IL-17 and TNF-α co-operation contributes to the proinflammatory response of hepatic stellate cells

Beringer, Audrey; Miossec, Pierre

doi:10.1111/cei.13316

Cited by 24 publications

(14 citation statements)

References 32 publications

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“… 37 Moreover, IL-6, IL-8, and IL-1β are increased following CCl 4 -induced TNF-α release. 37 , 38 Among these inflammatory mediators, pro-inflammatory cytokines including TNF-α, IL-8, IL-1β, and IL-6 play an important role in the activation of HSCs and synthesis of ECM. 37 , 39 IL-10 acts as an anti-inflammatory and antifibrotic mediator.…”

Section: Discussionmentioning

confidence: 99%

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Liu¹,

Sun²,

Chen³

et al. 2021

Journal of Clinical and Translational Hepatology

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Background and Aims:The pathogenesis of liver fibrosis involves liver damage, inflammation, oxidative stress, and intestinal dysfunction. Indole-3-propionic acid (IPA) has been demonstrated to have antioxidant, anti-inflammatory and anticancer activities, and a role in maintaining gut homeostasis. The current study aimed to investigate the role of IPA in carbon tetrachloride (CCl 4 )-induced liver fibrosis and explore the underlying mechanisms. Methods: The liver fibrosis model was established in male C57BL/6 mice by intraperitoneal injection of CCl 4 twice weekly. IPA intervention was made orally (20 mg/kg daily). The degree of liver injury and fibrosis were assessed by serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and histopathology. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction (qPCR) were used to detect the inflammatory cytokines. The malondialdehyde (MDA), glutathione, glutathione peroxidase, superoxide dismutase, and catalase were determined via commercial kits. Hepatocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. The expression of mRNA and protein was assayed by qPCR, Western blotting, or immunohistochemical staining. Results: After IPA treatment, the ALT and AST, apoptotic cells, and pro-inflammatory factor levels were enhanced significantly. Moreover, IPA intervention up-regulated the expression of collagen I, α-smooth muscle actin, tissue inhibitor of matrix metalloproteinase-1, matrix metalloproteinase-2, transforming growth factor-β1 (TGF-β1), Smad3, and phosphorylated-Smad2/3. Additionally, IPA intervention did not affect the MDA level. Attrac-tively, the administration of IPA remodeled the gut flora structure. Conclusions: IPA aggravated CCl 4 -induced liver damage and fibrosis by activating HSCs via the TGF-β1/ Smads signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Liu¹,

Sun²,

Chen³

et al. 2021

Journal of Clinical and Translational Hepatology

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“…TNF-α is known to trigger cell activation, migration, or proliferation against pathogens, and is involved in the pathogenesis of inflammatory and autoimmune diseases. TNF-α can induce the release of cytokines IL-6, IL-1β, and IL-8, which can be enhanced by IL-17 ( 40 ). MMP-9 is produced by a variety of cells including epithelial cells, fibroblasts, dendritic cells, macrophages, and granulocyteshas in response to P. aeruginosa infection, and has the capacity to degrade both elastin and partially hydrolyzed collagen resulting in lung structure injury ( 41 ).…”

Section: Discussionmentioning

confidence: 99%

IL-17 Aggravates Pseudomonas aeruginosa Airway Infection in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Ding

Han

et al. 2022

Front. Immunol.

