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Antrum mucosa in H. pylori-associated gastritis: CD68+ macrophages in infiltrate of lamina propria, magnitude ×400.
Source publication
Helicobacter pylori is one of the most common causes of chronic gastritis. With the development of the disease cellular inflammatory infiltrates composed of lymphocytes, plasma cells, and macrophages are formed in epithelium and lamina propria of the stomach. These cells are capable of secreting a number of active substances, including inducible ni...
Citations
... This adaptation by H. pylori is crucial for its persistent colonization and chronic infection in the host. (Calam et al., 1997;Fowler et al., 2006;Cullen et al., 2011;Moran, 2008;Wang et al., 2000;Ciesielska et al., 2021;Cherdantseva et al., 2014) (Continued) (Akazawa et al., 2013;Sewald et al., 2011;Ji et al., 2020) (Continued) Fan et al. 10.3389/fcimb.2024.1342913 Frontiers in Cellular and Infection Microbiology frontiersin.org ...
... H. pylori's pathogenic factors, including urease and outer membrane lipopolysaccharides, stimulate the expression of iNOS, facilitating the conversion of L-arginine to nitric oxide (NO). This process leads to LPS+IFNg-induced mitochondrial dysfunction and inhibition of the electron transport chain, intensifying the inflammatory response and impeding the transition from M1 to M2 macrophages (Cherdantseva et al., 2014). In vivo experiments have shown that inhibiting NO production can improve mitochondrial function and reprogramming towards the M2 macrophage phenotype (Van den Bossche et al., 2016), underscoring the role of NO as a critical regulator of M1 macrophage activity. ...
Helicobacter pylori (H. pylori) is the predominant pathogen causing chronic gastric mucosal infections globally. During the period from 2011 to 2022, the global prevalence of H. pylori infection was estimated at 43.1%, while in China, it was slightly higher at approximately 44.2%. Persistent colonization by H. pylori can lead to gastritis, peptic ulcers, and malignancies such as mucosa-associated lymphoid tissue (MALT) lymphomas and gastric adenocarcinomas. Despite eliciting robust immune responses from the host, H. pylori thrives in the gastric mucosa by modulating host immunity, particularly by altering the functions of innate and adaptive immune cells, and dampening inflammatory responses adverse to its survival, posing challenges to clinical management. The interaction between H. pylori and host immune defenses is intricate, involving evasion of host recognition by modifying surface molecules, manipulating macrophage functionality, and modulating T cell responses to evade immune surveillance. This review analyzes the immunopathogenic and immune evasion mechanisms of H. pylori, underscoring the importance of identifying new therapeutic targets and developing effective treatment strategies, and discusses how the development of vaccines against H. pylori offers new hope for eradicating such infections.
... However, in the scenario of HP negative gastritis cases, mild chronic inflammation was predominant with 82.6%. Many studies indicate increased lymphocytic infiltration with H.pylori associated gastritis [12][13][14] , but some of the literature also contradicts the above mentioned findings 15 . ...
... Similarly, previous literature strongly indicates the association of metaplasia with infectious gastritis, which contradicted the findings of our research. Only one patient (1.4%) had metaplastic change in HP positive gastritis group 11,12,13,16,17 . ...
