Lack of IL-6 during Coxsackievirus Infection Heightens the Early Immune Response Resulting in Increased Severity of Chronic Autoimmune Myocarditis

• DOI: 10.1371/journal.pone.0006207
• Publication Date: 2009-07-08T23:03:40Z
• Authors: Maya C. Poffenberger; Nadine Straka; Nahida El Warry; Dianne Fang; Iryna Shanina; Marc S. Horwitz
• Keywords: Coxsackievirus; Viral Myocarditis

Background Chronic myocarditis is often initiated by viral infection, the most common of which coxsackievirus infection. The precise mechanism infection leads to chronic autoimmune pathology poorly understood, however it clear that early immune response plays a critical role. Previous results have shown inflammatory cytokine interleukin (IL)-6 integral development experimental-induced myocarditis. However, function IL-6 during viral-mediated autoimmunity has yet be elucidated. Methods and Results To address requirement disease induction, deficient mice were infected with B3 (CB3). Following lacking developed increased compared wild type controls without corresponding change in level replication heart. This increase severity was accompanied elevated levels TNF-α, MCP-1, IL-10, activated T cells cardiac infiltrating macrophage/monocytes. Injection recombinant following sufficient lower serum cytokines TNF-α IL-10 as well chemokines MIP-1β, RANTES MIG decrease strongly suggests an important regulatory role for response. Conclusions While pathogenic disease, its viral-induced not reprised. By regulating thereby controlling directs outcome