TLR4 signaling protects from excessive muscular damage induced byBothrops jararacussusnake venom

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Abstract

Immune cells and skeletal muscle express Toll-like receptors (TLRs) that participate as sensors of tissue injury triggering signals for activation of innate and adaptive immune responses. This study aimed to investigate the involvement of TLR4 in the process of skeletal muscle repair. Muscular injury was induced by injection of 0.6 mg/kg of Bothrops jararacussu snake venom in the gastrocnemius muscle of C3H/HeJ mice that express a non-functional TLR-4 receptor and C3H/HeN mice with functional receptor. TLR4-deficient mice had persistent muscular inflammation with few F4/80 macrophages at onset but increased MMP9 activity and collagen deposition during resolution of injury. Since such effect was not observed in the mouse strain with functional receptor it is concluded that TLR4 signaling exerts a protective role preventing from excessive muscular damage induced by B. jararacussu venom.

Highlights

▸ TLR4-deficient and control mice had similar acute tissue damage after intramuscular injection with Bothrops jararacussu venom. ▸ TLR4-deficient mice had persistent inflammation, increased MMP9 activity and collagen deposition. ▸ Lack of TLR signaling delayed resolution of muscular injury. ▸ TLR4 signaling exerts a protective role in the muscular injury induced by B. jararacussu venom.

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