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Curr Pharm Des. 2017 Mar 16. doi: 10.2174/1381612823666170316123736. [Epub ahead of print]
Cytokines induced during influenza virus infection.
Bet?kov? T1, Kostrabova A2, Lachova V1, Turianova L1.
Author information
Abstract
Influenza A virus is one of the major human pathogens. The influenza infection can pass out without any subclinical symptoms or infestation can appear in upper respiratory tract as well as in lower respiratory tract where it can result in lethal outcome. Both innate and adaptive immune responses are activated shortly after infection providing protection against infection. Many activities of the cells of innate and adaptive immunity are coordinated by cytokines. However, inordinate or disbalanced immune response may result in overproduction of cytokines as well as chemokines what can lead to severe inflammation, including excessive recruitment of neutrophils and mononuclear cells at the site of infection. These may damage lung tissue, reduce respiratory capacity, and cause severe disease and mortality. Recently, the role of cytokines induced by virus infection has been reevaluated. While moderate inflammatory response protects against development of severe illness, the hyper-inflammatory response can elevate the disease progression. In this minireview we summarized the data on cytokines and chemokines induced in the sera of hospitalized patients infected with human and avian high pathogenic influenza viruses and define their possible role in pathogenesis. Interleukine IL-6 and chemokines CCL-2/MCP-1, CCL-4, MIP/1β, CXCL-8/IL-8, CXCL-9/MIG, and CXCL-10/IP-10 are associated with pathogenicity of both avian (H5N1 and H7N9) and human (pdmH1N1 and H3N2) viruses. Chemokines CCL-2/MCP-1, CXCL-8/IL-8, CXCL-9/MIG, and CXCL-10/IP-10 are also connected with mortality. These cytokines may be used as targets for new, more complex therapy in the extenuation of unfavorable effects of hyper inflammatory response.
Copyright? Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
KEYWORDS:
B cell; NK cell; T cell; chemokines; cytokines; immunity; influenza virus; interferon; interleukin; macrophage; pathogenesis
PMID: 28302021 DOI: 10.2174/1381612823666170316123736
Cytokines induced during influenza virus infection.
Bet?kov? T1, Kostrabova A2, Lachova V1, Turianova L1.
Author information
Abstract
Influenza A virus is one of the major human pathogens. The influenza infection can pass out without any subclinical symptoms or infestation can appear in upper respiratory tract as well as in lower respiratory tract where it can result in lethal outcome. Both innate and adaptive immune responses are activated shortly after infection providing protection against infection. Many activities of the cells of innate and adaptive immunity are coordinated by cytokines. However, inordinate or disbalanced immune response may result in overproduction of cytokines as well as chemokines what can lead to severe inflammation, including excessive recruitment of neutrophils and mononuclear cells at the site of infection. These may damage lung tissue, reduce respiratory capacity, and cause severe disease and mortality. Recently, the role of cytokines induced by virus infection has been reevaluated. While moderate inflammatory response protects against development of severe illness, the hyper-inflammatory response can elevate the disease progression. In this minireview we summarized the data on cytokines and chemokines induced in the sera of hospitalized patients infected with human and avian high pathogenic influenza viruses and define their possible role in pathogenesis. Interleukine IL-6 and chemokines CCL-2/MCP-1, CCL-4, MIP/1β, CXCL-8/IL-8, CXCL-9/MIG, and CXCL-10/IP-10 are associated with pathogenicity of both avian (H5N1 and H7N9) and human (pdmH1N1 and H3N2) viruses. Chemokines CCL-2/MCP-1, CXCL-8/IL-8, CXCL-9/MIG, and CXCL-10/IP-10 are also connected with mortality. These cytokines may be used as targets for new, more complex therapy in the extenuation of unfavorable effects of hyper inflammatory response.
Copyright? Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
KEYWORDS:
B cell; NK cell; T cell; chemokines; cytokines; immunity; influenza virus; interferon; interleukin; macrophage; pathogenesis
PMID: 28302021 DOI: 10.2174/1381612823666170316123736