Chemokine-receptor upregulation and disease severity in Respiratory Syncytial Virus infection

Morrison, Paul T.; Thomas, Lynette H.; Manna, Soumendu; Handforth, Jennifer; Tibby, Shane M.; Friedland, Jon S.

doi:10.1016/j.clim.2008.03.460

Cited by 12 publications

(11 citation statements)

References 45 publications

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“…Patients with ARI were mainly infected by RSV. This virus is involved in serious lower respiratory tract disease in children and can induce the produce of several cytokines (IL‐6, IL‐1, TNF‐α, IL‐8 and GM‐CSF), chemokines (IL‐8, IP‐10, MCP‐1 and RANTES) and chemokine receptor expressions in vivo and in vitro . Accordingly, in this study, serum from RSV‐infected patients had increased levels of IL‐1β, TNF‐α, IL‐4, IL‐5, MCP‐1 and RANTES.…”

Section: Discussionmentioning

confidence: 52%

Increased Systemic Cytokine/Chemokine Expression in Asthmatic and Non‐asthmatic Patients with Bacterial, Viral or Mixed Lung Infection

et al. 2017

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This study was aimed to determine the profiles of serum cytokines (IL-1β, TNF-α, IL-4, IL-5) and chemokines (MCP-1: monocyte chemoattract protein-1 and RANTES: regulated on activation normal T cell expressed and secreted) in individuals with an asthmatic versus a non-asthmatic background with bacterial, viral or mixed acute respiratory infection. Asthmatic (n = 14) and non-asthmatic (n = 29) patients with acute viral, bacterial or mixed (bacterial and viruses) respiratory infection were studied. Patients were also analysed as individuals with pneumonia or bronchitis. Healthy individuals with similar age and sex (n = 10) were used as controls. Cytokine/chemokine content in serum was determined by ELISA. Increased cytokine/chemokine concentration in asthmatic and non-asthmatic patients was observed. However, higher concentrations of chemokines (MCP-1 and RANTES) in asthmatic patients infected by viruses, bacteria or bacteria and viruses (mixed) than in non-asthmatic patients were observed. In general, viral and mixed infections were better cytokine/chemokine inducers than bacterial infection. Cytokine/chemokine expression was similarly increased in both asthmatic and non-asthmatic patients with pneumonia or bronchitis, except that RANTES remained at normal levels in bronchitis. Circulating cytokine profiles induced by acute viral, bacterial or mixed lung infection were not related to asthmatic background, except for chemokines that were increased in asthmatic status.

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Section: Discussionmentioning

confidence: 52%

Increased Systemic Cytokine/Chemokine Expression in Asthmatic and Non‐asthmatic Patients with Bacterial, Viral or Mixed Lung Infection

et al. 2017

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“…Several chemokine receptors been shown to be involved in the host response to RSV infection, particularly CCR1 and CXCR1 [37, 38]. The ligands of CCR1 include MIP-1α, RANTES, and MCP [37], and an important ligand for CXCR1 is IL-8 [39–41].…”

Section: Resultsmentioning

confidence: 99%

Respiratory Syncytial Virus F and G Proteins Induce Interleukin 1α, CC, and CXC Chemokine Responses by Normal Human Bronchoepithelial Cells

et al. 2010

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Human respiratory syncytial virus (RSV) is a ubiquitous respiratory virus causing serious lower respiratory tract disease in infants and young children worldwide. Studies have shown that RSV infection modulates chemokine expression patterns suggesting that particular cytokine expression profiles may be indicators of disease severity. In this study, we show that RSV F or G protein treatment of fully differentiated primary human bronchial epithelial (NHBE) cells induces apical and basolateral secretion of IL-8, IP-10, MCP-1, and RANTES. Purified RSV G (attachment) protein was shown to stimulate the secretion of IL-1α, and RANTES, while purified F (fusion) protein elicited the production of IL-8, IP-10, and RANTES. Studies with UV-inactivated RSV showed that treatment of NHBE cells induces apical IL-8, IP-10, and MCP-1 secretion independent of infection suggesting that RSV proteins alone modify the chemokine response pattern which may affect the early immune response prior to infection.

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“…Suppressing SOCS signals improved influenza infection and inhibited HRSV replication [68,69]. CCR2 mRNA upregulation was correlated with HRSV-disease severity [70]. CCR2 antagonism reduced pathology, morbidity, and mortality during influenza A (H1N1) infection [71].…”

Section: Discussionmentioning

confidence: 99%

MERS-CoV infection is associated with downregulation of genes encoding Th1 and Th2 cytokines/chemokines and elevated inflammatory innate immune response in the lower respiratory tract

et al. 2020

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A B S T R A C TMERS-CoV, a highly pathogenic virus in humans, is associated with high morbidity and case fatality. Inflammatory responses have a significant impact on MERS-CoV pathogenesis and disease outcome. However, CD4 + T-cell induced immune responses during acute MERS-CoV infection are barely detectable, with potent inhibition of effector T cells and downregulation of antigen presentation. The local pulmonary immune response, particularly the Th1 and Th2-related immune response during acute severe MERS-CoV infection is not fully understood. In this study, we offer the first insights into the pulmonary gene expression profile of Th1 and Th2related cytokines/chemokines (Th1 & Th2 responses) during acute MERS-CoV infection using RT 2 Profiler PCR Arrays. We also quantified the expression level of primary inflammatory cytokines/chemokines. Our results showed a downregulation of Th2, inadequate (partial) Th1 immune response and high expression levels of inflammatory cytokines IL-1α and IL-1β and the neutrophil chemoattractant chemokine IL-8 (CXCL8) in the lower respiratory tract of MERS-CoV infected patients. Moreover, we identified a high viral load in all included patients. We also observed a correlation between inflammatory cytokines, Th1, and Th2 downregulation and the case fatality rate. Th1 and Th2 response downregulation, high expression of inflammatory cytokines, and high viral load may contribute to lung inflammation, severe infection, the evolution of pneumonia and ARDS, and a higher case fatality rate. Further study of the molecular mechanisms underlying the Th1 and Th2 regulatory pathways will be vital for active vaccine development and the identification of novel therapeutic strategies.

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Chemokine-receptor upregulation and disease severity in Respiratory Syncytial Virus infection

Cited by 12 publications

References 45 publications

Increased Systemic Cytokine/Chemokine Expression in Asthmatic and Non‐asthmatic Patients with Bacterial, Viral or Mixed Lung Infection

Increased Systemic Cytokine/Chemokine Expression in Asthmatic and Non‐asthmatic Patients with Bacterial, Viral or Mixed Lung Infection

Respiratory Syncytial Virus F and G Proteins Induce Interleukin 1α, CC, and CXC Chemokine Responses by Normal Human Bronchoepithelial Cells

MERS-CoV infection is associated with downregulation of genes encoding Th1 and Th2 cytokines/chemokines and elevated inflammatory innate immune response in the lower respiratory tract

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