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RvE1 protected the disruption of cytoskeletal structure caused by CSE or acrolein in RAW264.7 cells. RAW264.7 cells were incubated with RvE1 or vehicle for 30 min, CSE (10%, A) or acrolein (10 μM, B) was then added, followed by incubation for 4 h. Representative florescent images with TRITC-labeled phalloidin are shown. Cell size was measured under a microscope after collecting 30 cells from each culture. Open bar: vehicle-treated cells. Dark gray bar: CSE- or acrolein-treated cells. Light gray bar: acrolein-treated cells in the presence of RvE1 (10 nM). The line in each column indicates the mean value. *P < 0.05 vs. control. †P < 0.05 vs. CSE or acrolein alone (n = 4). Scale bar: 25 μM.
Source publication
Cigarette smoke (CS) induces oxidative stress, which disables macrophage function. In this study, we examined whether Resolvin E1 (RvE1), a pro-resolving mediator known to enhance macrophage functions, attenuates the damage of macrophages by CS extract (CSE) induced oxidative stress. RvE1 blocked p47phox translocation to plasma membrane induced by...
Contexts in source publication
Context 1
... in an impaired phagocytic function in macrophages [8]. Therefore, the attenuation of CSE impaired-phagocytic function by RvE1 prompted us to examine whether RvE1 was capable of restoring CSE induced- actin modification. Polymerized actin fibers were stained with phal- loidin and analyzed by laser scanning confocal microscopy. As shown in Fig. 3(A), 4 h-CSE exposure evoked a retraction in the leading- edge that occurred simultaneously with the reduction of cell size. The mean size of the CSE-exposed RAW264.7 cells was 66 ± 17% that of the control cells. When we treated RAW 264.7 cells with 10 nM RvE1 30 min prior to CSE-exposure, CSE-induced cytoskeletal disrup- tion was ...Context 2
... mean size of the CSE-exposed RAW264.7 cells was 66 ± 17% that of the control cells. When we treated RAW 264.7 cells with 10 nM RvE1 30 min prior to CSE-exposure, CSE-induced cytoskeletal disrup- tion was recovered to 87 ± 21% that of the control cells. Stabilizing actions of RvE1 were also observed when the stimulus was replaced with acrolein ( Fig. ...Context 3
... coli [21]. Therefore, we speculated that RvE1 could ameliorate the impaired phagocytosis in CSE-treated RAW264.7 cells. As we expected, RvE1 at a concen- tration of 10 nM concentration restored the phagocytic function of macrophages ( Fig. 2(B) and (C)), and showed protective effects against the disruption of cytoskeletal structure caused by CSE (Fig. ...Similar publications
Cigarette smoking is the most commonly encountered risk factor for chronic obstructive pulmonary disease (COPD). However, it is not the only one and there is consistent evidence from epidemiologic studies that nonsmokers may develop chronic airflow limitation. A history of tuberculosis has recently been found to be associated with airflow obstructi...
Background:
The present study was done to compare serum heart type-fatty acid-binding protein (H-FABP) levels in patients with stable chronic obstructive pulmonary disease (COPD) and healthy subjects and address the correlation of this marker with airflow limitation and health-related quality of life using the COPD assessment test (CAT).
Material...
Background
The incidence and prevalence of chronic kidney disease (CKD) continue to rise worldwide. Increasing age, diabetes, hypertension, and cigarette smoking are well-recognized risk factors for CKD. Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation leading to airway obstruction and parenchymal lung de...
The recruitment and activation of inflammatory cells into the respiratory system is considered a crucial feature in the pathophysiology of chronic obstructive pulmonary disease (COPD). Since dendritic cells (DCs) have a pivotal role in the onset and regulation of immune responses, we investigated the effect of modulating of DC subsets on airway inf...
COPD is a chronic inflammatory disease of the lungs associated with an abnormal inflammatory response to noxious particles, the most prevalent of which is cigarette smoke. Studies have demonstrated that cigarette smoking is associated with activation of the bone marrow, and chronic smoking can lead to the inflammatory changes seen in COPD. Due to t...
