Inhibitory Effect of Recombinant IL-25 on the Development of Dextran Sulfate Sodium-Induced Experimental Colitis in Mice

Mchenga, S.S. Salum; Wang, Danan; Cheng, Li; Shan, Fengping; Lu, Cuihua

doi:10.1038/cmi.2008.53

Cited by 49 publications

(54 citation statements)

References 36 publications

(44 reference statements)

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“…IL-25 is a member of the IL-17 cytokine family that is reduced in the colonic mucosa of patients with IBD (6). Moreover, treatment with recombinant IL-25 attenuates experimental colitis in mice (6,32). In the present study, colonic IL-25 levels were significantly lower in DSS-treated mice previously exposed to C. jejuni.…”

Section: Discussionsupporting

confidence: 51%

Campylobacter jejuni Disrupts Protective Toll-Like Receptor 9 Signaling in Colonic Epithelial Cells and Increases the Severity of Dextran Sulfate Sodium-Induced Colitis in Mice

et al. 2012

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Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation associated with a dysregulated immune response to commensal bacteria in susceptible individuals. The relapse of IBD may occur following an infection with Campylobacter jejuni. Apical epithelial Toll-like receptor 9 (TLR9) activation by bacterial DNA is reported to maintain colonic homeostasis. We investigated whether a prior C. jejuni infection disrupts epithelial TLR9 signaling and increases the severity of disease in a model of mild dextran sulfate sodium (DSS) colitis in mice. In a further attempt to identify mechanisms, T84 monolayers were treated with C. jejuni followed by a TLR9 agonist. Transepithelial resistance (TER) and dextran flux across confluent monolayers were monitored. Immunohistochemistry, Western blotting, and flow cytometry were used to examine TLR9 expression. Mice colonized by C. jejuni lacked any detectable pathology; however, in response to low levels of DSS, mice previously exposed to C. jejuni exhibited significantly reduced weight gain and increased occult blood and histological damage scores. Infected mice treated with DSS also demonstrated a significant reduction in levels of the anti-inflammatory cytokine interleukin-25. In vitro studies indicated that apical application of a TLR9 agonist enhances intestinal epithelial barrier function and that this response is lost in C. jejuni-infected monolayers. Furthermore, infected cells secreted significantly more CXCL8 following the basolateral application of a TLR9 agonist. Surface TLR9 expression was reduced in C. jejuni-infected monolayers subsequently exposed to a TLR9 agonist. In conclusion, infection by C. jejuni disrupts TLR9-induced reinforcement of the intestinal epithelial barrier, and colonization by C. jejuni increases the severity of mild DSS colitis.

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Section: Discussionsupporting

confidence: 51%

Campylobacter jejuni Disrupts Protective Toll-Like Receptor 9 Signaling in Colonic Epithelial Cells and Increases the Severity of Dextran Sulfate Sodium-Induced Colitis in Mice

et al. 2012

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“…IL-17E expression is significantly reduced in IBD [29]. IL-17E could prevent chemical-induced colitis if administered prior to induction or ameliorate the disease severity if administered after the induction [29][30][31][32][33]. Our results, however, showed a strong expression of IL-17E in both healthy control and CRC with no difference between them.…”

Section: Discussioncontrasting

confidence: 51%

Distinctive expression pattern of interleukin-17 cytokine family members in colorectal cancer

et al. 2015

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Colorectal cancer (CRC) is one of the most common cancers in both genders. Even though interleukin (IL)-17A was shown to play an important role in intestinal tumourigenesis and CRC, other IL-17 family members were not studied well. We therefore studied the expression of IL-17 cytokine family members in CRC. Ten healthy colons and ten CRC mucosa were immunostained for IL-17B, IL-17C, IL-17E, and IL-17F, and their receptors IL-17RA, IL-17RB, and IL-17RC. Double immunofluorescence staining of the CRC mucosa was done for IL-17B with markers of neutrophils, endothelial cells, macrophages, T cells, mast cells, or fibroblasts. While IL-17B was increased in CRC with a strong presence both in the epithelial and stromal compartments, IL-17C showed different expression depending on the grade of differentiation and IL-17E remained unchanged. In contrast, IL-17F was decreased in CRC compared to healthy control. Colon epithelial cells stained positive for IL-17RA, IL-17RB, and IL-17RC in both healthy control and CRC. Neutrophils were the main source of IL-17B in the stroma. family members demonstrated distinct expression patterns in CRC, suggesting a differential role exerted by each member in colon carcinogenesis.

