IL-17 is a protection effector against the adherent-invasive Escherichia coli in murine colitis

Zhang, Hai-jia; Xu, Bin; Wang, Hu; Xu, Bing; Wang, Guodong; Jiang, Mingzuo; Ding, Meiling; Yu, Pengfei; Nie, Yongzhan; Wu, Kaichun; Sha, Sumei; Li, Mengbin

doi:10.1016/j.molimm.2017.11.020

Cited by 17 publications

(13 citation statements)

References 42 publications

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“…We next tested whether our novel mAIEC colonizes mouse intestine and causes disease in vivo in the absence of SFB, since SFB is known to elicit a Th17 response which prevents AIEC colonization. 69 Whereas H Figure 2(a)). These data demonstrate that mAIEC caused mild and transient disease activity.…”

Section: Maiec Colonizes and Causes Mild Disease In Sfb-free Micementioning

confidence: 98%

The autoimmune susceptibility gene, PTPN2, restricts expansion of a novel mouse adherent-invasive E. coli

et al. 2020

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Inflammatory bowel disease (IBD) pathogenesis involves significant contributions from genetic and environmental factors. Loss-of-function single-nucleotide polymorphisms (SNPs) in the protein tyrosine phosphatase non-receptor type 2 (PTPN2) gene increase IBD risk and are associated with altered microbiome population dynamics in IBD. Expansion of intestinal pathobionts, such as adherent-invasive E. coli (AIEC), is strongly implicated in IBD pathogenesis as AIEC increases proinflammatory cytokine production and alters tight junction protein regulationsuggesting a potential mechanism of pathogen-induced barrier dysfunction and inflammation. We aimed to determine if PTPN2 deficiency alters intestinal microbiome composition to promote expansion of specific bacteria with pathogenic properties. In mice constitutively lacking Ptpn2, we identified increased abundance of a novel mouse AIEC (mAIEC) that showed similar adherence and invasion of intestinal epithelial cells, but greater survival in macrophages, to the IBD-associated AIEC, LF82. Furthermore, mAIEC caused disease when administered to mice lacking segmented-filamentous bacteria (SFB), and in germ-free mice but only when reconstituted with a microbiome, thus supporting its classification as a pathobiont, not a pathogen. Moreover, mAIEC infection increased the severity of, and prevented recovery from, induced colitis. Although mAIEC genome sequence analysis showed >90% similarity to LF82, mAIEC contained putative virulence genes with >50% difference in gene/protein identities from LF82 indicating potentially distinct genetic features of mAIEC. We show for the first time that an IBD susceptibility gene, PTPN2, modulates the gut microbiome to protect against a novel pathobiont. This study generates new insights into geneenvironment-microbiome interactions in IBD and identifies a new model to study AIEC-host interactions.

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Section: Maiec Colonizes and Causes Mild Disease In Sfb-free Micementioning

confidence: 98%

The autoimmune susceptibility gene, PTPN2, restricts expansion of a novel mouse adherent-invasive E. coli

et al. 2020

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“…Unfortunately, pathogenic Escherichia was observed in the biomarkers of LA4%. Previous studies showed that in ammation caused by Crohn's disease and colitis was characterized by the increased abundance of Escherichia in intestinal microbiota [59][60][61]. And as mentioned above, 4% maternal dietary LA supplementation promote in ammation.…”

Section: Discussionmentioning

confidence: 82%

Maternal Dietary Linoleic Acid Altered Intestinal Barrier Function in Domestic Pigeons (Columba Livia)

Zou

Dong

2020

Preprint

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BackgroundLinoleic acid (LA) is predominantly essential for poultry. Deficiency of LA in poultry were manifested in various aspects such as retarded growth and reduced resistance to disease. The effects of LA on intestinal health in vitro and in mammals has been studied, whereas research related to the effects of LA on intestine health in poultry was scanty. Intestinal health and immune function play an important role in pigeon squab growth. Considering squabs are fed by their parents, the purpose of this study was to explore the effects of maternal dietary LA on intestinal barrier function in squabs by determining intestinal morphology, gene expression of tight junction protein, immune cytokines, and microbial flora.ResultsA completely randomized design with a control group, 1% dietary LA supplementation group, 2% dietary LA supplementation group, and 4% dietary LA supplementation group was used. Six squabs from each treatment were randomly sampled at 21 posthatch. Results indicated that LA supplementation improved intestinal morphology as reflected by increased villus height, villus area and the ratio of villus to crypt, and the promotion at dosage of 1% was most significant. Besides, 1% LA supplementation elevated distribution density of goblet cell in intestine, and strengthened tight junction between enterocytes by up-regulating claudin3 and occludin gene expression, but down-regulating claudin2 gene expression. Moreover, 1% LA supplementation reduced secretion of pro-inflammation cytokines and increased anti-inflammation cytokines partly. The diversity index Chao1 of intestinal microbiota in 1% LA supplementation group was higher than other groups. And Butyrivibrio as beneficial bacteria was the biomarker of LA1%. However, excessive (4%) LA supplementation led to adverse impact on intestinal immunity and microbiota.ConclusionsMaternal dietary LA in three levels all could improve intestinal morphology in squabs. Therein, appropriate dosage (1%) supplementation might enhance mucosal protection and epithelium barrieer in squabs, and furthermore consolidated intestine immunity and luminal microbial environment. However, excessive (4%) LA supplementation might lead to adverse impact on immunity and microbiota. Maternal dietary LA might alter intestinal barrier function in pigeon squabs in a dose-dependent manner.

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“…Colonization with the pathobiont adherent-invasive E. coli (AIEC) was shown to potentiate the expression of IL-33 and ST2 in the intestine mediated by the bacterial flagellin 35 . Furthermore, AIEC colonization of Il17 −/− mice resulted in increased intestinal epithelial damage, systemic bacterial dissemination and mortality, indicating that IL-17 plays a protective role in AIEC-induced colitis 36 . Thus, we suggest that the flagellin-driven expansion of ST2 and IL-33 could be a self-protective mechanism of AIEC to counterbalance the induction of Th17-mediated responses.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity

et al. 2021

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A wide range of microbial pathogens is capable of entering the gastrointestinal tract, causing infectious diarrhea and colitis. A finely tuned balance between different cytokines is necessary to eradicate the microbial threat and to avoid infection complications. The current study identified IL-33 as a critical regulator of the immune response to the enteric pathogen Citrobacter rodentium. We observed that deficiency of the IL-33 signaling pathway attenuates bacterial-induced colitis. Conversely, boosting this pathway strongly aggravates the inflammatory response and makes the mice prone to systemic infection. Mechanistically, IL-33 mediates its detrimental effect by enhancing gut permeability and by limiting the induction of protective T helper 17 cells at the site of infection, thus impairing host defense mechanisms against the enteric pathogen. Importantly, IL-33-treated infected mice supplemented with IL-17A are able to resist the otherwise strong systemic spreading of the pathogen. These findings reveal a novel IL-33/IL-17A crosstalk that controls the pathogenesis of Citrobacter rodentium-driven infectious colitis. Manipulating the dynamics of cytokines may offer new therapeutic strategies to treat specific intestinal infections.

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IL-17 is a protection effector against the adherent-invasive Escherichia coli in murine colitis

Cited by 17 publications

References 42 publications

The autoimmune susceptibility gene, PTPN2, restricts expansion of a novel mouse adherent-invasive E. coli

The autoimmune susceptibility gene, PTPN2, restricts expansion of a novel mouse adherent-invasive E. coli

Maternal Dietary Linoleic Acid Altered Intestinal Barrier Function in Domestic Pigeons (Columba Livia)

Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity

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