Abstract:
:Inactivation of the Staphylococcus aureus tricarboxylic acid (TCA) cycle delays the resolution of cutaneous ulcers in a mouse soft tissue infection model. In this study, it was observed that cutaneous lesions in mice infected with wild-type or isogenic aconitase mutant S. aureus strains contained comparable inflammatory infiltrates, suggesting the delayed resolution was independent of the recruitment of immune cells. These observations led us to hypothesize that staphylococcal metabolism can modulate the host immune response. Using an in vitro model system involving RAW 264.7 cells, the authors observed that cells cultured with S. aureus aconitase mutant strains produced significantly lower amounts of nitric oxide (NO(•)) and an inducible nitric oxide synthase as compared to those cells exposed to wild-type bacteria. Despite the decrease in NO(•) synthesis, the expression of antigen-presentation and costimulatory molecules was similar in cells cultured with wild-type and those cultured with aconitase mutant bacteria. The data suggest that staphylococci can evade innate immune responses and potentially enhance their ability to survive in infected hosts by altering their metabolism. This may also explain the occurrence of TCA cycle mutants in clinical S. aureus isolates.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Massilamany C,Gangaplara A,Gardner DJ,Musser JM,Steffen D,Somerville GA,Reddy Jdoi
10.1007/s11010-011-0840-3subject
Has Abstractpub_date
2011-09-01 00:00:00pages
75-82issue
1-2eissn
0300-8177issn
1573-4919journal_volume
355pub_type
杂志文章abstract::In view of the accumulation of H2O2 in the myocardium due to ischemia-reperfusion and changes in beta-adrenoceptor mechanisms in the ischemic-reperfused heart, we investigated the effects of H2O2 on the beta-adrenoceptor, G-protein and adenylyl cyclase complex. Rat hearts were perfused with 1 mM H2O2 for 10 min before...
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