The human host selleck chem inhibitor immune response to nvH1N1 infection is unknown at this time and studies on its contribution to disease pathogenesis are desperately needed to improve prevention and treatment strategies.By analyzing 29 cytokines and chemokines and the hemagglutination inhibition activity, Bermejo-Martin and colleagues [1] assessed the early host innate and adaptive immune responses in patients both mildly and severely infected with nvH1N1. While infection with nvH1N1 induces a typical innate response in both mild and severe cases, severe infections with respiratory involvement are characterized by an early secretion of Th17 and Th1 cytokines. Thus, hospitalized patients tend to show high systemic levels of mediators that stimulate Th17 (IL-8, IL-9, IL-17, IL-6) and Th1 responses (IFN-��, TNF-��, IL-15, IL-12p70) [1].
Based on this finding, this study was able to highlight similarities between the cytokine response to severe H1N1 infection and the pathogenesis of asthma and some autoimmune diseases.The Th1 response is primarily involved with host immune defense against intracellular pathogens by activating cellular immunity. This response is effective in eradicating infectious agents such as viruses [3]. Indeed, Th1 cells produce IFN-�� and cytokines that are involved in monocyte/macrophage-mediated inflammatory responses [4]. When the Th1 response is exhaustively prolonged, it may result in host damage. Moreover, other authors have reported that Th1-dominated responses may be implicated in the pathogenesis of autoimmune disorders and chronic inflammatory diseases [5].
Bermejo-Martin and colleagues [1] found IL-15, IL-12p70, and IL-6 to be particularly elevated following severe nvH1N1 infection. These three cytokines are known to mediate both antiviral and pro-inflammatory responses. The authors [1] also found a significant inverse relationship of IL-6 and IL-8 with the pressure of oxygen in arterial blood in severely infected patients. Interestingly, previous studies had already reported high levels of specific proinflammatory cytokines and chemokines in severe SARS coronavirus, H5N1 and respiratory syncytial virus infections [6-11].Th17 cells are required for host defense against intracellular pathogens [12]. Th17 promotes inflammation by inducing various pro-inflammatory cytokines and chemokines, recruiting neutrophils, enhancing antibody production, and activating T cells [12].
Th17 cells secrete IL-17, IL-17F, and IL-22, thereby inducing a massive tissue reaction. Also, these cells secrete IL-21 to communicate with the cells of the immune system [13]. However, uncontrolled production of these cytokines induces Entinostat tissue damage in infected tissues [12]. In addition, Th17 cells have a well-known role in clearing pathogens during infections and inducing tissue inflammation in autoimmune disease [13].
No related posts.