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@#Specific pro-resolving mediators(SPM)are a class of lipid mediators that trigger and orchestrate the resolution of inflammation, which formed in cells by the metabolism of polyunsaturated fatty acids. SPM pathway and receptors are highly expressed inocular surface, and constitute endogenous SPM networks which are important for maintaining ocular surface health and immune homeostasis. Recent evidence indicates that SPM and their analogs are essential mediators in promoting corneal wound healing, corneal nerve regeneration, and inhibiting the immune inflammatory response of corneal transplant rejection, allergic conjunctivitis and microbial keratitis. In addition, they are potential therapeutic drug targets of dry eye disease, and provide novel insight on the research and treatment of ocular surface diseases. Here, we will review and discuss evidence for SPM as important endogenous regulators of ocular surface health and disease and their therapeutic potential.
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Objective:To investigate the effect and mechanism of Fuzheng Touxie prescription （FZTX） on the immune homeostasis of drug-resistant <italic>Pseudomonas aeruginosa</italic> lung infection in rats at different time points. Method:A total of 168 rats were divided into a blank group （<italic>n</italic>=8），a model group （<italic>n</italic>=40），a Touxie （TX） group （<italic>n</italic>=40），an early Fuzheng （FZ） group （<italic>n</italic>=40）， and a delayed FZ group （<italic>n</italic>=40）. The blank group was given distilled water by gavage， the model group was given distilled water by gavage after infection，the TX group was given clear heat and penetrate evil drug free decoction granules（3.5 g·kg<sup>-1</sup>） by gavage after infection， the early FZ group was given Fuzheng Touxie whole formula free decoction granules（10.75 g·kg<sup>-1</sup>） by gavage after infection， the delayed FZ group was given clear heat and penetrate evil drug free decoction granules by gavage after infection， on the third day plus Fuzheng drug free decoction granules［（3.5+10.75） g·kg<sup>-1</sup>］ by gavage， the three treatment groups were gavaged twice a day， 2 mL each time .Each drug treatment group was divided into five groups according to five time points （3 h，1 d，3 d，5 d， and 7 d）， with eight rats in each group. The levels of tumor necrosis factor-<italic>α</italic>（TNF-<italic>α</italic>），high mobility group protein 1（HMGB1），interleukin-10（IL-10）， and tumor necrosis factor -<italic>α</italic>-induced protein-8-like2 （TIPE2） were measured by enzyme-linked immunosorbent assay （ELISA）， and HMGB1 protein expression level by Western blot. Result:At 3 h，the TNF-<italic>α</italic> content in the drug treatment groups was higher than that in the blank group and the model group （<italic>P</italic><0.05）. At 3 d，the TNF-<italic>α</italic> content in the early FZ group and the delayed FZ group was lower than that in the model group （<italic>P</italic><0.05） and the TX group （<italic>P</italic><0.05）. At 1 d，the HMGB1 content in the TX group and the delayed FZ group was higher than that in the model group （<italic>P</italic><0.05）. At 5 d，the HMGB1 content was lower in the delayed FZ group than in the model group （<italic>P</italic><0.05）. At 7 d，HMGB1 protein expression in the model group was higher than that in the blank group （<italic>P</italic><0.05） and the early FZ group （<italic>P</italic><0.05）. At 3 d，the IL-10 content was significantly higher in both the early FZ group and the delayed FZ group than that in the model group （<italic>P</italic><0.05）. At 5 d，the IL-10 content was higher in the early FZ group than that in the TX group （<italic>P</italic><0.05）. At 7 d，the IL-10 content in the early FZ group and the delayed FZ group was lower than that in the TX group （<italic>P</italic><0.05）. At 5 d，the TIPE2 content in the early FZ group was lower than that in the model group （<italic>P</italic><0.05）. At 7 d，the TIPE2 content in the TX group and the delayed FZ group was lower than that in the model group （<italic>P</italic><0.05）. Conclusion:FZTX or modified prescription can promote the inflammatory response to eliminate pathogenic bacteria in the early stage and suppress the inflammatory response in the late stage to avoid the inflammatory cascade effect and lung tissue damage，indicating that Fuzheng drugs have an important role in maintaining the immune homeostasis of the body after infection.
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The normal immune system has the ability to distinguish between "self" and "non-self". Because of its dynamic balance of "immune activity-immune tolerance", it will produce immune response to the non-self antigen, but with no response or weak response to the self-antigen. However, if the balance was broken, T cell in the abnormal immune activation state will respond continually to the self-antigen, with an abnormal immune response, which caused autoimmune disease. Pathologically, "invalid" immune recognition and immune response become the main causes for autoimmune diseases. Co-stimulatory molecule is an important link between Attach antigen presenting cells（APC） and immune cells (T cell and B cell). Studies have proved that excessive co-stimulation and/or insufficient co-inhibition could cause detect of self-tolerance and induce autoimmunity. Although co-stimulatory and co-inhibitory pathways have a significant impact on all ADS, this paper focuses on their effect on two systemic autoimmune diseases [systemic lupus erythematosus （SLE） and rheumatoid arthritis（RA）] and two organ-specific autoimmune diseases [multiple sclerosis （MS） and type 1 diabetes （T1DM）], in order to discuss the pathogenesis and relationship between co-stimulatory molecules and autoimmune diseases.
