Macrophages produce IL-33 by activating MAPK signaling pathway during RSV infection

Qi, Feifei; Bai, Shan; Wang, Dandan; Liu, Xu; Hu, Haiyan; Zhang, Sheng; Chai, Renjie; Liu, Beixing

doi:10.1016/j.molimm.2017.05.008

Cited by 39 publications

(33 citation statements)

References 40 publications

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“…Besides the studies mentioned above in HCV, MAPK signalling pathway could also be carried out in other fields. 8,9 For example, data in the study of Li et al showed that Angiotensin II regulated the expression of miR-143/145 through p38 MAPK signalling pathway in the pathogenesis of aortic dissection. 9 However, the mechanisms of MAPK signalling pathway remain to be explored and supplemented.…”

mentioning

confidence: 99%

Inhibition of miR‐148a‐3p resists hepatocellular carcinoma progress of hepatitis C virus infection through suppressing c‐Jun and MAPK pathway

Deng

Wang

Huang

et al. 2018

J Cellular Molecular Medi

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ObjectivesThe present study was committed to investigate the role of miR‐148a‐3p in HCC infected with hepatitis C virus (HCV) and the regulatory mechanism of miR‐148a‐3p/c‐Jun/MAPK signalling pathway.MethodsDifferential analysis and GSEA analysis were performed with R packages. QRT‐PCR and Western blot were used to detect RNA or protein level, respectively. The targeted relationship between miR‐148a‐3p and c‐Jun was predicted by TargetScan database and determined by double luciferase reporter assay. MTT assay and flow cytometry were used to evaluate cell proliferation, cell cycle and cell apoptosis, respectively.Results C ‐Jun was up‐regulated, and MAPK signalling pathway was activated in HCV‐infected HCC cells. C‐Jun expression regulated inflammation‐related gene expression and had an influence on cell proliferation, cell cycle and cell apoptosis. MiR‐148a‐3p, down‐regulated in HCV‐infected HCC cells, could target c‐Jun mRNA to suppress c‐Jun protein expression.ConclusionsMiR‐148a‐3p suppressed the proliferation of HCC cells infected with HCV through targeting c‐Jun mRNA.

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mentioning

confidence: 99%

Inhibition of miR‐148a‐3p resists hepatocellular carcinoma progress of hepatitis C virus infection through suppressing c‐Jun and MAPK pathway

Deng

Wang

Huang

et al. 2018

J Cellular Molecular Medi

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“…In addition, we demonstrated that these inhibitors also decreased the expression of IL-33 in HBECs from COPD patients, which suggest that MAPK signaling is involved in the regulation of IL-33 expression in airway epithelial cells in COPD. Using murine alveolar epithelial cells or macrophage cells, the involvement of the MAPK signal pathway has been demonstrated in the IL-6 group of cytokines, oncostatin M- or respiratory syncytial virus infection-augmented IL-33 expression and production [ 40 , 41 ]. These reports support our current results.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress enhances the expression of IL-33 in human airway epithelial cells

