Systemic interleukin-9 in inflammatory bowel disease: Association with mucosal healing in ulcerative colitis

Matusiewicz, Małgorzata; Neubauer, Katarzyna; Bednarz−Misa, Iwona; Górska, Sabina; Krzystek−Korpacka, Małgorzata

doi:10.3748/wjg.v23.i22.4039

Cited by 23 publications

(14 citation statements)

References 27 publications

(42 reference statements)

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“…The role of IL-9 in the process of mucosal healing is not fully understood, we evaluated its effect on intestinal epithelial cells. IL-9 significantly inhibited the growth of RKO and SW480 cells into the gap in scratch assays, which was consistent with the report that systemic IL-9 level corresponds with endoscopic inflammation, may serve as a negative marker of mucosal healing in UC [ 22 , 23 ]. Moreover, SW480 cells were stimulated freshly with IL-9, the level of pSTAT3 increased but SOCS3 did not change.…”

Section: Discussionsupporting

confidence: 90%

IL-9 promotes the pathogenesis of ulcerative colitis through STAT3/SOCS3 signaling

Zhang

et al. 2018

Bioscience Reports

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Ulcerative colitis (UC) is a chronic condition in which the overreacting immune system may play an important role. It has been confirmed that the interleukin (IL) 9 (IL-9) participates in the pathogenesis of UC but the molecular mechanism is not fully illustrated. Here, we show that levels of peripheral blood cytokines IL-9, IL-8, IL-10, IL-6, IL-1β, IL-12, and tumor necrosis factor (TNF) were higher in patients with UC than normal control, and serum and local IL-9 levels were positively correlated with the disease activity grade. Moreover, IL-9 stimulation inhibited suppressor of cytokine signaling 3 (SOCS3) expression and wound healing ability in colonic epithelial cells and promoted the phosphorylation level of signal transducers and activators of transcription 3 (STAT3). And IL-9 stimulation promoted claudin-2 expression while inhibited claudin-3 and occludin expression. Furthermore, SOCS3 overexpression rescued the IL-9-induced effects. Altogether, IL-9 participates in the pathogenesis of UC through STAT3/SOCS3 signaling pathway and has the potential to serve as a possible therapeutic candidate in patients with UC.

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Section: Discussionsupporting

confidence: 90%

IL-9 promotes the pathogenesis of ulcerative colitis through STAT3/SOCS3 signaling

Zhang

et al. 2018

Bioscience Reports

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“…Further studies have also revealed that in UC patients, activated peripheral blood lymphocytes produced increased amounts of IL-9 ( 186 ). Clinically, patients with increased serum IL-9 levels have been shown to have a worsened prognosis ( 187 ) and higher levels of systemic IL-9 were also associated with cachexia and lower hemoglobin concentrations in IBD patients ( 188 ).…”

Section: Th9 Cellsmentioning

confidence: 99%

Effector T Helper Cell Subsets in Inflammatory Bowel Diseases

Imam¹,

Park²,

Kaplan³

et al. 2018

Front. Immunol.

205

157

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The gastrointestinal tract is a site of high immune challenge, as it must maintain a delicate balance between tolerating luminal contents and generating an immune response toward pathogens. CD4+ T cells are key in mediating the host protective and homeostatic responses. Yet, CD4+ T cells are also known to be the main drivers of inflammatory bowel disease (IBD) when this balance is perturbed. Many subsets of CD4+ T cells have been identified as players in perpetuating chronic intestinal inflammation. Over the last few decades, understanding of how each subset of Th cells plays a role has dramatically increased. Simultaneously, this has allowed development of therapeutic innovation targeting specific molecules rather than broad immunosuppressive agents. Here, we review the emerging evidence of how each subset functions in promoting and sustaining the chronic inflammation that characterizes IBD.

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“…The level of IL-9 mRNA expression in intestinal tissue from UC patients correlates with the endoscopic disease score and histological disease activity [202,203]. Higher serum levels of IL-9 also associate with disease activity in UC [204]. In support of this, Th9-like inflammatory profile, IL-9 promoter-binding Smad2 and Smad3 proteins activated by TGF-β and Notch signaling are up-regulated in the inflamed mucosa of UC patients [205].…”

Section: The Role Of Il-9 Secreting Cd4 + T-cells In Ibdmentioning

confidence: 83%

Dissecting the Heterogeneity in T-Cell Mediated Inflammation in IBD

Tindemans

Joosse

Samsom

2020

Cells

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Infiltration of the lamina propria by inflammatory CD4+ T-cell populations is a key characteristic of chronic intestinal inflammation. Memory-phenotype CD4+ T-cell frequencies are increased in inflamed intestinal tissue of IBD patients compared to tissue of healthy controls and are associated with disease flares and a more complicated disease course. Therefore, a tightly controlled balance between regulatory and inflammatory CD4+ T-cell populations is crucial to prevent uncontrolled CD4+ T-cell responses and subsequent intestinal tissue damage. While at steady state, T-cells display mainly a regulatory phenotype, increased in Th1, Th2, Th9, Th17, and Th17.1 responses, and reduced Treg and Tr1 responses have all been suggested to play a role in IBD pathophysiology. However, it is highly unlikely that all these responses are altered in each individual patient. With the rapidly expanding plethora of therapeutic options to inhibit inflammatory T-cell responses and stimulate regulatory T-cell responses, a crucial need is emerging for a robust set of immunological assays to predict and monitor therapeutic success at an individual level. Consequently, it is crucial to differentiate dominant inflammatory and regulatory CD4+ T helper responses in patients and relate these to disease course and therapy response. In this review, we provide an overview of how intestinal CD4+ T-cell responses arise, discuss the main phenotypes of CD4+ T helper responses, and review how they are implicated in IBD.

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Systemic interleukin-9 in inflammatory bowel disease: Association with mucosal healing in ulcerative colitis

Cited by 23 publications

References 27 publications

IL-9 promotes the pathogenesis of ulcerative colitis through STAT3/SOCS3 signaling

IL-9 promotes the pathogenesis of ulcerative colitis through STAT3/SOCS3 signaling

Effector T Helper Cell Subsets in Inflammatory Bowel Diseases

Dissecting the Heterogeneity in T-Cell Mediated Inflammation in IBD

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