title: The Role of Virus Infection in Deregulating the Cytokine Response to Secondary Bacterial Infection.
abstract: Proinflammatory cytokines are produced by macrophages and dendritic cells (DCs) after infection to stimulate T helper (Th) cells, linking innate and adaptive immunity. Virus infections can deregulate the proinflammatory cytokine response like tumor necrosis factor-α and interleukin (IL)-2, making the host more susceptible to secondary bacterial infections. Studies using various viruses such as lymphocytic choriomeningitis virus, influenza A virus, and human immunodeficiency virus have revealed several intriguing mechanisms that account for the increased susceptibility to several prevalent bacterial infections. In particular, type I interferons induced during a virus infection have been observed to play a role in suppressing the production of some key antibacterial proinflammatory cytokines such as IL-23 and IL-17. Other suppressive mechanisms as a result of cytokine deregulation by viral infections include reduced function of immune cells such as DC, macrophage, natural killer, CD4(+), and CD8(+) T cells leading to impaired clearance of secondary bacterial infections. In this study, we highlight some of the immune mechanisms that become deregulated by viral infections, and can thus become defective during secondary bacterial infections.
authors: Department of Biomedical and Molecular Sciences, Queen's University , Kingston, Ontario, Canada .
authors: Divya
authors: D
authors: Mehta
authors: Department of Biomedical and Molecular Sciences, Queen's University , Kingston, Ontario, Canada .
authors: Carlene
authors: C
authors: Petes
authors: Department of Biomedical and Molecular Sciences, Queen's University , Kingston, Ontario, Canada .
authors: Katrina
authors: K
authors: Gee
authors: Department of Biomedical and Molecular Sciences, Queen's University , Kingston, Ontario, Canada .
authors: Sameh
authors: S
authors: Basta
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D060085:Coinfection; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D056747:Immunomodulation; D018836:Inflammation Mediators / Q000378:metabolism; D007370:Interferon Type I / Q000378:metabolism; D008217:Lymphocytic choriomeningitis virus / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D014777:Virus Diseases / Q000276:immunology* / Q000378:metabolism* / Q000821:virology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D007370:Interferon Type I