Background and Objectives: The intention of this study was to compare the histopathological features of helicobacter pylori positive gastritis (HPPG) and helicobacter pylori negative gastritis (HPNG) reported at Department of Pathology, Sahiwal Medical College & Allied Hospitals, Sahiwal, Pakistan. Methodology: It was a descriptive cross-sectional study carried out at Histopathology Section, Department of Pathology, Sahiwal Medical College, Sahiwal. It included all the gastritis cases proven on histopathology on endoscopic biopsies sent from Gastroenterology Department GHAQTH Sahiwal from January 2020 to December 2020. HPPG and HPNG cases were sorted and the data was analyzed with help of SPSS version 20. Chi-square test was used to find p-value and the value of p <0.05 was taken as significant. Results: In all 95 cases of gastritis were identified out of which 75.8% were HPPG and 24.2% were HPNG. More than 90% of HPPG had moderate and severe chronic inflammation in the biopsies as compared to only 17% in cases of HPNG and the difference was significant statistically (p < 0.00001). About 98% cases of HPPG showed activity as compared to 8.7% cases of HPNG and this difference was statistically significant (p < 0.00001). Lymphoid follicles were seen in biopsies of 34.7% cases of HPPG while this feature was absent in all HPNG cases and this difference was statistically significant (p= 0.00994). No statistically significant variance was found in relation to age group, gender, location of biopsy and intestinal metaplasia in our study. Conclusion: HPPG more frequently shows moderate/severe chronic inflammation, activity and lymphoid follicles in endoscopic biopsies as compared to HPNG. Our data, first of its kind from Sahiwal, is in accordance with the available literature. Keywords: Helicobacter pylori, gastritis, endoscopic biopsy, histopathology
... H. suis might, similar to H. pylori, evoke a local oxidative stress reaction whereby superoxide radicals are produced by the bacteria themselves, and ROS and inducible nitric oxide synthase (iNOS) production by gastric epithelial cells and immune cells is induced [60][61][62][63][64][65][66][67]. The presence of moderate levels of ROS activates transcription factors that increase the antioxidant potential, thus diminishing damage by oxidative stress [51]. ...
The exact etiology of Parkinson’s disease (PD) remains largely unknown, but more and more research suggests the involvement of the gut microbiota. Interestingly, idiopathic PD patients were shown to have at least a 10 times higher prevalence of Helicobacter suis (H. suis) DNA in gastric biopsies compared to control patients. H. suis is a zoonotic Helicobacter species that naturally colonizes the stomach of pigs and non-human primates but can be transmitted to humans. Here, we investigated the influence of a gastric H. suis infection on PD disease progression through a 6-hydroxydopamine (6-OHDA) mouse model. Therefore, mice with either a short- or long-term H. suis infection were stereotactically injected with 6-OHDA in the left striatum and sampled one week later. Remarkably, a reduced loss of dopaminergic neurons was seen in the H. suis/6-OHDA groups compared to the control/6-OHDA groups. Correspondingly, motor function of the H. suis-infected 6-OHDA mice was superior to that in the non-infected 6-OHDA mice. Interestingly, we also observed higher expression levels of antioxidant genes in brain tissue from H. suis-infected 6-OHDA mice, as a potential explanation for the reduced 6-OHDA-induced cell loss. Our data support an unexpected neuroprotective effect of gastric H. suis on PD pathology, mediated through changes in oxidative stress.
... Polyphenols, an example of flavonoids, are an important factor for gastroprotective activity and are substances that have been showing good activity against urease [74] , acting in an antioxidant way and consequently contributing to antiulcer activity since urease, H. pylori and arginase are inhibitors of macrophage phagocytic function and are related to stimulating the activity of lymphocytes and neutrophils with a high production of ROS, which affects the transduction of signals from the gastric mucosal epithelium and allows the formation of neoplastic mass [75][76][77][78] . With regard to other applications, E. umbellata latex has the potential for obtaining molluscicidal agents that can be used to control schistosomiasis mansoni due to the presence of triterpenes [9] . ...
... Furthermore, in the infected mucosa, nitric oxide is generated in the lymphocytes, macrophages, and gastric cells by inducible nitric oxide synthetase. This results in the production of the highly toxic peroxynitrite, and the consequent damage to proteins and DNA through the generation of nitrotyrosine and DNA adducts, respectively (Sakaguchi et al., 1999;Cherdantseva et al., 2014;Valenzuela et al., 2015). However, this oxidative stress induced by H. pylori infection of gastric cells can be attenuated through the production of scavenger molecules, such as metallothionines, a role for which has been demonstrated in animal models (Mita et al., 2008). ...
Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a "type I carcinogen." Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa's cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett's esophagus, but also asthma and allergies, through discussion of the "hygiene hypothesis. " This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa's cascade, to improve prevention and therapy of gastric carcinoma.