Citations
... Успешное разрешение воспалительного процесса неизменно связано с вовлечением механизмов, направленных на предотвращение нежелательного рекрутинга и трансэндотелиальной миграции нейтрофилов Таблица 1. Краткая характеристика основных биологических эффектов резолвинов на таргетные клеточные популяции Table 1. Summary of the main biological effects of resolvins on target cell populations Типы резолвинов и их эффекты Нейтрофилы • RvE1 -регуляция экспрессии интегрина CD18, подавление сигнальных путей AKT и MAPK, ингибирование образования радикалов и трансэпителиальной/трансэндотелиальной миграции [ 16,17 ] • RvD1 -подавление хемотаксиса, миграции, агрегации и адгезии нейтрофилов [ 18 ] • RvD2 -регуляция экспрессии CD62, подавление хемотаксиса, миграции и агрегации нейтрофилов [ 19 ] • RvT -дозозависимое подавление образования внеклеточных нейтрофильных ловушек (NET) и миграции нейтрофилов [ 12 ] Клетки моноцитарно-макрофагального ряда • RvE1 -подавление экспрессии субъединицы HO-1 и NADPH-оксидазы P47PHOX регуляция экспрессии L-селектина и интегрина CD18 [ 20 ] • RvD1 -индукция поляризации популяции макрофагальных клеток от провоспалительных M1-макрофагов к противовоспалительным M2-макрофагам, подавление экспрессии CD11B, CD68 и GR-1 [ 21 ] • RvD2 -регуляция фактора транскрипции IRF4 [ 22 ] • RvD3 и RvD5 -стимуляция фагоцитарной активности субпопуляции макрофагов M2 [ 23 ] • RvT2 -стимулирование фагоцитоза NET посредством сигнального пути цАМФ и АМФ-активируемой протеинкиназы (AMPK) [ 12 ] Клетки лимфоидного ряда • RvD1 -подавление продукции IgE плазматическими клетками, подавление дифференцировки Th17 с восстановлением противовоспалительного паттерна соотношения Th17/Treg, ингибированием секреции IL-17, усиление миграции NK-клеток, снижение секреции TNF-α и IL-6 [ 24,25 ] • RvD2 -снижение количества CD4 + -T-лимфоцитов, подавление секреции провоспалительных цитокинов [ 26 ] • RvD5 -подавление дифференцировки и пролиферации Th17 [ 27 ] Эндотелиальные клетки • RvD1 -активация сигнальных путей ENAC и Na + /K + -АТФазы с блокированием взаимодействия между эндотелиальными клетками и клетками моноцитарно-макрофагального ряда [ 28 ] • RvD2 -регуляция выработки NO и экспрессии рецепторов адгезии на эндотелиальных клетках [ 29 ] • RvE1 -подавление экспрессии белков pro-IL-1β и генерации комплексов воспаления NLRP3 [ 30 ] Клетки фибробластического ряда • RvE1 -подавление пролиферации клеток фибробластического ряда in vitro и in vivo [ 31 ] , подавление активации клеток фибробластического ряда за счет снижения ядерной транслокации NF-κβ [ 32 ] • RvD1 -активация пролиферации фибробластов, подавле- ...
Представлены данные, касающиеся современных представлений о разрешающей фазе воспаления и роли резолвинов в качестве нового класса эндогенных веществ — производных омега-3-полиненасыщенных жирных кислот (эйкозапентаеновой и докозагексаеновой), применительно к хроническому воспалению тканей пародонта. Основываясь на первоначальных исследованиях резолвинов, а также на данных исследований in vitro и in vivo в экспериментальных моделях пародонтита, в систематизированном виде представлены данные в отношении ключевых биологических эффектов резолвинов, а также их влияния на течение воспалительного ответа и резорбцию костной ткани альвеолярного отростка челюсти. С учетом выявленных эффектов и основных патогенетических механизмов, вовлеченных в развитие пародонтита, систематизированы данные в отношении потенциальных ключевых точек приложения резолвинов на течение пародонтита, а также обозначены перспективные направления дальнейших исследований.
The literature review presents data on modern ideas about the resolving phase of inflammation and the role of resolvins as a new class of endogenous substances — derivatives of omega-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid), in relation to chronic inflammation of periodontal tissues. Based on initial studies of resolvins, as well as data from in vitro and in vivo studies in experimental models of periodontitis, data are presented in a systematic way regarding the key biological effects of resolvins, as well as their impact on the course of the inflammatory response and bone resorption of the alveolar process of the jaw. Taking into account the identified effects and the main pathogenetic mechanisms involved in the development of periodontitis, data on potential key points of application of resolvins on the course of periodontitis are systematized, as well as promising areas for further research are identified.
