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International Digital Organization for Scientific Research IDOSRJSR1.1.11.100
IDOSR JOURNAL OF SCIENTIFIC RESEARCH 9(1) 1-11, 2024.
https://doi.org/10.59298/IDOSRJSR/2024/1.1.11.100
Immunological Changes with Age and Innovative Approaches to
Bolster Immune Function in Older Adults
Nkiruka R Ukibe1, Chizoba Rita Dike 1, A.C. Ihim1, Ezinne G. Ukibe2, Blessing C. Ukibe2,
Victory Ezennia Ukibe3 and *Emmanuel Ifeanyi Obeagu4
1Department of Medical Laboratory Science, College of Health Sciences, Nnamdi Azikiwe University, Awka,
P. M. B 5025, Anambra State, Nigeria
2Department of Medicine, College of Health Sciences, Nnamdi Azikiwe University, Awka, P. M. B 5025,
Anambra State, Nigeria
3Department of Radiography and Radiological Sciences, Nnamdi Azikiwe University, Awka, P. M. B 5025,
Anambra State, Nigeria
4Department of Medical Laboratory Science, Kampala International University, Uganda
*Corresponding author: Emmanuel Ifeanyi Obeagu, Department of Medical Laboratory Science, Kampala
International University, Uganda, emmanuelobeagu@yahoo.com, ORCID: 0000-0002-4538-0161
ABSTRACT
Aging is accompanied by a progressive decline in immune function, known as immunosenescence, which renders
elderly individuals more susceptible to infections, reduced vaccine efficacy, and increased incidence of autoimmune
diseases and cancer. This decline in immunity is characterized by alterations in both innate and adaptive immune
responses, including reduced T-cell diversity, impaired function of antigen-presenting cells, and dysregulated
cytokine production. Additionally, inflammaging, a chronic low-grade inflammatory state, further contributes to
age-related immune dysfunction. Strategies aimed at enhancing immunity in aging individuals have garnered
significant attention. Promising interventions include lifestyle modifications encompassing regular exercise,
balanced nutrition, and adequate sleep, which can positively impact immune function. Furthermore, vaccination
strategies tailored for the elderly, such as high-dose vaccines or adjuvanted formulations, aim to bolster vaccine
efficacy. Immunomodulatory therapies, including supplementation with specific micronutrients and pharmacological
interventions targeting immune senescence, hold promise for rejuvenating immune responses in older individuals.
Understanding the mechanisms underlying immunosenescence and inflammaging is critical in developing targeted
approaches to enhance immunity in aging populations. A holistic approach combining lifestyle interventions,
vaccination strategies, and innovative immunomodulatory therapies holds potential for mitigating the impact of age-
related immune decline and improving overall healthspan in the elderly.
Keywords: Immunosenescence, Aging, Immunity, Inflammaging, Elderly, Immunomodulation, Vaccination
Strategies, Immune Rejuvenation, Geriatrics
INTRODUCTION
Immunology began with two significant discoveries
in the last quarter of the nineteenth century. The first
was Elias Metchnikff's (1845-1916) discovery of
phagocytic cells, which absorb and eliminate
pathogens. This created the groundwork for innate
immunity. The second breakthrough was the
identification of antibodies that neutralize microbial
poisons by Emil Behring (1854-1917) and Paul
Ehrlich (1854-1915). This served as the foundation
for acquired immunity [1]. The immune system
exists to protect the host from harmful environmental
agents, particularly pathogenic organisms such as
bacteria, viruses, fungus, or parasites [2]. Immunity
is an organism's ability to defend itself (and be
resistant) against antigens from both the external and
internal environment. In general, an antigen is any
molecule capable of generating an immune system
reaction [3-6]. Our body is endlessly exposed to
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microbial agents and environmental noxious
substances. These may cause serious illness, or
toxicity to the body; therefore, they must be
eliminated [7-10].
The innate immune system is the first line of host
defense, recognizing invading pathogens by sensing
pathogen-associated molecular patterns (PAMPs)
such as foreign polysaccharides, glycoproteins,
lipoproteins, and nucleic acids, as well as damaage-
associated molecular patterns (DAMPs) such as
molecules produced as a result of host cell and tissue
damage [11-16]. Four categories of protective
barriers are considered to be part of innate immunity:
physiologic (temperature, low pH, and chemical
mediators), endocytic and phagocytic, inflammatory,
and anatomic (skin and mucous membrane) [17].
