Enteric infections complicating ulcerative colitis

Micic, Dejan; Hirsch, Ayal; Setia, Namrata; Rubin, David T.

doi:10.5217/ir.2018.16.3.489

Cited by 6 publications

(2 citation statements)

References 18 publications

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“…The current study particularly focused on the differences in the taxa at the genus level. A significantly higher proportions of the genus Turicibacter, Ruminococcaceae, and Lactobacillus were detected in the control group than those in DSS group, which was similar to previous research 22–24 , while a great abundance of the genera Klebsiella , Parabacteroides was observed in the DSS group, which was also validated by other studies 25,26 . Moreover, the administration of CRH further aggravated these changes in IBD (Fig.…”

Section: Resultssupporting

confidence: 91%

Intestinal autophagy links psychosocial stress with gut microbiota to promote inflammatory bowel disease

et al. 2019

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Psychosocial stress is a critical inducing factor of inflammatory bowel diseases (IBD), while autophagy is a novel central issue of IBD development. The present study investigated the potential role of autophagy in stress-related IBD in patients and animal model. The correlation between psychosocial stress and intestinal autophagy was determined in 23 patients with IBD. Corticotropin-releasing hormone (CRH), a well-established inducer of psychosocial stress, was administrated in dextran sulfate sodium (DSS)-induced IBD mice and lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDM). In IBD patients, the autophagy markers beclin-1, LC3-II/I ratio, Atg16L1, and Atg4B were significantly enhanced. The psychosocial stress score was positively associated with the levels of beclin-1 and the LC3II/I ratio in intestinal biopsy specimens. In IBD mouse model, CRH significantly aggravated intestinal inflammation, increased Paneth cell metaplasia, and enhanced intestinal autophagy (beclin-1, Atg16L1, PIK3R4, and Atg4B upregulation; GAA, CTSD, and PPKAA1 downregulation). Additionally, the CRH-induced gut microbial dysbiosis was evidenced by a marked increase in the number of detrimental bacteria. In LPS-stimulated BMDM, CRH substantially increased M1/M2 polarization and thus promoted inflammation. In both IBD mice and LPS-treated BMDM, blockade of autophagy by chloroquine abrogated the unbeneficial effects of CRH, whereas autophagy inducer rapamycin resulted in a pronounced protective effect against IBD lesion. Our data demonstrate that psychosocial stress may link the enhanced intestinal autophagy by modulating gut microbiota and inflammation to aggravate IBD. These data indicate autophagy as a promising therapeutic target for psychosocial stress-related IBD.

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Section: Resultssupporting

confidence: 91%

Intestinal autophagy links psychosocial stress with gut microbiota to promote inflammatory bowel disease

et al. 2019

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“…28 In addition, there has been at least one case study suggesting the association of K. oxytoca with refractory colitis independent of antibiotic treatment. 29 The source of K. oxytoca infection often comes from the hospital environment 30 and as such may pose a danger to patients undergoing treatment, such as with K. oxytoca contamination upon intravenous injection causing septic arthritis. 31 Despite the emerging importance of K. oxytoca as a human pathogen, to the best of our knowledge, no studies on the interaction between this bacteria and T cells in colitis are available.…”

Section: Discussionmentioning

confidence: 99%

Animal unit hygienic conditions influence mouse intestinal microbiota and contribute to T-cell-mediated colitis

Cázares-Olivera

Miroszewska

et al. 2022

Exp Biol Med (Maywood)

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Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders of the gastrointestinal tract with worldwide increasing incidence. Recent studies indicate that certain species of intestinal bacteria are strongly associated with IBD. Helper T lymphocytes are not only the key players in mediating host defense against a wide variety of pathogens but also contribute to pathogenesis of many immune-related diseases. Here, using the T cell transfer model of colitis, we observed that the mice maintained in a specific-pathogen free (SPF) unit after receiving naïve CD4+ T cells developed mild disease. The same mice developed different degrees of disease when they were maintained in a conventional animal facility (non-SPF), where some pathogens were detected during routine health monitoring. Consistently, increased circulating inflammatory cytokines as well as Th1 and Th17 cells were detected in mice housed in non-SPF units. 16S rRNA sequencing of feces samples enabled us to identify changes in the microbiota composition of mice kept in different facilities. Our data indicate that environmental factors influence gut microbiota composition of mice, leading to development of colitis in a T-cell-dependent manner. In conclusion, changes in environmental conditions and microbial status of experimental animals appear to contribute to progression of colitis.

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Gut Microbiota-Mediated NLRP12 Expression Drives the Attenuation of Dextran Sulphate Sodium-Induced Ulcerative Colitis by Qingchang Wenzhong Decoction

Sun

Pei

Guo

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Qingchang Wenzhong Decoction (QCWZD) is a newly developed, effective traditional Chinese herbal formulation for ulcerative colitis (UC). In earlier studies, we found that QCWZD could relieve the clinical symptoms of UC patients, reduce inflammation, and improve the intestinal barrier function in dextran sulphate sodium (DSS)-induced UC rats. However, the relationship between QCWZD and the gut microbiota in colitis was not clarified. In this study, we established a rat model of DSS-induced UC and then investigated the regulatory effects of QCWZD on the gut microbiota using 16S rRNA analysis. We also determined the expression of NLRP12 after QCWZD administration. Our findings suggested that QCWZD administration could modulate gut microbiota composition and selectively promote the protective strains such asButyricimonas,Blautia,andOdoribacter,whereas the enteric pathogens includingClostridiumandDoreawere significantly reduced after QCWZD treatment. It is noteworthy that QCWZD administration was identified to promote gut microbiota-mediated NLRP12 expression by inhibiting the activity of the TLR4/Blimp-1 axis. In conclusion, our study supports the potential of QCWZD administration as a beneficial therapeutic strategy for UC.

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Enteric infections complicating ulcerative colitis

Cited by 6 publications

References 18 publications

Intestinal autophagy links psychosocial stress with gut microbiota to promote inflammatory bowel disease

Intestinal autophagy links psychosocial stress with gut microbiota to promote inflammatory bowel disease

Animal unit hygienic conditions influence mouse intestinal microbiota and contribute to T-cell-mediated colitis

Gut Microbiota-Mediated NLRP12 Expression Drives the Attenuation of Dextran Sulphate Sodium-Induced Ulcerative Colitis by Qingchang Wenzhong Decoction

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