Role of GapC in the pathogenesis of Staphylococcus aureus

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• 作者：Oudessa Kerro-Dego¹ ; Tracy Prysliak ; Jose Perez-Casal² ; ^{jose.perez-casal@usask.ca} ; Andrew A. Potter²
• 关键词：Staphylococcus aureus ; Pathogenesis ; GAPDH ; In vivo ; In vitro
• 刊名：Veterinary Microbiology
• 出版年：2012
• 出版时间：4 May, 2012
• 年：2012
• 卷：156
• 期：3-4
• 页码：443-447
• 全文大小：572 K

文摘

Staphylococcus aureus is recognized worldwide as a major pathogen causing clinical or subclinical intramammary infections in lactating cows, sheep and goats. S. aureus produces a wide arsenal of cell surface and extracellular proteins involved in virulence. Among these are two conserved proteins with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity named glyceraldehyde-3-phosphate dehydrogenase-B (GapB) and -C (GapC). In this study, we used the S. aureus wild type strain RN6390 and its isogenic gapC mutant H330 in in vitro and in vivo studies and determined that the S. aureus GapC protein plays a role on adherence to and internalization into bovine mammary epithelial (MAC-T) cells. In addition, we found that S. aureus H330 did not caused mastitis after an experimental infection of ovine mammary glands. Together, these results show that GapC is important in the pathogenesis of S. aureus mastitis.