Innate immune responses limit viral entry,
translation, replication and assembly, help identify
and remove infected cells and coordinate and
accelerate the development of adaptive immunity.
The development of adaptive immunity is accelerated
and coordinated by innate immune responses, which
also help detect and eliminate infected cells and
restrict viral entrance, translation, replication, and
assembly. Using a variety of PRRs, innate immune
cells, such as macrophages, monocytes, dendritic
cells, neutrophils, and innate lymphoid cells (ILCs),
such as natural killer (NK) cells, can trigger cells, and
inflammatory signaling pathways and immune
responses by identifying PAMPs, or damage-
associated molecular patterns [18].
Immunity and Aging
Aging is a multimodal process that happens at
multiple levels and involves significant, simultaneous
remodeling of organs, tissues, and cells, traditional
molecular biology techniques are limited in their
ability to address this complexity. Among the main
characteristics of aging are the loss of physiological
integrity, disruption of tissue homeostasis, and
growing decline of numerous biological systems,
including the immune system [19]. Full blood
counts, T and B cell counts including their subsets,
the amount of immunoglobulin in the serum, and the
presence of particular antibodies are among the tests
that clinicians may use to assess immune competency.
Although this gives a broad overview of some
immune system components, unless values are
significantly below the usual ranges, it does not give
a useful indicator of a person's ability to respond to a
particular threat. An older individual with immune
parameters within the normal levels who may have
immune dysfunction would thus not be easily
identified. So, any attempt to restore immunity in
older individuals first requires that simple methods of
assessment are derived to determine the effectiveness
of the process as a whole. These techniques of
assessment must: (i) be related to function; (ii) yield
results reasonably quickly; (iii) be relatively non-
invasive; and (iv) call for relatively basic equipment
[20]. Thymic atrophy, a decrease in peripheral blood
naïve cells, and a relative increase in memory cell
frequency are the results of aging-related declines in
adaptive immune responses. These changes result in
weakened immune responses to vaccinations,
heightened susceptibility to infectious illnesses,
reactivation of dormant viral infections like varicella-
zoster virus (VZV), commonly known as chickenpox,
and lowered cancer immunosurveillance.
Inflammaging, a long-term state of innate
immunological activation linked to aging, plays a role
in the pathophysiology of the chronic immune
disorders associated with aging [21]. Crucially, they
also demonstrated that increased levels of CCL2, a
chemokine that attracts immune cells and is
recognized by the proinflammatory monocytes'
CCR2 receptor, was a major factor in drawing those
detrimental innate immune cells to the injection site
in older people. Senescent tissue fibroblasts, which
are significantly more prevalent in the elderly,
produce CCL2. The well-known, largely
proinflammatory senescence-associated secretory
phenotype (SASP), which includes CCL2 secretion,
has been linked to a number of detrimental effects of
aging, such as tissue loss (sarcopenia), an increased
risk of cancer, and a collection of degenerative
changes in various organ systems collectively
referred to as "inflammaging." [21]. One
characteristic of immunological aging that is
sometimes referred to as "inflammageing" is an
unresolved systemic inflammation in the absence of
pathogens in elderly organisms. An imbalance in the
production of pro- and anti-inflammatory molecules
is a hallmark of inflammation, and it is a strong
predictor of death and chronic illnesses [20]. The
immune system undergoes change as we age. This
eventually results in a decrease in immunological
function, which raises the risk of contracting
infectious diseases, reduces the benefit of
immunizations, and increases the risk of developing
age-related inflammatory illnesses [22].
Immunosenescence
Immunosenescence, a process brought on by aging
that affects the makeup, number, and functionality of
immunological organs, immune cells, and cytokines,
is the immune system's decline in function.
Immunosenescence increases the risk of several age-
related illnesses, such as cancer, cardiovascular
disease, autoimmune disorders, neurodegenerative
diseases, and COVID-19, which can ultimately lead to
organ failure and death. Immunosenescence is defined
by age-related reductions in coping skills and
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concurrent elevations in proinflammatory state.
Stress and a persistent antigen load are the root
causes of this syndrome, which Claudio Franceschi
initially described in 200012 and dubbed
"inflammaging." Thymic involution has also been one
of the most notable and pervasive modifications. Both
the innate and adaptive immune systems are impacted
by immunosenescence, with some immune cell types
being more severely affected [23].