... The finding that plasma RvE1 was elevated in smokers has not been previously reported and may be a homeostatic response to counter inflammation that is known to occur in smokers [33]. There is some support for this argument from the work by Takamiya et al. who showed that RvE1 maintained macrophage function under cigarette smoke induced oxidative stress [34]. ...
Background
Inadequate inflammation resolution may contribute to persistent low-grade inflammation that accompanies many chronic conditions. Resolution of inflammation is an active process driven by Specialized Pro-resolving Mediators (SPM) that derive from long chain n-3 and n-6 fatty acids. This study examined plasma SPM in relation to sex differences, lifestyle and a broad range cardiovascular disease (CVD) risk factors in 978, 27-year olds from the Australian Raine Study.
Methods
Plasma SPM pathway intermediates (18-HEPE, 17-HDHA and 14-HDHA), and SPM (E- and D-series resolvins, PD1, MaR1) and LTB4 were measured by liquid chromatography-tandem mass spectrometry (LCMSMS). Pearson correlations and multiple regression analyses assessed relationships between SPM and CVD risk factors. Unpaired t-tests or ANOVA assessed the effect of sex, smoking, unhealthy alcohol consumption and obesity on SPM.
Results
Women had higher 17-HDHA (p = 0.01) and lower RvE1 (p < 0.0001) and RvD1 (p = 0.05) levels compared with men. In univariate analysis, obesity associated with lower RvE1 (p = 0.002), whereas smoking (p < 0.001) and higher alcohol consumption (p < 0.001) associated with increased RvE1. In multiple regression analysis, plasma RvE1 was negatively associated with a range of measures of adiposity including BMI, waist circumference, waist-to-height ratio, abdominal subcutaneous fat volume, and skinfold thicknesses in both men and women.
Conclusion
This population study suggests that a deficiency in plasma RvE1 may occur in response to increasing adiposity. This observation could be relevant to ongoing inflammation that associates with CVD and other chronic diseases.
... Cigarette smoke has been shown to impair macrophage phagocytic activity and activate macrophages to produce chemotactic molecules, which recruit additional inflammatory cells (neutrophils, monocytes, and lymphocytes) and perpetuates inflammation and oxidative stress. 8 Macrophages produce inflammatory mediators such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1 β (IL-1β). 9 Studies have indicated that rats exposed to e-cigarette aerosol exhibit similar vascular endothelial dysfunction as those exposed to t-cigarettes in vascular endothelial function. ...
With the advancement of society, electronic cigarettes (e-cigarettes) have gained popularity among a growing number of individuals. While numerous toxicological studies have suggested that e-cigarettes are a safer alternative to traditional cigarettes, there is also a body of literature presenting contrasting findings. This in vitro study aimed to compare the effects of e-cigarettes and tobacco cigarettes (t-cigarettes) on RAW264.7 cells by using four e-cigarette aerosol extracts (ECA) and cigarette smoking extracts (CS) containing different nicotine concentrations. The results revealed that low concentration of nicotine in CS as well as in ECA with grape, watermelon, and cola flavors could promote cell viability. Conversely, high nicotine concentration in CS and ECA with four flavors decreased cell viability. Furthermore, our study demonstrated that CS significantly reduced the phagocytic capability of RAW264.7 cells and increased the levels of inflammatory cytokines (IL-6, TNF-α, and IL-1β) and reactive oxygen species (ROS) compared to ECA. Overall, our findings indicate all four e-cigarettes induced less cytotoxicity to RAW264.7 cells and might be safer than t-cigarettes.
... An imbalance between the production of proinflammatory factors and specialized pro-resolving lipid mediators contributes to the persistence of inflammation. Resolvin E1, which belongs to the group of specialized pro-resolving lipid mediators, plays an important role in preserving macrophage function during oxidative stress induced by cigarette smoke [99]. At the same time, cigarette smoke can induce an unbalanced release of lipid mediators that is characterized by a reduced prostacyclin (prostaglandin I2 or PGI2)/thromboxane A2 (TXA2) ratio, which may contribute to pulmonary vascular remodeling [100]. ...
Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD) and atherosclerotic cardiovascular disease (ASCVD). These diseases share common pathogenesis and significantly influence each other’s clinical presentation and prognosis. There is increasing evidence that the mechanisms underlying the comorbidity of COPD and ASCVD are complex and multifactorial. Smoking-induced systemic inflammation, impaired endothelial function and oxidative stress may contribute to the development and progression of both diseases. The components present in tobacco smoke can have adverse effects on various cellular functions, including macrophages and endothelial cells. Smoking may also affect the innate immune system, impair apoptosis, and promote oxidative stress in the respiratory and vascular systems. The purpose of this review is to discuss the importance of smoking in the mechanisms underlying the comorbid course of COPD and ASCVD.
... Our study shows in this respect contrary results compared to previous literature. In these studies, it has been shown that cigarette smoke increases NOX2 expression and superoxide production by NOX2 in vitro and in vivo [36,64]. Also, smoking e-cigarettes as well as traditional cigarettes led to a significant increase in NOX2 levels in human volunteers with a lower impact of e-cigarettes [10]. ...
Monocytes exhibiting a pro-inflammatory phenotype play a key role in adhesion and development of atherosclerotic plaques. As an alternative to smoking, next-generation tobacco and nicotine products (NGP) are now widely used. However, little is known about their pro-inflammatory effects on monocytes. We investigated cell viability, anti-oxidant and pro-inflammatory gene and protein expression in THP-1 monocytes after exposure to aqueous smoke extracts (AqE) of a heated tobacco product (HTP), an electronic cigarette (e-cig), a conventional cigarette (3R4F) and pure nicotine (nic). Treatment with 3R4F reduced cell viability in a dose-dependent manner, whereas exposure to alternative smoking products showed no difference to control. At the highest non-lethal dose of 3R4F (20%), the following notable mRNA expression changes were observed for 3R4F, HTP, and e-cig respectively, relative to control; HMOX1 (6-fold, < 2-fold, < 2-fold), NQO1 (3.5-fold, < 2-fold, < 2-fold), CCL2 (4-fold, 3.5-fold, 2.5-fold), IL1B (4-fold, 3-fold, < 2-fold), IL8 (5-fold, 2-fold, 2-fold), TNF (2-fold, 2-fold, < 2-fold) and ICAM1 was below the 2-fold threshold for all products. With respect to protein expression, IL1B (3-fold, < 2-fold, < 2-fold) and IL8 (3.5-fold, 2-fold, 2-fold) were elevated over the 2-fold threshold, whereas CCL2, TNF, and ICAM1 were below 2-fold expression for all products. At higher doses, greater inductions were observed with all extracts; however, NGP responses were typically lower than 3R4F. In conclusion, anti-oxidative and pro-inflammatory processes were activated by all products. NGPs overall showed lower responses relative to controls than THP-1 cells exposed to 3R4F AqE.
... Studies involving its metabolites, such as resolverins and maresins, have revealed potent anti-inflammatory, analgesic, and antineoplastic activities, mainly by reducing the production of cytokines/chemokines derived from neoplastic cells (TNF-α, IL-6, CXCL10, and MCP-1) and CD11bþLy6G myeloid cells induced by tumor mediators and nociception. A decrease in ROS production and improvement in the phagocytic activity of macrophages were also observed in one study [75][76][77][78]. Treatment with maresin 1, a lipid mediator derived from omega-3 AGP, was associated with protection against UVB radiation in hairless mice. ...
Simple Summary
Hemangiosarcoma is a mesenchymal neoplasm that originates in the endothelial cells of blood vessels. According to the location of origin, they can be classified as non-visceral and visceral types. Hemangiosarcoma can be very aggressive and metastasize to distant organs. The aim of this critical review is to present data on the epidemiology, etiology, diagnosis, staging, therapeutic modalities, and prognosis of canine hemangiosarcoma based on a consensus meeting organized by the Brazilian Association of Veterinary Oncology (ABROVET) in September 2022. Recent information from the literature, as well as new results from consensus participants, are presented and discussed.