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“…[142][143][144] Mechanistically, the anti-colitic effect mediated by IL-17E is probably dependent on the activation of anti-inflammatory alternatively activated macrophages (AAMs) and the inhibition of CD4 + T-cell activation and their differentiation into inflammatory Th1/Th17 cells in the colon. 141,142,144,145 Recombinant IL-17E even ameliorates oxazolone-induced type 2 colitis, indicating that IL-17E has a broad anti-inflammatory effect in the colon rather than selectively suppressing Th1/Th17 cytokine production. 144 A recent study showed that IL-17E was produced by intestinal epithelial cells during acute colitis and that mice deficient in IL-17E were protected from DSS-induced colitis.…”

Section: Il-17dmentioning

confidence: 99%

“…Il-17E expression is downregulated in inflamed colons from IBD patients and DSS-treated mice. 141,142 In vivo delivery of recombinant IL-17E inhibits the development of DSS-, 2,4,6-trinitrobenzenesulphonic acid (TNBS)-, or peptidoglycan (PGN)-induced acute colitis in mice. [142][143][144] Mechanistically, the anti-colitic effect mediated by IL-17E is probably dependent on the activation of anti-inflammatory alternatively activated macrophages (AAMs) and the inhibition of CD4 + T-cell activation and their differentiation into inflammatory Th1/Th17 cells in the colon.…”

Section: Il-17dmentioning

confidence: 99%

“…141,142 In vivo delivery of recombinant IL-17E inhibits the development of DSS-, 2,4,6-trinitrobenzenesulphonic acid (TNBS)-, or peptidoglycan (PGN)-induced acute colitis in mice. [142][143][144] Mechanistically, the anti-colitic effect mediated by IL-17E is probably dependent on the activation of anti-inflammatory alternatively activated macrophages (AAMs) and the inhibition of CD4 + T-cell activation and their differentiation into inflammatory Th1/Th17 cells in the colon. 141,142,144,145 Recombinant IL-17E even ameliorates oxazolone-induced type 2 colitis, indicating that IL-17E has a broad anti-inflammatory effect in the colon rather than selectively suppressing Th1/Th17 cytokine production.…”

Section: Il-17dmentioning

confidence: 99%

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The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity

et al. 2016

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The mucosal immune system serves as our front-line defense against pathogens. It also tightly maintains immune tolerance to self-symbiotic bacteria, which are usually called commensals. Sensing both types of microorganisms is modulated by signalling primarily through various pattern-recognition receptors (PRRs) on barrier epithelial cells or immune cells. After sensing, proinflammatory molecules such as cytokines are released by these cells to mediate either defensive or tolerant responses. The interleukin-17 (IL-17) family members belong to a newly characterized cytokine subset that is critical for the maintenance of mucosal homeostasis. In this review, we will summarize recent progress on the diverse functions and signals of this family of cytokines at different mucosal edges.

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Inhibitory Effect of Recombinant IL-25 on the Development of Dextran Sulfate Sodium-Induced Experimental Colitis in Mice

Cited by 49 publications

References 36 publications

Campylobacter jejuni Disrupts Protective Toll-Like Receptor 9 Signaling in Colonic Epithelial Cells and Increases the Severity of Dextran Sulfate Sodium-Induced Colitis in Mice

Campylobacter jejuni Disrupts Protective Toll-Like Receptor 9 Signaling in Colonic Epithelial Cells and Increases the Severity of Dextran Sulfate Sodium-Induced Colitis in Mice

Distinctive expression pattern of interleukin-17 cytokine family members in colorectal cancer

The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity

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