Immunosenescence is characterized by three main
features: (i) a decreased capacity to react to novel
antigens; (ii) the build-up of memory T cells; and (iii)
a persistent state of low-grade inflammation known
as "inflamm-aging." (Anna Aiello et al., 2019).
Although T cells are significantly impacted, this
multifactorial phenomenon—which Roy Walford
named "immunosenescence"—affects both acquired
and innate immunity [22].
Cellular Senescence
Cellular senescence is defined as the irreversible exit
from the cell cycle in response to various types of
stress such as uncontrolled DNA replication and
genotoxic, oxidative and inflammatory stress. SnCs
are characterized by evidence of telomere associate
foci (TAFs), senescence-associated distension of
satellites (SADS), senescence-associated
heterochromatin foci (SAHF), senescence-associated
ß-galactosidase (SA-ß-gal) and upregulation of at
least 1 cell cycle dependent kinase inhibitor (e.g.,
p16INK4a, p21Cip1). Most tissues, including
lymphoid tissues, have been observed to have an
increase in cellular senescence, a cell fate that affects
various cell types. Additionally, the quantity of
senescent cells (SnCs) rises with age. The slow
deterioration of a cell's capacity for division,
proliferation, and physiological function over time is
known as cellular senescence. Research on the
molecular mechanisms and signaling pathways that
influence aging has yielded significant findings for
scientists. In this context, we examine and synthesise
these novel developments on three fronts: molecular
(genomic instability, telomere dysfunction, epigenetic
modifications, proteostasis loss, autophagy
compromise, mitochondrial dysfunction), cellular
(cellular senescence, stem cell exhaustion, and
intercellular communication), and systemic
(deregulated nutrient sensing) [24].
Impact of Immunosenescence on both Innate and adaptive system
The innate immune system can also be stimulated by
the so-called internal GARBage system. Thus, a
heightened inflamm-aging state is produced as a
consequence of (1) dysfunctional mitochondria, (2)
defective autophagy/mitophagy (disposal of
dysfunctional organelles), (3) endoplasmic reticulum
stress, (4) activation of inflammasome by cell debris
and misplaced self-molecules, (5) defective
ubiquitin/proteasome system (misfolded/oxidized
proteins), (6) activation of DNA damage response, (7)
senescent T cells and their senescence-associated
secretory phenotype (SASP), and (8) age-related
changes in the composition of gut microbiota
(dysbiosis). Intracellular alterations including altered
autophagy, mitochondrial malfunction, and
modifications to DNA repair processes coincide with
chronic problems associated with aging.
Chronic low-grade inflammation
However, because of persistent low-grade
inflammation, immune cells are always kept on guard.
As demonstrated in the case of centenarians, anti-
inflammatory chemicals may, however,
counterbalance this state. As long as chronic low-
grade inflammation (also known as "inflamm-aging")
is kept under control, it can serve as an effective
defensive mechanism in response to lifelong antigenic
stress. Now once anti-inflammatory molecules are
missing, as is the case with age, it is evident how
detrimental this physiological state may be to the
entire body [25]. Age-related changes in adaptive
immunity are striking and can be boiled down to two
main issues: (1) bone marrow reorganization and the
pool's differentiation into the myeloid lineage, which
outnumbers the lymphoid compartment; and (2)
physiological thymic involution, which jeopardizes
the generation of naïve T cells. The combination of
these two elements can aid in the explanation of the
previously documented decline in lymphocytes'
ability to regenerate in older individuals when
compared to myeloid-derived cells. Elderly people are
more likely to contract infectious infections. The
elderly are more likely than their younger
counterparts to come with respiratory and urinary
tract infections, and their prognosis is often worse.
Mucosae's compromised barrier function and a
weakened humoral and cellular adaptive immune
response could be the causes of the elderly's
heightened vulnerability to pathogenic microbes.
