Mechanisms of Methicillin-Resistant Staphylococcus aureus Pneumonia–Induced Intestinal Epithelial Apoptosis

• DOI: 10.1097/shk.0b013e318259abdb
• Publication Date: 2012-05-16T13:04:02Z
• Authors: Erin E. Perrone; Enjae Jung; Elise Breed; Jessica A. Dominguez; Zhe Liang; Andrew T. Clark; W. Michael Dunne; Eileen M. Burd; Craig M. Coopersmith
• Keywords: FADD

Methicillin-resistant Staphylococcus aureus (MRSA) pneumonia-induced sepsis is a common cause of morbidity in the intensive care unit. Although pneumonia initiated lungs, extrapulmonary manifestations occur commonly. In light key role intestine plays pathophysiology sepsis, we sought to determine whether MRSA induces intestinal injury. FVB/N mice were subjected or sham and killed 24 h later. Septic animals had marked increase epithelial apoptosis by both hematoxylin-eosin active caspase 3 staining. S. aureus-induced was associated with an expression proapoptotic proteins Bid Bax antiapoptotic protein Bcl-xL mitochondrial pathway. receptor-mediated pathway, induced Fas ligand but decreased levels Fas, FADD, pFADD, TNF-R1, TRADD. To assess functional significance these changes, genetic manipulations either pathways. Both Bid-/- intestine-specific overexpression Bcl-2 compared wild-type animals. contrast, ligand-/- no alterations apoptosis. if findings organism-specific, similar experiments performed Pseudomonas aeruginosa pneumonia. gut apoptosis, unlike MRSA, this increased TNF-R1 Fas. thus organism-specific changes via pathways, although former may be more functionally significant.