Microbial sensing in the intestine

The gut microbiota plays a key role in host health and disease, particularly through their interactions with the immune system. Intestinal homeostasis is dependent on the symbiotic relationships between the host and the diverse gut microbiota, which is influenced by the highly co-evolved immune-microbiota interactions. The first step of the interaction between the host and the gut microbiota is the sensing of the gut microbes by the host immune system. In this review, we describe the cells of the host immune system and the proteins that sense the components and metabolites of the gut microbes. We further highlight the essential roles of pattern recognition receptors (PRRs), the G protein-coupled receptors (GPCRs), aryl hydrocarbon receptor (AHR) and the nuclear receptors expressed in the intestinal epithelial cells (IECs) and the intestine-resident immune cells. We also discuss the mechanisms by which the disruption of microbial sensing because of genetic or environmental factors causes human diseases such as the inflammatory bowel disease (IBD).

Changes of the immunological barrier of intestinal mucosa in rats with sepsis / 世界急诊医学杂志（英文）

BACKGROUND:Sepsis has become the greatest threat to in-patients, with a mortality of over 25％.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsis. This dysfunction occurs after surgery, but the magnitude of change does not differentiate patients with sepsis from those without sepsis. Increased intestinal permeability before surgery is of no value in predicating sepsis. The present study aimed to observe the changes of intestinal mucosal immunologic barrier in rat models of sepsis induced by cecal ligation and puncture. METHODS:Sixty Sprague-Dawley rats were randomly divided into a sepsis group (n=45) and a control group (n=15). The rats in the sepsis group were subjected to cecal ligation and puncture (CLP), whereas the rats in the control group underwent a sham operation. The ileac mucosa and segments were harvested 3, 6 and 12 hours after CLP, and blood samples were collected. Pathological changes, protein levels of defensin-5 (RD-5) and trefoil factor-3 (TFF3) mRNA, and lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected. RESULTS:The intestinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of lamina propria, hemorrhage and ulceration in the sepsis group. The expression of TFF3 mRNA and level of RD-5 protein were decreased and the apoptosis of mucosal lymphocyte increased (P<0.05) in the sepsis group compared with the control group. Significant differences were observed in RD-5 and TFF3 mRNA 3 hours after CLP and they were progressively increased 6 and 12 hours after CLP in the sepsis group compared with the control group (P<0.05, RD-5 F=11.76, TFF3 F=16.86 and apoptosis F=122.52). In addition, the gut-origin bacterial DNA detected in plasma was positive in the sepsis group. CONCLUSION:The immunological function of the intestinal mucosa was impaired in septic rats and further deteriorated in the course of sepsis.

Effect of Scarring-moxibustion on Peyer’s Patch and T Cells Subsets of Intraepithelial Lymphocyte of Tumor-bearing Mice with Cyclophosphamide / 中国中医药信息杂志

Objective To explore the effect of scarring-moxibustion on Peyer’s patch and T cells subsets of intraepithelial lymphocyte of tumor-bearing mice with cyclophosphamide. Method The mucosal immune deficiency model was made by in site inoculating C-26 colon carcinoma with repeated intragastric administration of cyclophosphamide. The mice were treated with scarring- moxibustion for seventeen days after inoculation. The area of Peyer’s patch were measured, and T cells subsets of Lamina propria lymphocyte (LPL) were separated and detected by immunofluorescence test and flow cytometer. Result Tumor weight of tumor-bearing group was higher than cyclophosphamide group significantly (P

Relationship between anti-tumor necrosis factor -? monoclonal antibody and chronic colitis in mice / 中国实用内科杂志

Objective To investigate the role of tumor necrosis factor -?(TNF-?)in the pathogenesis of experimental murine colitis.Methods From Apr.1999 to May 2002,in the First Affiliated Hospital of Zhengzhou University,an experimental colitis model was established in which chronic colitis was induced by transfer of syngeneic CD45RB,CD~+_4T cells into severe combined immunodeficient(SCID)mice.These SCID recipients were treated with anti-TNF-? mAb,and the efficacy was observed and the mechanism was studied.Results Anti-TNF-? effectively prevented intestinal mucosal inflammation.Anti-TNF-? mAb also significantly suppressed leukocyte infiltration(e.g,CD~+_4 T cells,mononuclear macrophages)in the inflamed colon,and down-regulated production of proinflammatory cytokines interferon(IFN-?)and IL-2 of CD~+_4T cells in lamina propria.Conclusion The data suggests that administration of anti-TNF-? reverses mucosal inflammation via down-regulation of proinflammatory cytokines and decreases leukocyte infiltration in the bowel,thus providing additional support for TNF-?-targeted therapy in human Crohn's disease.