Furthermore, the senescence of natural killer (NK)
cells may impact the immune system's homeostasis in
the elderly, raising the risk of viral infections and
cancer. Finally, aging-related cell dysfunctions that
result in an exhausted phenotype are a crucial aspect
of the immune system remodeling process. These
dysfunctions may hasten tissue damage and impair
modulatory mechanisms [26]. Apart from their
ability to carry out phagocytosis, neutrophils can also,
in certain situations, release a structure resembling a
mesh, known as neutrophil extracellular traps (NET),
which help to physically confine the pathogenic
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agent—mostly microorganisms—and make it easier
for it to come into contact with microbicidal peptides
and enzymes. Free radicals known as reactive oxygen
species (ROS) are created following oxidative bursts
in phagosomes and are essential to the phagocytes'
microbicidal activity. In actuality, ROS can actually
cause NET formation in addition to directly aiding in
the removal of microorganisms. In older adults,
neutrophils produce less free radicals (ROS) [26].
Thymic Involution
Thymic involution, which is characterized by a
decrease in TECs and an increase of adipose tissue
within the thymus, is one of the most common
changes during immune system senescence and
affects most vertebrates. The thymus plays a critical
role in the cellular immune system by generating T
lymphocytes, which are involved in anti-tumor
immunity, anti-viral, and anti-intracellular infections,
as well as the establishment of self-tolerance to avoid
autoimmune disorders. During the entire process of
thymus organogenesis, maturation, and involution,
gene regulation not only occurs at the transcriptional
level via transcription factors, but is also affected at
the post-transcriptional level by microRNA (miRNA)
transcripts. By producing T cells, the thymus
contributes significantly to the cellular immune
system. T lymphocytes fight viruses, tumors, and
intracellular infections. They also help build self-
tolerance to prevent autoimmune diseases. Gene
control happens at the transcriptional level through
transcription factors and at the post-transcriptional
level through microRNA (miRNA) transcripts during
the whole thymus organogenesis, maturation, and
involution process. One of the animal body's most
active organs is the thymus. It experiences three
processes: involution (cell senescence and apoptosis),
development (proliferation, differentiation, and
apoptosis), and organogenesis (cell migration,
proliferation, and differentiation). T lymphocytes are
also produced by the thymus to assist the cellular
immune system. Generally speaking, during thymus
growth, two key processes interact and regulate each
other: T lymphocyte development, which produces
functional T cells, and stromal cell development,
which, mostly through TECs, builds and maintains
the thymic milieu to promote T cell maturation.
These two procedures show sequential or gradual
developmental routes [27]. The organ grows quickly
during development, reaches its maximum size
during adolescence, and then starts to shrink with
aging; in humans and mice, involution starts as early
as birth and ends no later than the onset of puberty.
Reduced thymocyte counts and naïve T cell
production are the outcomes of this thymic
regression, which also involves reductions in thymic
bulk, loss of thymic structure, and disarray to thymic
architecture. Acute atrophy of the thymus can occur
during physiological stress situations, including
illness, pregnancy, and cancer treatments, in addition
to chronic age-related involution. Reduced naïve T
cell production and weakened host immunity are the
outcomes of stressed-induced thymic involution,
which is typically reversible and returns to normal in
terms of size and function after the insult is removed
[28]. But as we age, the thymus becomes less able to
create central tolerance, which leads to more self-
reactive T cells escaping to the periphery and taking
part in the inflammatory process. There have
historically been two schools of thinking about the
possible causes of diminished thymopoiesis associated
with aging. The first is the notion of impaired
hematopoietic stem cells, as older bone marrow (BM)
produces fewer hematopoietic stem cell (HSC)
progenitors. Consequently, the thymus shrinks as a
result of fewer early T-cell progenitors (ETP)
entering the thymus from the BM. Second is the idea
of a defect in stromal niches of the BM or thymus. As
a result, the thymic niche is where age-related
characteristics of thymic involution predominantly
manifest themselves before having an effect on the
formation of ETPs [29].
Effect of T cell development and repertoire diversity
A wide repertory of T-cell receptors (TCRs), the main
factor influencing the probability of identifying
certain antigens, is necessary for the best immune
response to a wide range of unknown antigens. Both
chronic dysfunctions, such as those linked to age-
associated involution and recurring infections, and
acute immunological insults, such as those brought
on by infections, stress, or antineoplastic therapy, can
seriously impair thymic function and T-cell output.
Highly varied TCR repertoires are necessary for
effective T-cell responses because they guarantee the
capacity to recognize a broad variety of Ags.
Together with diversity, repertoire diversity is
frequently employed as a metric of the effectiveness of
the immune response. Clonality, which describes the
quantity and frequency of detected TCRs within a
sample, is inversely correlated with repertoire
diversity [30].
