ABSTRACT
As the first line of defense between the intestinal environment and the outside world， the intestinal mucosal barrier is essential for maintaining the intestinal homeostasis. The intestinal mucosal barrier injury will change the intestinal permeability and allow bacterial translocation and the entry of endotoxins into blood， thus triggering a series of inflammatory responses， followed by the injury of related tissues and the aggravation of primary diseases. The spleen， the acquired foundation， is responsible for maintaining the internal and external balance of the body and resisting external evils. Its physiological function is similar to that of the intestinal mucosal barrier. Spleen deficiency easily leads to intestinal mucosal barrier dysfunction. Therefore， replenishing Qi， invigorating spleen， and restoring the efficacy of spleen and stomach qi in defensing and governing transportation and transformation are the keys to prevent and treat intestinal mucosal barrier injury. In recent years， studies have shown that the spleen-invigorating Chinese medicinals repair the intestinal mucosal injury by promoting the expression of intestinal epithelial tight junction proteins， regulating the intestinal immune function， microbial flora， and metabolites， and supplementing the intestinal nutrition， enabling them to gradually become a research hotspot. After reviewing the relevant articles published in China and abroad， this paper expounded the common syndrome types of traditional Chinese medicine （TCM）， the changes in intestinal mucosal barrier induced by spleen deficiency， the repairing effects of spleen-invigorating Chinese medicinals on intestinal mucosal barrier injury， in order to provide some clues for the research on the treatment of intestinal mucosal barrier dysfunction-related diseases with spleen-invigorating Chinese medicinals.
ABSTRACT
Butyrate-producing bacteria are specific intestinal bacteria with butyrate as the main metabolite, and most of them are Firmicutes.Butyrate-producing bacteria can synthesize butyrate with non-digestible carbohydrates in the diet, and then regulate intestinal microecology and microenvironment, thereby supplying energy to intestinal epithelial cells, affecting intestinal mucosal barrier, adjusting intestinal flora structure and regulating host immunity, so as to alleviate obesity, hypertension and other diseases.Therefore, the targeted regulation of butyrate-producing bacteria and butyrate has become a potential vital method for the prevention and treatment of many diseases.After oral administration, Chinese herbal medicine (CHM) enters the body, and first contacts gastrointestinal tract, so the interaction between CHM and microbiota existing in the intestine is an inevitable important process.It has been confirmed that CHM could regulate intestinal flora; and due to its complex composition and numerous components, CHM can exert interventional effects at multiple levels, in multiple pathways and on multiple targets.Its effect on the butyrate-producing bacteria is as follows.In the intestinal tract, CHM can play a " prebiotic" role, and enrich the beneficial butyrate-producing bacteria, and polysaccharides in CHM can be used as a fermentation substrate to promote the synthesis of butyrate, so as to achieve the effective regulation of butyrate-producing bacteria and butyrate.Based on that, this paper explored the relationship among butyrate-producing bacteria, butyrate and intestinal microecology, and reviewed relevant researches about the intervention of CHM on butyrate-producing bacteria to regulate intestinal microecology in recent years, in order to provide new research ideas for the application of CHM to prevent and treat diseases, as well as drug development.
ABSTRACT
<p><b>Background</b>Imbalance of interferon-gamma (IFN-γ), interleukin (IL)-4, and IL-17 producing by T cells is confirmed to contribute to the pathogenesis of systemic lupus erythematosus (SLE). Autophagy is now emerging as a core player in the development and the function of the immune system. Therefore, we investigated the autophagic behavior in IFN-γ-, IL-4-, and IL-17-producing T cells from patients with SLE.</p><p><b>Methods</b>Thirty patients with SLE and 25 healthy controls matched for gender and age were recruited between September 2016 and May 2017. The autophagic levels in IFN-γ T cells, IL-4 T cells, and IL-17 T cells from patients with newly diagnosed SLE and healthy controls were measured using flow cytometry. The plasma levels of IFN-γ were determined by enzyme-linked immunosorbent assay in SLE patients and healthy controls. Unpaired t-tests and the nonparametric Mann-Whitney U-test were used to compare data from patients with SLE and controls. Spearman's rank correlation coefficient was applied for calculation of the correlation between parallel variables in single samples.</p><p><b>Results</b>Our results showed increased percentage of autophagy in IFN-γ T cells from patients with SLE and healthy controls ([8.07 ± 2.72]% vs. [3.76 ± 1.67]%, t = 5.184, P < 0.001), but not in IL-4 T cells or IL-17 T cells (P > 0.05) as compared to healthy donors. Moreover, the plasma levels of IFN-γ in SLE patients were significantly higher than those in healthy controls ([68.9 ± 29.1] pg/ml vs. [24.7 ± 17.6] pg/ml, t = 5.430, P < 0.001). Moreover, in SLE patients, the percentage of autophagy in IFN-γ T cells was positively correlated with the plasma levels of IFN-γ (r = 0.344, P = 0.046), as well as the disease activity of patients with SLE (r = 0.379, P = 0.039).</p><p><b>Conclusion</b>The results indicate that autophagy in IFN-γ T cells from SLE patients is activated, which might contribute to the persistence of T cells producing IFN-γ, such as Th1 cells, and consequently result in the high plasma levels of IFN-γ, and then enhance the disease activity of SLE.</p>