Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. Mammary pathogenic E. coli (MPEC) are a leading cause of acute mastitis in dairy animals worldwide. To date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. Using the murine mastitis model we have previously showed that the TLR4 and TLR2 ligands; LPS and bacterial lipoproteins, respectively, are sufficient virulence factor in the mammary gland. Other microbial associated molecular patterns that activate TLR and NLR signaling might also play a role as virulence factors. The objective of this research was to study the role of flagellin and flagellum function in virulence mechanisms of MPEC. We have screened 120 MPEC field isolates and found that 95% were motile, hence flagellar motility is a highly conserved trait in MPEC. Using challenge studies in murine mastitis model we next found reduced colonization and virulence of fliC isogenic mutant in comparison to the wt MPEC strain. Since the fliC mutant is completely devoid of flagellum, we next investigated the motA isogenic mutant which is producing flagellin and assemble non-motile flagella. Interestingly, although motA mutant is producing and secreting flagellin, loss of motility was associated with reduced colonization and virulence in the lactating mice. Our results indicate flagellum as a putative virulence mechanism of MPEC, albeit this mechanism might be related to bacterial motility rather than the potent proinflammatory activity of flagellin.