Inflammaging
Chronic low-grade inflammation associated with
aging. In order to improve species survival, the
inflammatory process is a vital immunological
defensive mechanism in living things. As a first line
of defense against viruses, poisons, or allergens,
short-term, acute inflammation is triggered. Under
normal circumstances, the elimination of pathogens,
infected cells, and repair of damaged tissues to restore
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body homeostasis are made possible by the closely
coordinated actions of multiple defense components,
including immune cells, endogenous anti-
inflammatory agents, and tissue remodeling
processes. However, additional defense mechanisms
are activated to produce a long-term unresolved
immune response known as chronic inflammation
when this complex acute inflammatory response is
unable to end and continues. Leukocytes collected by
macrophages and lymphocytes, together with a
variety of other cellular constituents, are involved in
chronic inflammation, which usually presents itself
over an extended period of time in a low-grade way.
It is crucial to understand that alterations in the
cellular redox state and signaling pathways leading
to cell death are causally related to this chronic
inflammation. An ongoing state of systemic
inflammation is brought on by the deregulation of the
immune response, which is one of the main aging-
related alterations. Cytokines and chemokines are
two of the dysregulated proinflammatory mediators
that play a crucial role in the development of chronic
inflammation and the immunosenescence process
[31]. The components of inflammatory cytoplasmic
multiprotein complexes, known as inflammasomes,
are adaptor apoptosis-associated speck-like (ASC)
protein, procaspasce-1, and NLR protein 3 (NLRP3).
When an inflammasome is activated, it causes
caspase-1 expression and maintains the release of
proinflammatory cytokines, such as IL-1β and IL-18.
Two steps are needed for the NLRP3 inflammasome
to assemble: the priming phase and the activation
phase. Priming involves post-translational changes
that are required for NLRP3-mediated gene
expression and facilitates accurate inflammasome
assembly. In order to cleave pro-IL-1β into IL-1β
paired with pro-IL-18, NLRP3 polymerizes to ASC
upon inflammasome activation and recruits
procaspase-1. With caspase-1 activation and
proinflammatory cytokine release (IL-1β/IL-18) in
response to cellular injury, the NLRP3 inflammasome
is a crucial component of the innate immune system.
As was previously indicated, "inflammaging" (also
known as "inflammaging, inflammageing") refers to
the low-grade, persistent, asymptomatic
inflammation that happens during aging in the
absence of infection. Atherosclerosis, chronic renal
disease, cardiovascular disease, adult diabetes, and
Alzheimer's disease are just a few of the age-related
chronic diseases that are exacerbated by inflammation
and have a detrimental impact on health. The exact
reasons of inflammation are still mostly unknown, but
they include the following: (i) the release of damaged
cells and the accumulation of altered molecules
(microRNA, mitochondrial DNA, or histones), which
are recognized by immune system cells and cause
inflammation to activate and develop; (ii) the growth
of senescent cells that release pro-inflammatory
molecules into the blood; (iii) chronic stress
conditions; and (iv) disruption of autophagic
processes (v) alteration of the intestinal microbiota;
(vi) immunosenescence, defining the steady waning of
immune system function during ageing. Autophagy
and microbiome homeostasis are rhythmically
regulated by the biological clock and their
derangement cause several pathological processes
underlying inflammatory, metabolic, degenerative,
and neoplastic diseases. An in-depth discussion of the
involvement of these processes in pathological
conditions and in age-related diseases goes beyond
the boundaries of this review; therefore, we refer to
exhaustive articles already present in the
international scientific literature. Innate and adaptive
immune response, including humoral and cellular
immunity, decays during aging [32]. Increasing
evidence shows that ageing significantly affects all
cell compartments of the innate immune system.
Numerous neutrophilic functions, for instance,
phagocytic capacity, ROS production, and
intracellular killing ability, are impaired in the
elderly. Similarly, macrophage functions, including
phagocytic activity, cytokine and chemokine
secretion, antigen presentation, infiltration and
wound repair and antibacterial proficiency decline
with ageing. Age-related reduction in mast cell and
eosinophil and alterations of functional properties
have been demonstrated [33].