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Pseudomonas aeruginosa airway infection increases risks of exacerbations and mortality in chronic obstructive pulmonary disease (COPD). We aimed to elucidate the role of IL-17 in the pathogenesis. We examined the expression and influences of IL-23/IL-17A in patients with stable COPD (n = 33) or acute COPD exacerbations with P. aeruginosa infection (n = 34). A mouse model of COPD (C57BL/6) was used to investigate the role of IL-17A in host inflammatory responses against P. aeruginosa infection through the application of IL-17A–neutralizing antibody or recombinant IL-17A. We found that P. aeruginosa infection increased IL-23/17A signaling in lungs of both COPD patients and COPD mouse models. When COPD mouse models were treated with neutralizing antibody targeting IL-17A, P. aeruginosa induced a significantly less polymorphonuclear leukocyte infiltration and less bacterial burden in their lungs compared to those of untreated counterparts. The lung function was also improved by neutralizing antibody. Furthermore, IL-17A-signaling blockade significantly reduced the expression of pro-inflammatory cytokine IL-1β, IL-18, TNF-α, CXCL1, CXCL15 and MMP-9, and increased the expression of anti-inflammatory cytokine IL-10 and IL-1Ra. The application of mouse recombinant IL-17A exacerbated P. aeruginosa-mediated inflammatory responses and pulmonary dysfunction in COPD mouse models. A cytokine protein array revealed that the expression of retinol binding protein 4 (RBP4) was down-regulated by IL-17A, and exogenous RBP4-recombinant protein resulted in a decrease in the severity of P. aeruginosa-induced airway dysfunction. Concurrent application of IL-17A-neutralizing antibody and ciprofloxacin attenuated airway inflammation and ventilation after inoculation of P. aeruginosa in COPD mouse models. Our results revealed that IL-17 plays a detrimental role in the pathogenesis of P. aeruginosa airway infection during acute exacerbations of COPD. Targeting IL-17A is a potential therapeutic strategy in controlling the outcomes of P. aeruginosa infection in COPD patients.

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“…There are four types of collagens in lung tissues, where collagen I and collagen III are the most abundant ( 47 ). Collagenous fibers are an aggregated form of collagen secreted by the fibroblasts ( 48 ).…”

Section: Discussionmentioning

confidence: 99%

Maiwei Yangfei decoction prevents bleomycin‑induced pulmonary fibrosis in mice

Peng

Han

et al. 2021

Exp Ther Med

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Maiwei Yangfei (MWYF) is a compound Chinese herb that is safe and effective in the clinical setting in patients with pulmonary fibrosis (PF). The aim of the present study was to assess the role of a (MWYF) decoction in a bleomycin (BLM)-induced PF mouse model and to investigate the underlying functional mechanism. Chemical components within the MWYF decoction were analysed using liquid chromatography-mass spectrometry. A total of 50 C57BL/6 mice were randomly assigned to one of the following five groups with 10 mice per group: Control, model, low dose MWYF (20 g/kg), medium dose MWYF (40 g/kg) and high dose MWYF (60 g/kg). A mouse PF model was established by the tracheal instillation of BLM (5 mg/kg) prior to MWYF treatment, except for mice in the control group. After 21 days of treatment with MWYF, the mice were sacrificed and the body weights were recorded. In addition, pulmonary tissues and bronchial alveolar lavage fluid were collected. TNF-α, IL-6, IL-17, hydroxyproline, pyridinoline and collagen I levels were determined using ELISA. Vimentin, α-smooth muscle actin (α-SMA), fibronectin, TGF-β1, Smad3, TNF-α, IL-6, IL-17, collagen I and collagen III were determined using western blotting. Vimentin and α-SMA levels were also determined using immunofluorescence analysis. Collagens I and III were detected using immunohistochemical analysis and TGF-β1 and Smad3 levels were determined using reverse transcription-quantitative PCR. Following treatment with MWYF decoction, the body weight of the mice in the PF group increased, the degree of pulmonary alveolitis and PF was reduced, collagen levels were reduced and the expression levels of α-SMA, vimentin and fibronectin were decreased. Although both protein and mRNA expression levels of TGF-β1 and Smad3 were reduced, they remained higher than those observed in the control group. To conclude, MWYF decoction delayed the development of BLM-induced PF in mice, where the functional mechanism was likely associated with the TGF-β1/Smad3 signalling pathway.

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IL-17 and TNF-α co-operation contributes to the proinflammatory response of hepatic stellate cells

Cited by 24 publications

References 32 publications

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

IL-17 Aggravates Pseudomonas aeruginosa Airway Infection in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Maiwei Yangfei decoction prevents bleomycin‑induced pulmonary fibrosis in mice

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