... H. suis might, similar to H. pylori, evoke an oxidative stress reaction whereby superoxide radicals are produced by the bacteria themselves, and reactive oxygen species (ROS) and inducible nitric oxide synthase (iNOS) production by gastric epithelial cells and inflammatory cells (i.e. monocytes/macrophages, neutrophils, and lymphocytes) is induced Flahou et al., 2011;Cherdantseva et al., 2014). ...
... Elevated levels of this mediator are associated with inflammation and injury to the stomach mucosa [55]. Also, NO metabolites are associated with gastric carcinogenesis [56]. A molecular docking study has shown that silybin has a high theoretical affinity for iNOS, showing that it can make versatile and efficient binding to the enzyme. ...
Aims
Silibinin is the major component of flavonolignans complex mixture (Silymarin), which is obtained from Silybum marianum (L.) Gaertn. Despite several reports about silibinin, little is known about its effects on gastric diseases. Then, the present study aims to evaluate the silibinin effect against Helicobacter pylori infection, gastric tumor cells and immunomodulation.
Main methods
The anti-H. pylori effect was performed on 43,504 and 43,629 strains by minimum inhibitory concentration (MIC) determination, observing morphological alterations by scanning electron microscopy and in silico evaluation by molecular docking. Immunomodulatory activity (Interleukins-6 and 10, TNF-α and NO inhibition) was determined in H. pylori-stimulated macrophages and the cytotoxic activity on gastric adenocarcinoma cells prior and after metabolization by S9 fraction.
Key findings
Silibinin showed anti-H. pylori activity with MIC of 256 μg/mL, promoted important morphological changes in the bacterial cell wall, as blebs and clusters, suggesting interaction with Penicillin Binding Protein (PBP) subunits. Immunomodulatory potential was observed at 50 μg/mL with the inhibition of produced cytokines and NO by H. pylori-stimulated macrophages of 100% for TNF-ɑ, 56.83% for IL-6, and 70.29% for IL-10 and 73.33% for NO. Moreover, silibinin demonstrated significant cytotoxic activity on adenocarcinoma cells (CI50: 60.17 ± 0.95 μg/mL) with a higher selectivity index (SI: 1.52) compared to cisplatin. After metabolization silibinin showed an increase of cytotoxicity with a CI50 six-fold decrease (10.46 ± 0.25).
Significance
The use of silibinin may become an important alternative tool in the prevention and treatment of H. pylori infection and, consequently, in gastric cancer.
... Many risk factors have been defined for H. pylori infection, such as living in crowded environments, poor hygiene conditions, low socioeconomic status, poor nutrition, smoking, alcohol consumption, blood groups, social status, and age [2,3]. H. pylori has been linked to chronic active gastritis, peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma [4][5][6][7]. According to 2015 data from 100,000 people in Turkey, the incidence of stomach cancer was reported to be 14.2% in men and 6.3% in women [8]. ...
Introduction
Helicobacter pylori (H. pylori) is a type of bacteria that affects more than half of the world’s population and has been associated with gastritis. The relationship between H. pylori and obesity is controversial. Laparoscopic sleeve gastrectomy (LSG) is the most commonly used surgery for morbidly obese patients. The aim of this study was to investigate the rate of H. pylori in patients undergoing LSG.
Methods
Biopsy specimens of 32,743 patients who underwent esophagogastroduodenoscopy (EGD) and resection materials from 1257 patients who underwent LSG were examined histopathologically. The relationships between body mass index (BMI), age, gender, H. pylori infection, and intestinal metaplasia (IM) were investigated in patients with gastritis.
Results
In patients undergoing EGD, the association of H. pylori infection was found to be increased in males and the elderly (p < 0.001). The presence of gastritis and IM was significantly higher with H. pylori infection (p < 0.001 and p = 0.001, respectively). H. pylori infection was significantly higher in patients over the age of 41 years (p < 0.001). There was no significant difference between the results of H. pylori before and after LSG surgery (p = 0.923). The presence of H. pylori together with gastritis and IM was found to be significant (p < 0.001).
Conclusions
H. pylori infection increases with age. No significant difference was found in the examination for H. pylori before and after LSG surgery. In addition, no relationship was found between H. pylori and excess weight. However, due to the low average age of patients who underwent LSG, further studies are needed in this area.