Contribution of inflammaging to age-related diseases
Decreases in cellular repair mechanisms occur with
aging and age-related diseases, resulting in the build-
up of damaged molecules, proteins, DNA, and lipids,
ultimately leading to the loss of effective cellular
function. Age-related decreases in the cell's ability to
undergo autophagic breakdown may also have an
impact on aging. Age-related slowdowns in both of
the primary intracellular protein degradation
mechanisms are accompanied by a physical decrease
in autophagy-related proteins, which adds to the
build-up of misfolded proteins and damaged
macromolecules within the cell. Conditions including
obesity, Crohn's disease, and cardiovascular disease
that are linked to elevated oxidative stress also slow
down cellular clearance and decrease autophagy,
which exacerbates the illness [34].
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Molecular Mechanism
Telomeres and cellular aging
The genomic regions at the ends of linear
chromosomes are called telomeres. In vertebrates,
telomeric DNA is composed of TTAGGG repeats
that are bound by a collection of proteins that control
their biological activities and prevent them from
being identified as DNA damage that would
otherwise set off a DNA damage response (DDR)
[35]. Many writers now acknowledge that TL is a
potent biomarker of aging and pathological disorders
linked to aging [36]. Furthermore, the molecular
mechanisms behind the age-related telomere
shortening phenomenon are still unclear and the
phenomenon itself is incredibly complex. Specifically,
it is still uncertain if telomeric aging is a reflection of
a process similar to the mitotic clock, or if it is a
biomarker of stress or a biological mechanism that
sends messages to the cell related to stress [37].
Because they shield chromosomes from end-to-end
fusions and chromosomal instability, telomeres are
essential for a variety of biological activities. At the
beginning of the end and in the middle of the
beginning: structure and maintenance of telomeric
DNA repeats and interstitial telomeric sequences.
The protective protein complex known as Shelterin
binds the repeated TTAGGG sequences that make up
telomeric DNA. This complex forms the telomere
structure, safeguarding chromosomal ends, together
with proteins that are involved in chromatin
remodeling [38]. The chromosomal ends' creation of
DNA loops, or T-loops, and the transcription of
telomeres to produce G-rich RNA, or TERRA, are
two important telomere characteristics. The 3′ end of
the G-rich strand projects as the G-overhang, a single
stranded overhang in the t-loop structure [39].
Increased susceptibility to infections
Respiratory infections
An age-related rise in viral infection susceptibility is
partly due to compromised innate and adaptive
immune systems. When it comes to respiratory viral
infections, such as influenza and severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2)
infections, aging is a significant factor that increases
morbidity and death [40-52]. The number of people
65 and older worldwide will nearly treble to 1.5
billion by 2050. (Population Division of the United
Nations Department of Economic and Social Affairs,
2020). This perspective calls for the creation of plans
aimed at enhancing the lives of the elderly [53-59].
Vaccine efficacy in the elderly
The best and most practical way to safeguard the
health of elderly patients is through preventive
medicine, and the best course of action is to vaccinate
against the most prevalent infectious diseases. Three
dangerous pathological conditions—seasonal
influenza, pneumococcus infection, and varicella
zoster virus reactivation—are major sources of
morbidity and mortality for elderly individuals, who
are more vulnerable than young persons [60]. The
elderly should also receive regular booster shots
against tetanus, diphtheria, pertussis, and polio. In
certain countries (Austria, France, Liechtenstein, and
Portugal), the booster intervals are shortened for
those over 65 due to a faster decline in antibodies with
age. The effectiveness of a vaccine, which measures
its ability to prevent a particular infection, and its
efficacy—a measure of its capacity to generally
improve an older person's health status and prevent
other related diseases—are what determine the value
of vaccines for the elderly. Therefore, it is crucial to
develop vaccination techniques that are especially
suited for the aged population, taking into account the
aging immune system and inflammatory processes in
both vaccine formulations and immunization
procedures. Geriatric medicine developed a number of
syndromes to manage the variability of elderly
physiology and pathophysiology. These syndromes
enable the elderly population to be categorized based
on their relative risk of developing certain diseases.
These include frailty, minor cognitive impairment,
and chronic obstructive pulmonary disease. The
elderly must receive vaccinations while maintaining a
careful balance between immunosenescence, which
reduces their receptivity to immunization, and
inflammation [60].
