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Impacts of enterotoxin gene cluster-encoded superantigens on local and systemic experimental Staphylococcus aureus infections

Artikel i vetenskaplig tidskrift
Författare Forough Nowrouzian
Abukar Ali
C. Badiou
O. Dauwalder
G. Lina
Elisabet Josefsson
Publicerad i European Journal of Clinical Microbiology & Infectious Diseases
Volym 34
Nummer/häfte 7
Sidor 1443-1449
ISSN 0934-9723
Publiceringsår 2015
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 1443-1449
Språk en
Länkar dx.doi.org/10.1007/s10096-015-2371-...
Ämnesord T-CELL-RECEPTOR, VIRULENCE, EXPRESSION, STRAINS, SHOCK, MICE, EGC, COLONIZATION, POLYMORPHISM, PREVALENCE, Infectious Diseases, Microbiology
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

Staphylococcus aureus is both a component of the normal skin flora and an important pathogen. It expresses a range of recognized and putative virulence factors, such as enterotoxins with superantigenic properties. Several superantigen genes, i.e., seg, sei, selm, seln, and selo, are encoded by the enterotoxin gene cluster (egc), which is found in the majority of S. aureus isolates. Carriage of egc is associated with fitness of S. aureus in the gut microbiota, but it is not known if it contributes to pathogenicity. We constructed egc+ (functional for the seg, selm, and selo genes) and isogenic egc- S. aureus mutants, and investigated their virulence profiles in murine infection models. No effect of egc was seen in a local skin and soft tissue infection model, but in an invasive infection model, increased weight loss was observed after infection with the egc+ as compared to the egc- mutant. Mortality and arthritis were not affected by egc status. Our data suggest that egc has limited effects on the virulence of S. aureus. It may primarily function as a colonization factor increasing commensal fitness, although it might have some aggravating effects on the infection when the bacteria reach the blood. DELNOUR A, 1994, EUROPEAN JOURNAL OF IMMUNOLOGY, V24, P1161 DELNOUR A, 1994, JOURNAL OF INFECTIOUS DISEASES, V170, P94

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