... Mucosal migration of macrophages and lymphocytes producing iNOS also takes place. 179 Once lymphocytes, plasma cells, and macrophages are chemotactically triggered, iNOS is generated, as seen by elevated concentrations of NO metabolites in Hp-infected patients. 42,43,179,180 Chronic antigenic stimulation, such as by superficial bacterial LPS upon exposure to inflammatory cells, regulates iNOS expression in order to generate NO and RNS. ...
... 179 Once lymphocytes, plasma cells, and macrophages are chemotactically triggered, iNOS is generated, as seen by elevated concentrations of NO metabolites in Hp-infected patients. 42,43,179,180 Chronic antigenic stimulation, such as by superficial bacterial LPS upon exposure to inflammatory cells, regulates iNOS expression in order to generate NO and RNS. This is especially true with peroxynitrite, which attempts to eliminate the pathogen, 149,179,180 although Hp could escape such attacks. ...
... 42,43,179,180 Chronic antigenic stimulation, such as by superficial bacterial LPS upon exposure to inflammatory cells, regulates iNOS expression in order to generate NO and RNS. This is especially true with peroxynitrite, which attempts to eliminate the pathogen, 149,179,180 although Hp could escape such attacks. ...
Nitric oxide (NO), a small molecule generated ubiquitously, targets a plethora of tissues to regulate both physiological and pathophysiological functions. NO overproduction, stimulated by microenvironmental conditions, is the main component that dysregulates the tight balance between its beneficial and damaging roles in ocular homeostasis. Considering the protective functions of NO against glaucoma, its endogenous release facilitates aqueous humor drainage and regulates ocular blood flow, maintaining a normal intraocular pressure. NO overproduction generates free radicals, such as peroxynitrite, which induce a vicious circle of vascular disharmony and dysregulation, transient ischemia, nitrosative stress, neuronal degeneration, and permanent glaucomatic injury. Helicobacter pylori (Hp) is considered a burdening factor of glaucoma. NO overproduction and possible systematic dispersion in Hp infection (Hp‐I) could suggest a potential pathophysiological bridge between these conditions. In this review, we aim to elucidate the role of NO in glaucoma with respect to Hp‐I, with the aim to stimulate further studies.
... CG develops subsequent to the infiltration of lymphocytes and plasma cells in the gastric mucosa. Patients with CG may exhibit atrophy and intestinal metaplasia in the gastric mucosa in later stages of the condition (3,4). The incidence of CG is high in the Chinese population, with ~30% afflicted chronic gastritis. ...
The current study aimed to evaluate the clinical value of using blue laser imaging combined with magnifying endoscopy in the diagnosis of chronic gastritis (CG). The groups used were as follows: The white light group (WLI, control group), linked color imaging group (LCI, observation group 1), blue laser imaging (BLI)-bright (brt) group (BLI-brt; observation group 2), BLI + magnified imaging (ME) group (observation group 3). WLI mode initially allowed the observation of mucosal suspicious lesions on the gastric mucosa. These lesions were photographed and the mode was changed to LCI, BLI-brt and BLI + ME. Different observational patterns were compared between modes to diagnose various grades of chronic gastritis. No significant differences were observed in the baseline information of enrolled patients. The LCI mode diagnosis rate was higher for Helicobacter pylori (HP) infection than in any other mode. LCI exhibited a high diagnostic rate for HP, BLI-brt exhibited a high diagnostic rate for atrophy and BLI/BLI + ME exhibited a high diagnostic rate for intestinal metaplasia and intraepithelial neoplasia. All modes exhibited higher diagnostic rates compared with the WLI mode. The pathological HP diagnosis rate (consistency) of HP infection was the greatest in the LCI group (endoscopic findings and pathological consistency). The BLI-BRT mode exhibited the highest pathological diagnosis rate for atrophic gastritis and the BLI/BLI + ME mode exhibited the highest diagnostic rate for intestinal metaplasia and low-grade intraepithelial neoplasia.
