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Yesilkaya H et al. – End–product analysis showed there was no formate, the main end product of the reaction catalysed by PFL, produced by mutants defective in SPD0420 and SPD1774, indicating that SPD0420 encodes for PFL and SPD1774 for putative PFL–AE. The results demonstrate that there is a direct link between pneumococcal fermentative metabolism and virulence.

Exclusive Author Commentary
Hasan Yesilkaya, 10/06/09

Traditionally, it was believed that the proteins involved in central metabolic pathways perform only housekeeping function, and therefore their contribution to the microbial virulence has been largely ignored. However, the recent research suggest that bacterial virulence is an integrated phenomenon and not mediated by few proteins but necessitates the concerted action of multiple pathways. I am interested in virulence determinant of Streptococcus pneumoniae, which is an important cause of otitis media, bacteremia, meningitis and pneumonia. Particularly, how this pathogen maintains its survival in host is of interest to me. Recently, I showed that mucin is important source of carbohydrate for the pathogen, and this compound is rich in its content of galactose. In our recent publication, we demonstrated that the use of galactose shifts the pneumococcal metabolism from homolactic to mixed acid fermentation. I also demonstrated that pyruvate formate lyase (PFL) is important for the shift and the inactivation of PFL results in attenuation of pneumococcal virulence in different tissue sites. Overall, our results demonstrate the integrated aspect of pneumococcal virulence.

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