Currently recommended vaccines for the elderly
1. Influenza Vaccine
One of the primary causes of illness and mortality in
the elderly is influenza infection. Annual influenza
outbreaks are thought to cause between 3 and 5
million instances of severe illness and between
290.000 and 650.000 fatalities globally.
http://www.who.int/news-room/detail/14-12-
2017-up-to-650-000-people-die-of-respiratory
diseases-linked-to-seasonal). The World Health
Organization (WHO) considers annual influenza
vaccination to be the most effective method of
preventing influenza, and many high-income
countries prescribe it for elderly individuals.
However, compared to adults, the effectiveness of
influenza vaccinations in older patients is just 30–50%
[60]. There are now two varieties of influenza
vaccines available: live attenuated influenza vaccine
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(LAIV) and inactivated influenza vaccine (IIV).
Antigens from one strain of influenza B (the
Yamagata or Victoria lineages) and two subtypes of
the influenza A strain (H1N1 and H3N2) are included
in the trivalent inactivated influenza vaccine (TIV).
The production of quadrivalent inactivated influenza
vaccines (QIV), which contain two A strains and two
B strains and have now been licensed in some
countries, was spurred by the frequent observations
of co-circulation of the two B lineages and the
frequent mismatch between the vaccine component
and the circulating strains. LAIV is primarily advised
for use in children. It was originally licensed and used
in Russia and North America in 2003. Because of a
phenomenon known as "antigenic drift," which is the
spontaneous change of the surface proteins
neuraminidase (NA) and hemagglutinin (HA),
influenza viruses are always changing [60].
Numerous tactics have been used to enhance
influenza shots administered to senior citizens. These
include the formulation of the inactivated vaccine
using oil-in-water emulsion adjuvants, the
administration of the vaccine via intradermal rather
than intramuscular route, and the increase of the
vaccine antigen from 15 to 60 μg of HA protein per
dose. Though these responses do not reach the
magnitude of those induced by the standard dose
vaccine in young adults, the high dose vaccine has
been linked to a stronger immune response and better
effectiveness than the regular dose flu vaccine in older
people. The high dose vaccine contains four times the
amount of HA antigen compared to the traditional
formulation [60].
2.Pneumococcal vaccine
Blood or cerebrospinal fluid are examples of
ordinarily sterile sites where the presence of the
bacteria is known as invasive pneumococcal disease
(IPD), which is caused by Streptococcus pneumoniae,
the most often isolated agent of community-acquired
pneumonia. The incidence of pneumococcal illness
rises sharply in those over 65, with the condition most
common at the extremes of age. Immunosenescence
and co-morbidities make people more vulnerable to
pneumococcal illness in particular and community-
acquired pneumonia in general. Therefore, it is
advised that older adults have a pneumococcal
immunization. The 23-valent pneumococcal
polysaccharidic vaccine (PPV23) contains 25 μg of
purified pneumococcal polysaccharide per serotype;
the 13-valent conjugated vaccine (PCV13) contains
2.2 μg of each polysaccharide type, with the exception
of 4.4 μg of serotype 6B, conjugated to the non-toxic
mutant of diphtheria toxin CRM197 and 0.125 mg of
aluminum phosphate as an adjuvant. These are the
licensed pneumococcal vaccines. PCV13 is advised for
use in older populations even though it covers fewer
serotypes since it can cause a T-dependent response
and high titers of functional (opsonophagocytic)
antibodies. Even in the presence of comorbidities,
PCV13 has shown to be immunogenic and safe in the
elderly, however there is currently no information on
the effectiveness of the vaccination in this population.
Vaccination techniques using PCV13 priming and
PCV13 or PPV23 boosting are also advised for the
older population, as the immune response to PPV23
is not ideal in this age group and repeated
administration of PPV23 may also cause
hyporesponsiveness.
3. Herpes zoster vaccine
The latent varicella zoster virus reactivates to cause
herpes zoster (HZ, or shingles). When elements of
cell-mediated immunity are weakened by illness,
medication side effects, or aging, viral reactivation
occurs. In actuality, the incidence of HZ increases
with age and is higher in the elderly (3–5/1000
persons/year in the general population, 8–12/1000
persons/year in adults over 80). With 65/100.000
hospitalizations in adults over 80 years of age, HZ is
a leading cause of hospitalization for the elderly. It
can also be compounded by postherpetic neuralgia,
which causes debilitating pain after the rash goes
away, or by eye involvement, which occurs when the
ophthalmic branch of the trigeminal nerve is afflicted.
