The clearance of cell remnants and the regeneration of the injured muscle depend on soluble pattern recognition receptor PTX3.

OBJECTIVE: The signals causing the resolution of muscle inflammation are only partially characterized. The long pentraxin PTX3, which modulates leukocyte recruitment and activation, could contribute.

METHODS: We analysed the expression of ptx3 after muscle injury and verified whether hematopoietic precursors are a source of the protein. The kinetics of regeneration and leukocytes infiltration, the accumulation of cell remnants and anti-histidyl-t-RNA synthetase autoantibodies were compared in wild-type and ptx3 -deficient mice.

RESULTS: Ptx3 expression was up-regulated three-five days after injury and restricted to the extracellular matrix. Cellular debris and leukocytes persisted in the muscle of ptx3 -deficient mice for a long time after wild-type animals had healed. ptx3 -deficient macrophages expressed receptors involved in apoptotic cell clearance and engulfed dead cells in vitro . Accumulation of cell debris in a pro-inflammatory microenvironment was not sufficient to elicit autoantibodies.

CONCLUSION: PTX3 generated in response to muscle injury prompts the clearance of debris and the termination of the inflammatory response.