et al. 2018

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BackgroundInterleukin-33 (IL-33) is a cytokine belonging to the IL-1 family, and its possible involvement in the pathophysiology of COPD and viral-induced exacerbations has been demonstrated. IL-33 has been shown to be increased in the airway epithelial cells from COPD patients, but the regulating mechanism of IL-33 expression in airway epithelial cells remains largely unknown. In the current study, we examined whether oxidative stress, which participates in the pathogenesis of COPD, affects the expression of IL-33 in airway epithelial cells and also evaluated the effect during viral infection.MethodsThe involvement of oxidative stress in the expression of IL-33, and its signal pathway was examined after stimulation with hydrogen peroxide (H2O2), with or without stimulation by polyinosinic-polycytidylic acid [poly (I:C)], a synthetic analogue of dsRNA that mimics viral infection, or rhinovirus infection in NCI-H292 cells and primary human bronchial epithelial cells (HBECs). In addition, the effect of antioxidant, N-acetylcysteine (NAC) in the expression of IL-33 was compared between HBECs from healthy subjects and those from COPD patients.ResultsTreatment with H2O2 significantly potentiated IL-33 expression in NCI-H292 cells, and the potentiation was reversed by NAC treatment. Mitogen-activated protein kinase (MAPK) inhibitors, but not nuclear factor-kappa B inhibitors, also significantly decreased the H2O2-potentiated IL-33 expression. In addition, H2O2 significantly potentiated the poly (I:C)- or rhinovirus-stimulated IL-33 expression. In HBECs from healthy subjects, H2O2-potentiated IL-33 expression and its reversal by NAC was also confirmed. Under the condition without H2O2-stimulation, treatment with NAC significantly decreased the expression of IL-33 in HBECs from COPD patients, but not in those from healthy subjects.ConclusionsThese results demonstrate that oxidative stress involves in the expression of IL-33 in airway epithelial cells via MAPK signal pathway and it augments IL-33 expression during viral infection. This mechanism may participate in the regulation of IL-33 expression in airway epithelial cells in COPD and the viral-induced exacerbations. Modulation of this pathway could become a therapeutic target for viral-induced exacerbations of COPD.Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0752-9) contains supplementary material, which is available to authorized users.

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“…Recently, the importance of ILC2 in shaping the immune response early during RSV infection has been revealed in infants [46]. AMs are one of the source of IL-33 upon RSV infection [45,47,48], and it was shown that deletion of IL-33 production by myeloid cells strongly affects IL-5 secretion and eosinophil recruitment upon RSV infection [45]. Furthermore, IL-33 treatment promotes IL-10 production by B-cells in adult mice, thus protecting these mice from induction of inflammatory bowel disease [49].…”

Section: Discussionmentioning

confidence: 99%

Regulatory B Lymphocytes Colonize the Respiratory Tract of Neonatal Mice and Modulate Immune Responses of Alveolar Macrophages to RSV Infection in IL-10-Dependant Manner

Laubreton

Drajac

Éléouët

et al. 2020

Viruses

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Respiratory syncytial virus (RSV) is the prevalent pathogen of lower respiratory tract infections in children. The presence of neonatal regulatory B lymphocytes (nBreg) has been associated with a poor control of RSV infection in human newborns and with bronchiolitis severity. So far, little is known about how nBreg may contribute to neonatal immunopathology to RSV. We tracked nBreg in neonatal BALB/c mice and we investigated their impact on lung innate immunity, especially their crosstalk with alveolar macrophages (AMs) upon RSV infection. We showed that the colonization by nBreg during the first week of life is a hallmark of neonatal lung whereas this population is almost absent in adult lung. This particular period of age when nBreg are abundant corresponds to the same period when RSV replication in lungs fails to generate a type-I interferons (IFN-I) response and is not contained. When neonatal AMs are exposed to RSV in vitro, they produce IFN-I that in turn enhances IL-10 production by nBreg. IL-10 reciprocally can decrease IFN-I secretion by AMs. Thus, our work identified nBreg as an important component of neonatal lungs and pointed out new immunoregulatory interactions with AMs in the context of RSV infection.

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Macrophages produce IL-33 by activating MAPK signaling pathway during RSV infection

Cited by 39 publications

References 40 publications

Inhibition of miR‐148a‐3p resists hepatocellular carcinoma progress of hepatitis C virus infection through suppressing c‐Jun and MAPK pathway

Inhibition of miR‐148a‐3p resists hepatocellular carcinoma progress of hepatitis C virus infection through suppressing c‐Jun and MAPK pathway

Oxidative stress enhances the expression of IL-33 in human airway epithelial cells

Regulatory B Lymphocytes Colonize the Respiratory Tract of Neonatal Mice and Modulate Immune Responses of Alveolar Macrophages to RSV Infection in IL-10-Dependant Manner

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