Currently, there are two licensed shingles vaccines:
the subunit zoster vaccine (GSK) and the HZ live
attenuated zoster vaccine (Zostavax, Merck). The
Oka strain, an attenuated VZV strain that was first
obtained in Japan and is also used in children to
prevent chickenpox, albeit at a lesser dose, is included
in the live attenuated vaccine in at least 20.000 PFU
form. The VZV glycoprotein E (gE), a significant part
of the viral surface, is present in 50 μg of the
recombinant subunit vaccine. This vaccine is
prepared with the AS01B adjuvant, which is made up
of 50 μg of Quillaja saponaria Molina, fraction 21, and
50 μg of 3-O-desacyl-4′-monophosphoryl lipid A
from Salmonella minnesota. The live attenuated
vaccine received a license in the United States in
2006. A recent meta-analysis evaluated the vaccine's
performance and found that it was 33% effective in
preventing HZ, but 74% effective in avoiding
hospitalizations for HZ and 57% effective in
preventing postherpetic neuralgia. After receiving its
license in 2017, the recombinant vaccine showed a
97% efficacy in preventing HZ in adults 50 years of
age and above. However, it had a moderate
reactogenicity, causing discomfort at the injection
site in 79.1% of recipients and myalgia in 46.3%.
According to immunological study, older persons
www.idosr.org Ukibe et al
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(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
who receive the recombinant vaccination that
contains AS01B adjuvant experience a strong and
long-lasting memory response.
Strategies for enhancing immunity in aging
We propose that lifestyle variables, including food
and exercise regimens, have a major impact on the
immunosenescence and inflammatory processes.
Consequently, the danger of maladaptive
immunological aging is reduced and effective immune
aging is supported by targeted nutrition and regular
exercise training.
1. Diet and nutrition
2. Physical activity
Engaging in regular physical activity has been linked
to several significant health advantages, such as a
lower risk of mortality, sarcopenia, diabetes, stroke,
and cardiovascular illnesses. However, the amount
and intensity of physical activity decrease sharply
with age, and most older persons do not achieve the
minimum standards of 150 minutes per week of
aerobic exercise set by the World Health
Organization (WHO). Lower levels of pro-
inflammatory cytokines including IL6 and TNFα
have been linked to exercise in older persons. Several
methods allow physical activity to have an anti-
inflammatory impact. Age-related increases in fat
mass have been linked to low-grade chronic
inflammation. Immune system performance is
directly impacted by physical activity, even in elderly
persons. According to a recent study, adults who
engage in high levels of physical activity had better
thymic output. This impact is probably due to an
improved thymic microenvironment, which includes
higher levels of IL7 and lower levels of IL6.
Furthermore, we discovered that the active older
adults maintained a frequency of peripheral naïve T
cells, which was linked to greater serum IL15 levels.
All things considered, engaging in regular physical
activity is a non-invasive, largely cost-neutral anti-
aging and anti-immunesenescence treatment.
CONCLUSION
The age-related decline in immune function poses
significant challenges to the health and well-being of
the elderly population. Immunosenescence and
inflammaging contribute to increased susceptibility
to infections and reduced responsiveness to
vaccinations. However, research efforts focused on
understanding the underlying mechanisms have
paved the way for the development of strategies to
enhance immunity in aging individuals. Interventions
targeting lifestyle modifications, specialized
vaccination approaches, and innovative
immunomodulatory therapies hold promise for
rejuvenating immune responses in the elderly. A
multidisciplinary approach that integrates knowledge
from immunology, geriatrics, and nutrition sciences
is crucial in devising effective strategies to counteract
age-related immune decline and promote healthy
aging. Implementation of these strategies may lead to
improved health outcomes and quality of life in aging
populations.
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CITE AS: Nkiruka R Ukibe, Chizoba Rita Dike, A.C. Ihim, Ezinne G. Ukibe, Blessing C. Ukibe, Victory
Ezennia Ukibe and Emmanuel Ifeanyi Obeagu (2024). Immunological Changes with Age and Innovative
Approaches to Bolster Immune Function in Older Adults. IDOSR JOURNAL OF SCIENTIFIC
RESEARCH 9(1) 1-11. https://doi.org/10.59298/IDOSRJSR/2024/1.1.11.100IDOSR JOURNAL OF
SCIENTIFIC RESEARCH 9(1) 1-11. https://doi.org/10.59298/IDOSRJSR/2024/1.1.11.100
