肠道微生态与肠道疾病

人类肠道微生态是一个包含大量肠道微生物的复杂生态系统,近年来研究发现肠道细菌过度繁殖可导致胃肠道动力失调及内脏神经敏感性改变,最终导致肠易激综合征的发生,而肠道菌群引起的肠粘膜异常免疫应答损伤被认为是炎症性肠病发病机制的关键所在,另外,肠道微生态还可过参与炎症性肠病的病理生理过程或直接代谢产生致癌物质影响肠道肿瘤的发生发展。由此我们发现,肠道微生态不仅参与了消化吸收、物质代谢等胃肠道基本生理过程,还直接关系到肠道疾病的发生。本文将就目前肠道微生态与肠道疾病的研究进展进行简单综述。     

Inhibitory effects of Geijigajakyak-Tang on trinitrobenzene sulfonic acid-induced colitis

Aim of the study

Water extract of Geijigajakyak-Tang (GJT) consisting of five crude drugs [dried root of P. lactiflora Peony (Paeoniaceae), dried trunk bark of C. cassia Blume (Lauraceae), seed of Z. jujube var. inermis Mill (Rhamnaceae), fresh root of Z. officinale Rocoe (Zingiberaceae) and dried trunk bark of G. uralensis Fish (Leguminosae)] is a folk medicine used for the treatment of chronic colitis. This study was designed to further elucidate the effect of GJT on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats.

Materials and methods

GJT orally given to mice before and after TNBS intoxication, and their clinical and morphological changes, myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels in colon tissues, were evaluated on Day 8 post-TNBS. Furthermore, the effect of six major constituents of individual herbs on ileum smooth muscle contraction and neutrophil chemotaxis was studied.

Results

GJT had a significant anti-inflammatory effect based on clinical and morphologic changes, MPO activity and MDA levels in colon tissues as compared with sham control. GJT and 5 major active constituents of individual herbs, paeoniflorin, cinnamaldehyde, jujuboside A, jujubogenin, and diammonium glycyrhhizinate significantly inhibited neutrophil chemotaxis. GJT significantly inhibited muscle contraction (IC₅₀; 2.10 ± 0.11 mg/ml), and 1,8-cineol has the most spasmolytic activity (IC₅₀; 0.10 ± 0.03 mg/ml).

Conclusion

GJT has significant anti-inflammatory effects on TNBS-induced colitis via inhibitions of smooth muscle contraction and neutrophil chemotaxis.     

Early‐life adversity,epigenetics, and visceral hypersensitivity

Abdominal pain is associated with many gastrointestinal dysfunctions, such as irritable bowel syndrome (IBS), functional dyspepsia, and inflammatory bowel disease (IBD). Visceral hypersensitivity is a key reason for development of abdominal pain that presents in these gastrointestinal disorders/diseases. The pathogenesis of visceral hypersensitivity is complex and still far from being fully understood. In animal studies, visceral hypersensitivity has been linked to several early‐life adverse (ELA) events. In humans, IBD, functional dyspepsia, and IBS can have adult onset, though the adverse events that lead to visceral hypersensitivity are largely uncharacterized. In this issue of the journal, Aguirre et al. report the interesting finding that epigenetics underlies the effects of ELA events on visceral hypersensitivity. This mini‐review examines models of ELA events leading to visceral hypersensitivity and the potential role of epigenetics, as reported by Aguirre et al. and others.     

Increase in fecal primary bile acids and dysbiosis in patients with diarrhea-predominant irritable bowel syndrome

Background Irritable bowel syndrome (IBS) is a multifactorial disease for which a dysbiosis of the gut microbiota has been described. Bile acids (BA) could play a role as they are endogenous laxatives and are metabolized by gut microbiota. We compared fecal BA profiles and microbiota in healthy subjects (HS) and patients with diarrhea‐predominant IBS (IBS‐D), and we searched for an association with symptoms. Methods Clinical features and stool samples were collected in IBS‐D patients and HS. Fecal BA profiles were generated using HPLC coupled to tandem mass spectrometry. The fecal microbiota composition was assessed by q‐PCR targeting dominant bacterial groups and species implicated in BA transformation. Key Results Fourteen IBS‐D patients and 18 HS were included. The two groups were comparable in terms of age and sex. The percentage of fecal primary BA was significantly higher in IBS‐D patients than in HS, and it was significantly correlated with stool consistency and frequency. Fecal counts of all bacteria, lactobacillus, coccoides, leptum and Faecalibacterium prausnitzii were similar. There was a significant increase of Escherichia coli and a significant decrease of leptum and bifidobacterium in IBS‐D patients. Conclusions & Inferences We report an increase of primary BA in the feces of IBS‐D patients compared to HS, correlated with stool consistency and frequency. A dysbiosis of different bacterial groups was detected, some of them involved in BA transformation. As the gut microbiota is the exclusive pathway to transform primary into secondary BA, this suggests a functional consequence of dysbiosis, leading to lower BA transformation.