Muscle Injury, Vimentin Expression, and Nonsteroidal Anti‐inflammatory Drugs Predispose to Cryptic Group A Streptococcal Necrotizing Infection
Open Access
- 1 December 2008
- journal article
- Published by Oxford University Press (OUP) in The Journal of Infectious Diseases
- Vol. 198 (11), 1692-1698
- https://doi.org/10.1086/593016
Abstract
Background. Myonecrosis due to group A streptococci (GAS) often develops at sites of nonpenetrating muscle injury, and nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the severity of these cryptic infections. We have previously shown that GAS bind to vimentin on injured skeletal muscles in vitro. The present study investigated whether vimentin up-regulation in injured muscles in vivo is associated with homing of circulating GAS to the injured site and whether NSAIDs facilitate this process. Methods. M type 3 GAS were delivered intravenously 48 h after eccentric contraction (EC)-induced injury of murine hind-limb muscles. Vimentin gene expression and homing of GAS were followed by real-time reverse-transcriptase polymerase chain reaction and quantitative bacteriology of muscle homogenates, respectively. In separate experiments, ketorolac tromethamine (Toradol) was given 1 h before GAS infusion. Results. Vimentin was up-regulated ∼8-fold 48 h after EC. Significantly more GAS were found in moderately injured muscles than in noninjured controls. NSAIDs greatly augmented the number of GAS in injured muscles. Conclusions. Vimentin may tether circulating GAS to injured muscle, and NSAIDs enhance this process. Strategies targeting the vimentin-GAS interaction may prevent or attenuate GAS myonecrosis. Use of NSAIDs should increase suspicion of cryptic GAS infection in patients with increasing pain at sites of nonpenetrating muscle injury.Keywords
This publication has 26 references indexed in Scilit:
- SevereStreptococcus pyogenesInfections, United Kingdom, 2003–2004Emerging Infectious Diseases, 2008
- Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesisThe Journal of Experimental Medicine, 2007
- Inflammatory processes in muscle injury and repairAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2005
- The COX-2 pathway is essential during early stages of skeletal muscle regenerationAmerican Journal of Physiology-Cell Physiology, 2004
- Rapid muscle-specific gene expression changes after a single bout of eccentric contractions in the mouseAmerican Journal of Physiology-Cell Physiology, 2004
- Contractile function, sarcolemma integrity, and the loss of dystrophin after skeletal muscle eccentric contraction-induced injuryAmerican Journal of Physiology-Cell Physiology, 2004
- Urokinase-dependent plasminogen activation is required for efficient skeletal muscle regeneration in vivoBlood, 2001
- Specific and Innervation-Regulated Expression of the Intermediate Filament Protein Nestin at Neuromuscular and Myotendinous Junctions in Skeletal MuscleThe American Journal of Pathology, 1999
- Could Nonsteroidal Antiinflammatory Drugs (NSAIDs) Enhance the Progression of Bacterial Infections to Toxic Shock Syndrome?Clinical Infectious Diseases, 1995
- Severe Group A Streptococcal Infections Associated with a Toxic Shock-like Syndrome and Scarlet Fever Toxin ANew England Journal of Medicine, 1989