Abstract
Hemangiosarcoma is a mesenchymal neoplasm originating in the endothelial cells of blood vessels; they can be classified as non-visceral and visceral types. Non-visceral hemangiosarcomas can affect the skin, subcutaneous tissues, and muscle tissues; visceral hemangiosarcomas can affect the spleen, liver, heart, lungs, kidneys, oral cavity, bones, bladder, uterus, tongue, and retroperitoneum. Among domestic species, dogs are most affected by cutaneous HSA. Cutaneous HSA represents approximately 14% of all HSA diagnosed in this species and less than 5% of dermal tumors, according to North American studies. However, Brazilian epidemiological data demonstrate a higher prevalence, which may represent 27 to 80% of all canine HSAs and 13.9% of all skin neoplasms diagnosed in this species. Cutaneous HSA most commonly affects middle-aged to elderly dogs (between 8 and 15 years old), with no gender predisposition for either the actinic or non-actinic forms. The higher prevalence of cutaneous HSA in some canine breeds is related to lower protection from solar radiation, as low skin pigmentation and hair coverage lead to greater sun exposure. Actinic changes, such as solar dermatosis, are frequent in these patients, confirming the influence of solar radiation on the development of this neoplasm. There are multiple clinical manifestations of hemangiosarcoma in canines. The diagnostic approach and staging classification of cutaneous HSAs are similar between the different subtypes. The definitive diagnosis is obtained through histopathological analysis of incisional or excisional biopsies. Cytology can be used as a presurgical screening test; however, it has little diagnostic utility in cases of HSA because there is a high risk of blood contamination and sample hemodilution. Surgery is generally the treatment of choice for dogs with localized non-visceral HSA without evidence of metastatic disease. Recently, electrochemotherapy (ECT) has emerged as an alternative therapy for the local ablative treatment of different neoplastic types; the use of radiotherapy for the treatment of dogs with cutaneous HSA is uncommon. There is greater consensus in the literature regarding the indications for adjuvant chemotherapy in subcutaneous and muscular HSA; doxorubicin is the most frequently used antineoplastic agent for subcutaneous and muscular subtypes and can be administered alone or in combination with other drugs. Other therapies include antiangiogenic therapy, photodynamic therapy, the association of chemotherapy with the metronomic dose, targeted therapies, and natural products. The benefits of these therapies are presented and discussed. In general, the prognosis of splenic and cardiac HSA is unfavorable. As a challenging neoplasm, studies of new protocols and treatment modalities are necessary to control this aggressive disease.
... RvE1 plays crucial roles in preserving macrophage effereocytosis, impaired due to their overexposure to ·O 2 − , as seen in cigratte smoke induced inflammation in the lungs. This is possible, as RvE1 are able to prevent membrane translocation of neutrophil cytosolic factor1(or p47phox), which in turn controls NADPH oxidase 2 (NOX2) [178], [187]. El Kebir et al reported that RvE1 enhances neutrophil apoptosis by promoting phagocytosis via the BLT1 receptor, and, mitigated ERK and Akt-mediated anti-apoptosis signals from MPO, serum amyloid A(SAA), and bacterial DNA constituent (CpG DNA), helps to accelerate resolution [188]. ...
Fatal "cytokine storms (CS)" observed in critically ill COVID-19 patients are consequences of dysregulated host immune system and over-exuberant inflammatory response. Acute respiratory distress syndrome (ARDS), multi-system organ failure, and eventual death are distinctive symptoms, attributed to higher morbidity and mortality rates among these patients. Consequent efforts to save critical COVID-19 patients via the usage of several novel therapeutic options are put in force. Strategically, drugs being used in such patients are dexamethasone, remdesivir, hydroxychloroquine, etc. along with the approved vaccines. Moreover, it is certain that activation of the resolution process is important for the prevention of chronic diseases. Until recently Inflammation resolution was considered a passive process, rather it's an active biochemical process that can be achieved by the use of specialized pro-resolving mediators (SPMs). These endogenous mediators are an array of atypical lipid metabolites that include Resolvins, lipoxins, maresins, protectins, considered as immunoresolvents, but their role in COVID-19 is ambiguous. Recent evidence from studies such as the randomized clinical trial, in which omega 3 fatty acid was used as supplement to resolve inflammation in COVID-19, suggests that direct supplementation of SPMs or the use of synthetic SPM mimetics (which are still being explored) could enhance the process of resolution by regulating the aberrant inflammatory process and can be useful in pain relief and tissue remodeling. Here we discussed the biosynthesis of SPMs, & their mechanistic pathways contributing to inflammation resolution along with sequence of events leading to CS in COVID-19, with a focus on therapeutic potential of SPMs.