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Allergic asthma is thought to arise from an imbalance of immune regulation, which is characterized by the production of large quantities of IgE antibodies by B cells and a decrease of the interferon-γ/interleukin-4 (Th1/Th2) ratio. Certain immunomodulatory components and Chinese herbal formulae have been used in traditional herbal medicine for thousands of years. However, there are few studies performing evidence-based Chinese medicine (CM) research on the mechanisms and effificacy of these drugs in allergic asthma. This review aims to explore the roles of Chinese herbal formulae and herb-derived compounds in experimental research models of allergic asthma. We screened published modern CM research results on the experimental effects of Chinese herbal formulae and herb-derived bioactive compounds for allergic asthma and their possible underlying mechanisms in English language articles from the PubMed and the Google Scholar databases with the keywords allergic asthma, experimental model and Chinese herbal medicine. We found 22 Chinese herb species and 31 herb-derived anti-asthmatic compounds as well as 12 Chinese herbal formulae which showed a reduction of airway hyperresponsiveness, allergen-specifific immunoglobulin E, inflflammatory cell infifiltration and a regulation of Th1 and Th2 cytokines in vivo, in vitro and ex vivo, respectively. Chinese herbal formulae and herbderived bioactive compounds exhibit immunomodulatory, anti-inflflammatory and anti-asthma activities in different experimental models and their various mechanisms of action are being investigated in modern CM research with genomics, proteomics and metabolomics technologies, which will lead to a new era in the development of new drug discovery for allergic asthma in CM.
Subject(s)
Animals , Asthma , Drug Therapy , Allergy and Immunology , Disease Models, Animal , Drugs, Chinese Herbal , Therapeutic Uses , Homeostasis , Hypersensitivity , Drug Therapy , Allergy and Immunology , Immunologic Factors , Therapeutic UsesABSTRACT
A healthy gut consists of commensal flora,epithelial layer and gut-associated lymphoid tissue (GALT). GALT is hyporesponsive to commensal flora and dietary antigens,but can recognize and at-tack pathogens. Accumulating evidence suggests that dendritic cells (DCs) play a crucial role in managing this paradoxical situation and maintaining the complex homeostasis in gut. Influenced by intestinal epithelial cells (IECs) and commensal flora,intestinal DCs possess unique properties that enable them to regulate T-helper 2 (Th2) cells,regulatory T cells (Tregs) and immunoglobulin A (IgA)-producing cells in a steady state. During infection,intestinal DCs are involved in the induction of effector lymphocytes, although they are also responsible for initiating pathogenic responses in inflammatory bowel diseases (IBDs). Therefore, intestinal DCs are associated with not only the maintenance of immune tolerance to commensal flora,but also the induction of protective immune responses against pathogens. This review outlines the roles of commensal flora, epithelial layer, and GALT in mucosal homeostasis and inflammation and summarizes recent progress in DCs-mediated intestinal immune homeostasis.
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Objective To demonstrate the effect of tumor necrosis factor-α induced protein 8 like-2 (TIPE2) expression in patients with acute respiratory distress syndrome (ARDS) and its mechanism. Methods A prospective observation was conducted. Thirty-nine patients with ARDS admitted to department of emergency of PLA General Hospital from July 2013 to July 2015 were enrolled, and 35 healthy persons served as control group. The acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score within 24 hours after admission, blood gas analysis, procalcitonin (PCT), and C-reactive protein (CRP) were recorded. The mRNA expressions of TIPE2 in peripheral blood mononuclear cell (PBMC) and myxoma resistance protein 1 (MX1) in plasma were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). The correlations were analyzed by Spearman rank correlation analysis. Results The mean of APACHE Ⅱ score in 39 patients with ARDS was 25±3, the mean of PCT was (1.85±0.41) μg/L, and the mean of CRP was (18.0±3.0) mg/L. The TIPE2 mRNA expression in PBMC of ARDS patients was significantly down-regulated as compared with that of healthy control group (2-ΔΔCt: 3.28±0.15 vs. 8.87±0.20, P 0.05). The MX1 mRNA expression was positively correlated with APACHE Ⅱ score (r = 0.893, P 0.05). Conclusion TIPE2 expression was decreased in ARDS patients, which negatively correlate with disease severity, and indicate TIPE2 might be involved in the pathogenic process of ARDS.