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Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Interferon+Cytokine+Res 2011 ; 31 (6): 501-8 Nephropedia Template TP
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Susceptibility to infection and inflammatory response following influenza virus (H1N1, A/PR/8/34) challenge: role of macrophages #MMPMID21352081
J Interferon Cytokine Res 2011[Jun]; 31 (6): 501-8 PMID21352081show ga
The precise role that macrophages play in both influenza-induced pathology and the host's cytokine-mediated response to infection remains largely unknown. We examined the effects of lung macrophage depletion on susceptibility to influenza virus (H1N1, A/PR/8/34) infection and how this relates to the inflammatory cytokine response in the lungs. ICR mice were administered 100 muL of clodronate (CL(2)MDP) or PBS-encapsulated liposomes via an intranasal route 2 days before infection. Then, mice were intranasally inoculated with influenza virus and monitored for morbidity, mortality, and symptom severity for 21 days. Additional mice were sacrificed at 2 and 5 days postinfection, and lung tissue was analyzed for viral replication and for gene expression and protein concentration of interleukin-1beta (IL-1beta), IL-6, and TNF-alpha. Macrophage depletion increased morbidity, mortality, and symptom severity (P < 0.05) and viral replication at 2 and 5 days postinfection (P < 0.05). IL-1beta, IL-6, and TNF-alpha mRNA was greater at day 2 (P < 0.05) and IL-6 and TNF-alpha was greater at day 5 postinfection (P < 0.05) in macrophage depleted mice. Macrophage depletion increased protein concentration of IL-1beta and IL-6 at day 2 postinfection (P < 0.05). These data suggest that macrophages play a necessary role in controlling susceptibility to influenza virus and the host's cytokine-mediated response to influenza infection.