@article{TEXTUAL,
      recid = {7119},
      author = {Malachowa, Natalia and Kobayashi, Scott D. and Porter,  Adeline R. and Braughton, Kevin R. and Scott, Dana P. and  Gardner, Donald J. and Missiakas, Dominique M. and  Schneewind, Olaf and DeLeo, Frank R.},
      title = {Contribution of <i>Staphylococcus aureus</i>  Coagulases and Clumping Factor A to Abscess Formation in a  Rabbit Model of Skin and Soft Tissue Infection},
      journal = {PLOS ONE},
      address = {2016-06-23},
      number = {TEXTUAL},
      abstract = {Staphylococcus aureus produces numerous factors that  facilitate survival in the human host. S. aureus coagulase  (Coa) and von Willebrand factor-binding protein (vWbp) are  known to clot plasma through activation of prothrombin and  conversion of fibrinogen to fibrin. In addition, S. aureus  clumping factor A (ClfA) binds fibrinogen and contributes  to platelet aggregation via a fibrinogen- or  complement-dependent mechanism. Here, we evaluated the  contribution of Coa, vWbp and ClfA to S. aureus  pathogenesis in a rabbit model of skin and soft tissue  infection. Compared to skin abscesses caused by the Newman  wild-type strain, those caused by isogenic coa, vwb, or  clfA deletion strains, or a strain deficient in coa and  vwb, were significantly smaller following subcutaneous  inoculation in rabbits. Unexpectedly, we found that fibrin  deposition and abscess capsule formation appear to be  independent of S. aureus coagulase activity in the rabbit  infection model. Similarities notwithstanding, S. aureus  strains deficient in coa and vwb elicited reduced levels of  several proinflammatory molecules in human blood in vitro.  Although a specific mechanism remains to be determined, we  conclude that S. aureus Coa, vWbp and ClfA contribute to  abscess formation in rabbits.},
      url = {http://knowledge.uchicago.edu/record/7119},
}