Intestinal mucosal layers are colonized by a complex microbiota that provides beneficial effects under normal physiological conditions, but is capable of contributing to chronic inflammatory disease such as inflammatory bowel disease (IBD) in susceptible individuals. Studies have shown that the enteric microbiota may drive the development of the gut immune system and can induce immune homeostasis as well as contribute to the development of IBD although the precise etiology is still unknown. Therefore, intestinal microbes seem to play a key role in the disease pathogenesis. Especially, dysbiosis, which is a shift in the composition of enteric microbiota to a nonphysiologic composition, is associated with one or more defects in mucosal immune functions, including microbe recognition, barrier function, intercellular communication, and anti-microbial effector mechanisms. This review focuses on the impact of enteric microbiota on the development and perpetuation of IBD. In addition, interactions with enteric bacteria and mucosal cells, including intestinal epithelial cells, dendritic cells, and T cells, to induce immune responses at mucosal surfaces have been discussed in the point of IBD pathogenesis. Further extension of the knowledge of enteric microbiota may lead to insights on the pathogenesis and new therapeutic strategies for IBD.
Bacterial Physiological Phenomena ; Host-Pathogen Interactions ; Humans ; Inflammatory Bowel Diseases/*microbiology/pathology ; Intestinal Mucosa/immunology/microbiology ; Intestines/microbiology/pathology ; T-Lymphocytes/immunology/metabolism

Proliferative enteropathy was reproduced in IFN-gamma receptor knockout (IFN-gamma R-) mice by experimental infection with Lawsonia intracellularis (L. intracellularis). The cecum and the colon of the infected mice were evidently enlarged 2 weeks post infection. The presence of L. intracellularis was identified in the stool and the cecum of the mice after infection. However, high levels of IFN-gamma were detected in the sera of the infected mice 2 weeks PI. These data indicated that the IFN-gamma produced in the infected mice should have been utilized by it's receptor to elicit protective immune responses against L. intracellularis infections.
Animals ; DNA, Viral ; Desulfovibrionaceae Infections/*immunology/microbiology ; Interferon Type II/*immunology ; Intestinal Diseases/*immunology/microbiology ; Intestinal Mucosa/immunology ; Lawsonia Bacteria/*immunology/isolation&purification ; Mice ; Mice, Knockout ; Polymerase Chain Reaction ; Receptors, Interferon/physiology

The human intestinal microbiota is a community of 10(13)-10(14) microorganisms that harbor in the intestine and normally participate in a symbiotic relationship with human. Technical and conceptual advances have enabled rapid progress in characterizing the taxonomic composition, metabolic capacity and immunomodulatory activity of the human intestinal microbiota. Their collective genome, defined as microbiome, is estimated to contain > or =150 times as many genes as 2.85 billion base pair human genome. The intestinal microbiota and its microbiome form a diverse and complex ecological community that profoundly impact intestinal homeostasis and disease states. It is becoming increasingly evident that the large and complex bacterial population of the large intestine plays an important role in colorectal carcinogenesis. Numerous studies show that gut immunity and inflammation have impact on the development of colorectal cancer. Additionally, bacteria have been linked to colorectal cancer by the production of toxic and genotoxic bacterial metabolite. In this review, we discuss the multifactorial role of intestinal microbiota in colorectal cancer and role for probiotics in the prevention of colorectal cancer.
Animals ; Bacteroides/metabolism ; Colorectal Neoplasms/immunology/*microbiology ; Fatty Acids, Nonesterified/metabolism ; Humans ; Hydrogen Sulfide/metabolism ; Intestinal Mucosa/immunology/microbiology ; Metagenome ; *Probiotics ; Reactive Oxygen Species/metabolism ; Toxins, Biological/metabolism

OBJECTIVETo investigate the potential effect of bifidobacterial supplement on intestinal mucosal immunity associated with severe burns.

METHODSWistar rats were randomly divided into burn control group (BC group, n = 30), treatment group (BT group, n = 30), and sham-burn group (NC group, n = 10). Rats in BT group were fed bifidobacterial preparation (5 x 10(9) CFU/ml) after 30% total body surface area full-thickness burns, 1.5 ml, twice daily. Rats in BC group and NC group were fed normal saline, 1.5 ml, twice daily. Samples were taken on post-burn 1-, 3-, and 5-day. The incidence of bacterial translocation and bifidobacteria counts in the cecum mucosa were determined with standard methods. The sIgA levels in the mucus of the small intestine were measured by RIA. The positive sIgA expression in the lamina propria was detected by immunohistochemical staining.

