Soluble interleukin-6 receptor is elevated during influenza A virus infection and mediates the IL-6 and IL-32 inflammatory cytokine burst

Wang, Jun; Wang, Qing; Han, Tao; Li, Yongkui; Zhu, Shengli; Ao, Fang; Feng, Jian; Jing, Ming-Zhen; Wang, Li; Ye, Linbai; Zhu, Ying

doi:10.1038/cmi.2014.80

Cited by 40 publications

(43 citation statements)

References 51 publications

(61 reference statements)

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“…Accordingly, silencing of IL-32 up-regulated the expression of sIL-6Ra during influenza virus infection. Thus, IL-32 simultaneously decreased sIL-6Ra while enhancing IL-6 production [85]. These results indicate that during influenza A virus infections PGE 2 , NO, sIL-6Ra, and IL-32 are produced, and these proinflammatory mediators influence each other.…”

Section: The Role Of Il-32 In Viral Infectionsmentioning

confidence: 62%

Interleukin 32: a novel player in the control of infectious diseases

Ribeiro‐Dias

Gomes

Silva

et al. 2016

Journal of Leukocyte Biology

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Interleukin 32 (IL-32) is a proinflammatory cytokine, expressed as 9 distinct isoforms. The most active isoform is the predominantly intracellular-functioning IL-32γ. Involvement of IL-32 in infectious diseases is increasingly being appreciated. Production of IL-32 promotes pathways that serve to control bacterial infection, especially those caused by mycobacteria. A similar role for this cytokine is observed in the cellular response to viral infections. In addition to its protective effects against microorganisms, IL-32 is involved in immunopathogenesis of some infectious diseases. In parasitic diseases, it has been demonstrated that this cytokine is induced by Leishmania infection. In this review, we summarize the present data on the role of IL-32 in infectious diseases, highlighting this cytokine as new target for control of infections.

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Section: The Role Of Il-32 In Viral Infectionsmentioning

confidence: 62%

Interleukin 32: a novel player in the control of infectious diseases

Ribeiro‐Dias

Gomes

Silva

et al. 2016

Journal of Leukocyte Biology

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“…Signaling of IL6 via the sIL6R promotes proinflammatory activities (33). Recent studies have found that sIL6R expression up-regulates the levels of its own ligand IL6 as well as the proinflammatory cytokine IL32 (34), and the circulating sIL6R elicited extensive antiviral activity through the induction of type I and type III IFNs (25,26). Furthermore, sIL6R was found to facilitate the nuclear translocation of IRF3 and NF-B (25).…”

Section: Il6r Is a Target Of Mir-590-5pmentioning

confidence: 99%

Inducible microRNA-590-5p inhibits host antiviral response by targeting the soluble interleukin-6 (IL6) receptor

Zhou

Xia

Cheng

et al. 2018

Journal of Biological Chemistry

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Edited by Charles E. SamuelMicroRNA (miR)-590-5p has been identified as an important regulator of some signaling pathways such as cell proliferation and tumorigenesis. However, little is known about its role during viral infection. Here, we report that miR-590-5p was significantly induced by various viruses and effectively potentiated virus replication in different viral infection systems. Furthermore, miR-590-5p substantially attenuated the virus-induced expression of type I and type III interferons (IFNs) and inflammatory cytokines, resulting in impaired downstream antiviral signaling. Interleukin-6 receptor (IL6R) was identified as a target of miR-590-5p. Interestingly, the role of miR-590-5p in virus-triggered signaling was abolished in IL6R knockout cells, and this could be rescued by restoring the expression of the soluble IL6R (sIL6R) but not the membrane-bound IL6R (mIL6R), suggesting that sIL6R is indispensable for miR-590-5p in modulating the host antiviral response. Furthermore, miR-590-5p down-regulated endogenous sIL6R and mIL6R expression through a translational repression mechanism. These findings thus uncover a previously uncharacterized role and the underlying mechanism of miR-590-5p in the innate immune response to viral infection.

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“…51,52 Impaired healing in animal models and age-related delayed healing of acute human wounds exhibit raised local and systemic levels of TNFα that may parallel the proinflammatory phenotype. 53,54 The pleiotropic cytokine IL6 is produced by macrophages, dendritic cells, mast cells, and other innate immune cells; consequently, this cytokine has long been considered a marker of inflammation. 55 Using ELISA to detect the concentration of TNFα and IL6 at different times, results showed that PACT treatment inhibited inflammation-factor secretion, significantly reduce the scalded-tissue concentration of TNFα and IL6, and prevent further deepening of the wound.…”

mentioning

confidence: 99%

Photodynamic antimicrobial chemotherapy for <em>Staphylococcus aureus</em> and multidrug-resistant bacterial burn infection in vitro and in vivo

Mai¹,

Gao²,

Li³

et al. 2017

IJN

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Background and objectives Antibiotic resistance has emerged as one of the most important determinants of outcome in patients with serious infections, along with the virulence of the underlying pathogen. Photodynamic antimicrobial chemotherapy (PACT) has been proposed as an alternative approach for the inactivation of bacteria. This study aims to evaluate the antibacterial effect of sinoporphyrin sodium (DVDMS)-mediated PACT on Staphylococcus aureus and multidrug resistant S. aureus in vitro and in vivo. Materials and methods Bacteria were incubated with DVDMS and exposed to treatment with light. After PACT treatment, colony-forming units were counted to estimate the bactericidal effect. Intracellular reactive oxygen-species production was detected by flow cytometry. Flow cytometry and fluorescence-microscopy detection of bacterial cell-membrane permeability. Enzyme-linked immunosorbent assays were used to determine expression of VEGF, TGFβ 1 , TNFα, IL6, and bFGF factors in burn infection. Results DVDMS-PACT effectively killed bacterial proliferation. Intracellular ROS levels were enhanced obviously in the PACT-treatment group. SYTO 9 and propidium iodide staining showed a decrease in the ratio of green:red fluorescence intensity in the PACT-treatment group in comparison to the control group. Enzyme-linked immunosorbent-assay results revealed that in the healing process, the expression of bFGF, TGFβ 1 , and VEGF in the treatment group were higher than in the control group, which inhibited inflammation-factor secretion. In addition, skin-tissue bacteria were reduced after treatment. Conclusion These results indicate that DVDMS-PACT presents significant bactericidal activity and promotes wound healing after burn infections.

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Soluble interleukin-6 receptor is elevated during influenza A virus infection and mediates the IL-6 and IL-32 inflammatory cytokine burst

Cited by 40 publications

References 51 publications

Interleukin 32: a novel player in the control of infectious diseases

Interleukin 32: a novel player in the control of infectious diseases

Inducible microRNA-590-5p inhibits host antiviral response by targeting the soluble interleukin-6 (IL6) receptor

Photodynamic antimicrobial chemotherapy for <em>Staphylococcus aureus</em> and multidrug-resistant bacterial burn infection in vitro and in vivo

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