... RvE1, RvD1, RvD2, RvD3, and RvD5 can all act on macrophages, but their effects are exerted in different ways. RvE1 reduces the expression of the HO-1 and NADPH oxidase subunit p47Phox, while RvD1 induces the transition from M1 macrophages to M2 macrophages [70,71]. RvD2 regulates the transcription factor IRF4, while RvD3 and RvD5 enhance efferocytosis and phagocytosis of M2 macrophages [34,55]. ...
An inflammatory response is beneficial to the organism, while an excessive uncontrolled inflammatory response can lead to the nonspecific killing of tissue cells. Therefore, promoting the resolution of inflammation is an important mechanism for protecting an organism suffering from chronic inflammatory diseases. Resolvins are a series of endogenous lipid mediums and have the functions of inhibiting a leukocyte infiltration, increasing macrophagocyte phagocytosis, regulating cytokines, and alleviating inflammatory pain. By promoting the inflammation resolution, resolvins play an irreplaceable role throughout the pathological process of some joint inflammation, neuroinflammation, vascular inflammation, and tissue inflammation. Although a large number of experiments have been conducted to study different subtypes of resolvins in different directions, the differences in the action targets between the different subtypes are rarely compared. Hence, this paper reviews the generation of resolvins, the characteristics of resolvins, and the actions of resolvins under a chronic inflammatory response and clinical translation of resolvins for the treatment of chronic inflammatory diseases.
... In contrast, the diminution of oxidative stress was associated with the upregulation of the Nrf2/Keap1 antioxidant pathway (Fig. 2). 83,84 The SPM derived from DHA RvD1 also has a positive role in lung injury and inflammation, as reported in patients with uncontrolled lung inflammation, such as exacerbated asthma and cystic fibrosis, that display a defect in the generation of SPMs. 85 The deficiency of SPMs such as lipoxin (Lx) A4, RvE1, and protectin D1 (PD1), is consistent with the failure to establish satisfactory protective counter-regulatory effects in lung disease. ...
Respiratory diseases include a wide range of pathologies with different clinical manifestations, affecting the normal airways and lung function. An increase in the inflammatory response is considered a characteristic hallmark of these diseases, being also a critical factor for their progression. The n-3 polyunsaturated fatty acids (n-3 PUFAs) eicosapentaenoic acid (C20:4n-3, EPA), docosahexaenoic acid (C22:6n-3, DHA) and their lipid mediators are known to have an inflammation pro-resolution effect. The effects of these n-3 PUFAs in the prevention and treatment of respiratory diseases are beginning to be understood. Consequently, this article aims to analyze the influence of n-3 PUFAs and their lipid mediators on the inflammatory response in respiratory health, emphasizing recent data concerning their beneficial effects in the prevention and possible treatment of different respiratory diseases, particularly asthma, airway allergic syndromes and chronic obstructive pulmonary disease. The review includes studies regarding the effects of EPA, DHA, and their specialized pro-resolving lipid mediators (SPMs) on in vivo and in vitro models of respiratory disease, concluding that EPA and DHA have a positive impact in attenuating the pro-inflammatory response in respiratory diseases, reducing symptoms like nasal congestion, fever and difficulty in breathing. Controversial data reported are probably due to differences in several factors, including the dosages, administration vehicles, and the supplementation times employed, which are aspects that remain to be addressed in future studies.
... Studies have shown that resolvins can induce macrophages to differentiate into the M2 lineage [132]. Studies on cigarette smoke-stimulated macrophages have shown that RvE1 promotes macrophages recruitment, significantly up-regulates expression of anti-inflammatory factors, and reduces levels of inflammatory response factors in culture supernatants [147]. Similarly, RvD1supplemented macrophages are significantly activated to the M2 type, which occurs concomitantly with an increase in IL-10 secretion and significant improvement in the phagocytic capacity of macrophages [148]. ...
Inflammation is an essential mechanism of various diseases. The development and resolution of inflammation are complex immune-modulation processes which induce the involvement of various types of immune cells. Specialized pro-resolving lipid mediators (SPMs) have been demonstrated to be signaling molecules in inflammation. SPMs are involved in the pathophysiology of different diseases, especially respiratory diseases, including asthma, pneumonia, and chronic obstructive pulmonary disease. All of these diseases are related to the inflammatory response and its persistence. Therefore, a deeper understanding of the mechanisms and development of inflammation in respiratory disease, and the roles of the SPM family in the resolution process, might be useful in the quest for novel therapies and preventive measures for pulmonary diseases.
