Probing the heat shock response of Corynebacterium pseudotuberculosis: The major virulence factor, phospholipase D, is downregulated at 43 °C

The complete genome sequence of Corynebacterium pseudotuberculosis FRC41 isolated from a 12-year-old girl with necrotizing lymphadenitis reveals insights into gene-regulatory networks contributing to virulence

“…The major virulence factor of C. pseudotuberculosis is the sphingomyelin-degrading phospholipase D that facilitates the persistence and spread of the bacterium within the host [5,6]. The expression of the pld gene is regulated by multiple environmental stimuli, including heat, and plays a role in the reduction of macrophage viability following infection [78,79]. The secreted corynebacterial protease CP40 was detected previously as a protective antigen of C. pseudotuberculosis and shown to be of the serine protease type, although BLAST searches revealed homology to endoglycosidases [80].…”

Expression of phospholipase D, the major virulence factor of Corynebacterium pseudotuberculosis, is regulated by multiple environmental factors and plays a role in macrophage death

“…Using a DNA macroarray approach, we have previously identified pld as being down-regulated following a 30 min heat shock from 37 to 43 u C (McKean et al, 2007). Northern analysis was performed to determine the time course of pld mRNA down-regulation following heat shock.…”

“…The chromosome contains a single copy of the gene and is transcribed as a monocistronic RNA of 1.1 kb (Hodgson et al, 1990). It has recently been established that expression of the pld gene is strongly down-regulated following heat shock (McKean et al, 2007). No other aspects of pld regulation have been reported to date.…”

Desenvolvimento de ensaio imunoenzimático (ELISA) indireto na detecção de anticorpos anti-Corynebacterium pseudotuberculosis em ovinos (Ovis aries, Linnaeus, 1758)

“…propriedade hemolítica e vasodilatadora, da virulência bacteriana e da higidez do animal (JOLLY, 1966;BURREL, 1981). Na forma visceral a bactéria atinge a circulação linfohematógena e atinge outros órgãos alvos, incluindo pulmão, fígado, rim e encéfalo, desencadeando a forma grave da doença (MCKEAN et al, 2007). Fontaine et al (2006) (WALKER, 1994;BAIRD;FONTAINE, 2007).…”

“…Os linfonodos acometidos geralmente apresentam aumento de volume, que possivelmente drenam material com grande quantidade de pus de coloração branca ou esverdeada, com consistência pastosa, contendo muitos microrganismos viáveis (COSTA, 2002;MCKEAN et al, 2007). ;FONTAINE, 2007;BINNS et al, 2002;RIBEIRO et al, 2001).…”