RESULTSThe incidence of bacterial translocation was 42% and 16% in BC and BT groups on post-burn day 3 (P = 0.004), 30% and 8% on day 5 (P = 0.002), respectively. Plasma endotoxin levels were markedly higher in BC and BT groups than in NC group at the early stage post-burn. There was a significant decrease between BT group and BC group on post-burn day 1 (P = 0.0412). Bifidobacteria counts in cecum mucosa were reduced by 10- to 60-fold after thermal injury, but there was a remarkable increase in bifidobacteria counts in animals fed with bifidobacteria. sIgA levels in the intestinal mucus were significantly decreased in group BC, but they returned to normal range in BT group on post-burn day 5. Similarly, sIgA expression in the lamina propria was also weakened after burns, and had a tendency to recover after prescription of a 5-day bifidobacteria-supplemented formula. A strong positive correlation was observed between the counts of bifidobacteria in the cecal mucosa and the levels of sIgA in the intestinal mucus (r = 0.7534, P = 0.0000).

CONCLUSIONSThe expression and excretion of sIgA in the intestine appear to be markedly inhibited following a severe thermal injury. The supplement of exogenous bifidobacteria could improve sIgA formation in the small intestine, thereby reducing the incidence of bacterial/endotoxin translocation secondary to major burns.

Animals ; Bacterial Translocation ; Bifidobacterium ; physiology ; Burns ; immunology ; microbiology ; Disease Models, Animal ; Female ; Immunoglobulin A, Secretory ; biosynthesis ; Intestinal Mucosa ; immunology ; microbiology ; Male ; Probiotics ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo explore the effects of Huoxiang Zhengqi liquid (HXZQ) on enteric mucosal immune responses in mice with Bacillus dysenteriae and Salmonella typhimurium induced diarrhea (BSD).

METHODMice were randomly divided into four groups with 10 mice in each group: control group (control), BSD group, Huoxiang Zhengqi liquid treated BSD groups at high dosage and low dosage (HXZQ high, HXZQ low). HXZQ was administrated from the day of diarrhea induction at dosage of 5.21 g kg(-1) and 0.52 g kg (-1) respectively. Peyer's patch and periphery lymphocytes were prepared for flow cytometry, and level of TNF-alpha in periphery and enteric tissue homogenate were determined with ELISA. Student's t-test was used for statistics.

RESULTMice in BSD group started showing continuous diarrhea at the day of induction till the fourth day when the mice were sacrificed. Diarrhea in the mice of HXZQ high and low groups lasted for 36 and 54 h respectively. There were more CD4+ and CD8+ cells in periphery, less CD4+ cells in peyer's patch in BSD mice comparing to normal mice. In peyer's patch, there were more CD8+ cells in mice in HXZQ high and low groups and more CD4+ in mice in HXZQ high group. Higher level TNF-alpha in periphery and intestinal tissue homogenate in BSD group were observed. Mice in HXZQ high group showed the decreased level TNF-alpha in periphery and enteric tissue homogenate.

CONCLUSIONThe immune regulation on peyer's patch CD4+ and CD8+ cells and suppression on TNF-alpha level in enteric homogenate might partially explain the effect of HXZQ on improvement of BSD.

Animals ; CD4-CD8 Ratio ; Colon ; immunology ; metabolism ; pathology ; Diarrhea ; immunology ; metabolism ; microbiology ; Drug Combinations ; Drugs, Chinese Herbal ; administration & dosage ; isolation & purification ; pharmacology ; Dysentery, Bacillary ; immunology ; metabolism ; microbiology ; Immunity, Mucosal ; drug effects ; Intestinal Mucosa ; immunology ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Peyer's Patches ; drug effects ; immunology ; pathology ; Plants, Medicinal ; chemistry ; Random Allocation ; Salmonella Infections ; immunology ; metabolism ; microbiology ; Salmonella typhimurium ; immunology ; Shigella dysenteriae ; immunology ; T-Lymphocyte Subsets ; drug effects ; immunology ; pathology ; Tumor Necrosis Factor-alpha ; blood ; metabolism