Increased interleukin-32 expression in chronic hepatitis B virus-infected liver

Xu, Qi-Huan; Pan, Xingfei; Shu, Xin; Cao, Hong; Li, Xuejun; Zhang, Ka; Lu, Jianxi; Zou, Yong; Li, Xueling; Liu, Hongcan; Zhang, Yeqiong; Yang, Di; Ning, Qin; Shen, Guanxin; Li, Gang

doi:10.1016/j.jinf.2012.05.009

Cited by 30 publications

(23 citation statements)

References 30 publications

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“…Several studies have shown that IL-32, an important proinflammatory cytokine in rheumatoid arthritis, enhanced IL-6 and IL-8 production in fibroblast-like synoviocytes [30–32]. Some studies also have shown that IL-32 is closely associated with liver fibrosis of chronic viral hepatitis [33, 34]. Furthermore, compared with primary blood monocytes, IL-1 β , TNF- α , or LPS can stimulate high levels of IL-32 expression through the I κ B kinase- β /NF- κ B and ERK pathways in human umbilical vein endothelial cells, aortic macrovascular endothelial cells, and cardiac and pulmonary microvascular endothelial cells [26].…”

Section: Discussionmentioning

confidence: 99%

Scropolioside B Inhibits IL-1βand Cytokines Expression through NF-κB and Inflammasome NLRP3 Pathways

Zhu

Zhang

Ling

et al. 2014

Mediators of Inflammation

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Chronic inflammation is associated with various chronic illnesses including immunity disorders, cancer, neurodegeneration, and vascular diseases. Iridoids are compounds with anti-inflammatory properties. However their anti-inflammatory mechanism remains unclear. Here, we report that scropolioside B, isolated from a Tibetan medicine (Scrophularia dentata Royle ex Benth.), blocked expressions of TNF, IL-1, and IL-32 through NF-κB pathway. Scropolioside B inhibited NF-κB activity in a dose-dependent manner with IC50 values of 1.02 μmol/L. However, catalpol, similar to scropolioside B, was not effective in inhibiting NF-κB activity. Interestingly, scropolioside B and catalpol decreased the expression of NLRP3 and cardiolipin synthetase at both the mRNA and protein level. Our results showed that scropolioside B is superior in inhibiting the expression, maturation, and secretion of IL-1β compared to catalpol. These observations provide further understanding of the anti-inflammatory effects of iridoids and highlight scropolioside B as a potential drug for the treatment of rheumatoid arthritis and atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Scropolioside B Inhibits IL-1βand Cytokines Expression through NF-κB and Inflammasome NLRP3 Pathways

Zhu

Zhang

Ling

et al. 2014

Mediators of Inflammation

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“…Based on link between IL-32 activity and production of IFNα, β or γ, various authors proposed that IL-32 exhibits its antiviral properties by all these interferons (39,21) (Figure 2). IL-32 expression is induced by hepatitis C and Epstein-Barr viruses (EBV) also (23,46,47). Human papillomavirus (HPV) induces IL-32 expression via E7-mediated COX-2 stimulation (41).…”

Section: Role In Viral Infectionsmentioning

confidence: 99%

“…In hepatitis B virus infection, HBx protein encoded by HBV genome, plays an important role in the hepatic inflammatory processes. Study of Pan X et al showed that HBx could induce IL-32 expression in Huh7 cell in a dosedependent manner by NF-κB pathway (46), and it is correlated with the severity of liver inflammation/fibrosis in patients with chronic HBV infection (48). In vitro and in vivo results of different studies showed that IL-32 expression in human macrophages serves to protect the host by facilitating apoptosis of the host cell and thereby depriving Mycobacterium tuberculosis of a protected survival as an intracellular microorganism (49,50).…”

Section: Role In Viral Infectionsmentioning

confidence: 99%

Interleukin-32 in Infection, Inflammation and Cancer Biology

Pavlovic

Jovanović

Arsenijević

2020

Serbian Journal of Experimental and Clinical Research

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“…Previous studies by our group determined that IL-32 expression is induced by hepatitis B virus protein X through the activation of NF-κB (19,20). IL-32 expression is increased in chronic hepatitis B virus-infected liver and is associated with HBV-related liver inflammation and fibrosis (19). Thus, it is hypothesized that IL-32 may participate in the pathogenesis of liver fibrosis through the integrin/FAK-signaling pathway.…”

Section: Introductionmentioning

confidence: 98%

“…Therefore, it serves a dual role in integrin signaling (18). Previous studies by our group determined that IL-32 expression is induced by hepatitis B virus protein X through the activation of NF-κB (19,20). IL-32 expression is increased in chronic hepatitis B virus-infected liver and is associated with HBV-related liver inflammation and fibrosis (19).…”

Section: Introductionmentioning

confidence: 99%

IL-32γ promotes integrin αvβ6 expression through the activation of NF-κB in HSCs

Liu

Pan

Cao

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Hepatic stellate cell (HSC) activation is important in the pathogenesis of liver fibrosis. However, the molecular mechanism of HSC activation is not completely understood. In the present study, it was demonstrated that interleukin-32γ (IL-32γ) is capable of enhancing intefgrin αvβ6 expression by inducing integrin αvβ6 promoter activity in a dose-dependent manner in HSCs. Furthermore, it was determined that nuclear factor κB (NF-κB) activation is required for IL-32γ-induced integrin αvβ6 expression. Increased integrin αvβ6 expression is then able to activate HSCs. These results indicate that NF-κB activation is required for IL-32γ to induce integrin αvβ6 expression and consequently promote HSC activation. Therefore, IL-32γ activates HSCs and therefore may be associated with hepatic fibrogenesis. These results may enable the development of novel effective strategies to treat hepatic fibrosis.

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Increased interleukin-32 expression in chronic hepatitis B virus-infected liver

Cited by 30 publications

References 30 publications

Scropolioside B Inhibits IL-1βand Cytokines Expression through NF-κB and Inflammasome NLRP3 Pathways

Scropolioside B Inhibits IL-1βand Cytokines Expression through NF-κB and Inflammasome NLRP3 Pathways

Interleukin-32 in Infection, Inflammation and Cancer Biology

IL-32γ promotes integrin αvβ6 expression through the activation of NF-κB in HSCs

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