TNF-α enhance Th2 and Th17 immune responses regulating by IL23 during sensitization in asthma model

Lee, Hyun Seung; Park, Heung-Woo; Song, Woo Jung; Jeon, E.; Bang, Bo-Ram; Shim, Eun Jin; Moon, Hyung‐Geun; Kim, Yoon Keun; Kang, Hye Ryun; Min, Kyung Up; Cho, Sang Heon

doi:10.1016/j.cyto.2015.12.001

Cited by 34 publications

(20 citation statements)

References 27 publications

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“…IL-23 has been proposed to stabilize Th17 cells and promote their production of IL-17, but also to promote Th2 differentiation and allergic inflammation (47). Furthermore, in some situations, TNF can promote both Th2 and Th17 inflammation by inducing IL-23 (48). However, we found that WT and TNFRdeficient mice had similar amounts of IL-23 in their airways after allergen challenge (G.S.…”

Section: Tnf Signaling Responses Contribute To Aec Transcriptional Recontrasting

confidence: 52%

TNF is required for TLR ligand–mediated but not protease-mediated allergic airway inflammation

Whitehead¹,

Thomas²,

Shalaby³

et al. 2017

Journal of Clinical Investigation

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Section: Tnf Signaling Responses Contribute To Aec Transcriptional Recontrasting

confidence: 52%

TNF is required for TLR ligand–mediated but not protease-mediated allergic airway inflammation

Whitehead¹,

Thomas²,

Shalaby³

et al. 2017

Journal of Clinical Investigation

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“…Thus, based on these results, we speculated that the overexpression of miR-802 might take part in the inflammatory process in IBD by suppressing SOCS5. Th17 and TNF-α are important factors for mediating inflammation during the development of inflammatory disease [26,27]. TNF-α contributes to the development of asthma by promoting Th17 expression during immune responses [28].…”

Section: Discussionmentioning

confidence: 99%

miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5

et al. 2020

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The present study aims to reveal the detailed molecular mechanism of microRNA (miR)-802 in the progression of inflammatory bowel disease (IBD). IBD tissues were obtained from IBD patients, followed by CD4+ cells isolation. Then, qRT-PCR and ELISA were used to detect the expression of miR-802, suppressor of cytokine signaling 5 (SOCS5), interleukin (IL)-17A and tumor necrosis factor (TNF)-α. Transfection of miR-802 mimics and miR-802 inhibitor in CD4+ cells was detected by Western blot. TargetScan and luciferase reporter assay were used to detect the relationship between SOCS5 and miR-802. Finally, colitis mice model was established to verify whether miR-802 inhibitor was involved in the protective effect of colonic mucosa. The miR-802 was highly expressed in inflamed mucosa and PBMC cells of IBD. The highest expression of miR-802 was observed in CD4+ T cells based on different immune cell subsets analysis. SOCS5 was the target gene of miR-802. The mice model experiments showed that blockade of miR-802 could alleviate mice colitis. Our study suggests that up-regulation of miR-802 plays an important role in inflammatory process of IBD via targeting SOCS5. Moreover, the differentiation of Th17 and secretion of TNF-α in IBD could be stimulated by miR-802.

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“…For example, leptin has been linked to body weight-gain associated asthma by modulating lung injury and repair 20 21 . Furthermore, IL-6, IL-1β, and IL-23 do not only exert a pro-inflammatory function, but also influence development of the lung and lung diseases, ultimately favouring asthmatic phenotype in adulthood 22 23 24 25 .…”

mentioning

confidence: 99%

Early-onset obesity dysregulates pulmonary adipocytokine/insulin signaling and induces asthma-like disease in mice

Dinger

Kasper

Hucklenbruch‐Rother

et al. 2016

Sci Rep

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Childhood obesity is a risk factor for asthma, but the molecular mechanisms linking both remain elusive. Since obesity leads to chronic low-grade inflammation and affects metabolic signaling we hypothesized that postnatal hyperalimentation (pHA) induced by maternal high-fat-diet during lactation leads to early-onset obesity and dysregulates pulmonary adipocytokine/insulin signaling, resulting in metabolic programming of asthma-like disease in adult mice. Offspring with pHA showed at postnatal day 21 (P21): (1) early-onset obesity, greater fat-mass, increased expression of IL-1β, IL-23, and Tnf-α, greater serum leptin and reduced glucose tolerance than Control (Ctrl); (2) less STAT3/AMPKα-activation, greater SOCS3 expression and reduced AKT/GSK3β-activation in the lung, indicative of leptin resistance and insulin signaling, respectively; (3) increased lung mRNA of IL-6, IL-13, IL-17A and Tnf-α. At P70 body weight, fat-mass, and cytokine mRNA expression were similar in the pHA and Ctrl, but serum leptin and IL-6 were greater, and insulin signaling and glucose tolerance impaired. Peribronchial elastic fiber content, bronchial smooth muscle layer, and deposition of connective tissue were not different after pHA. Despite unaltered bronchial structure mice after pHA exhibited significantly increased airway reactivity. Our study does not only demonstrate that early-onset obesity transiently activates pulmonary adipocytokine/insulin signaling and induces airway hyperreactivity in mice, but also provides new insights into metabolic programming of childhood obesity-related asthma.

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TNF-α enhance Th2 and Th17 immune responses regulating by IL23 during sensitization in asthma model

Cited by 34 publications

References 27 publications

TNF is required for TLR ligand–mediated but not protease-mediated allergic airway inflammation

TNF is required for TLR ligand–mediated but not protease-mediated allergic airway inflammation

miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5

Early-onset obesity dysregulates pulmonary adipocytokine/insulin signaling and induces asthma-like disease in mice

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