Role of a novel fimbrial adhesin in acid-induced host adhesion of escherichia coli 0157:H7

Enterohemorrhagic Eschericia coli (EHEC) 0157:H7 must be able to survive the acid stress of gastric passage. Previous studies show that adhesion of EHEC 0157:H7 to human epithelial cells is increased if EHEC was pre-exposed to acid. Whole genome array analysis of EHEC reveals that the putative fimbrial gene yadK is significantly upregulated after EHEC exposure to acid treatments. In this study, a YadK deficient mutant (△yadK) in EHEC 0157:H7 wild-type (WT) strain 85-170 was constructed and phenotyped. The results of this study demonstrate that △yadK exposed to acid stress showed no acid-induced increase in bacteria-host cell adhesion observed in similarly acid-induced wild type cells. This study concludes that YadK plays a role in acid-induced host adhesion of EHEC 0157:H7. It also indicates that acid stress, which is a part of the host’s natural assault to resist invasion, may regulate factors responsible for enhanced bacteria-host attachment, resulting in increased EHEC virulence.

Role of a novel fimbrial adhesin in acid-induced host adhesion of escherichia coli 0157:H7

Enterohemorrhagic Eschericia coli (EHEC) 0157:H7 must be able to survive the acid stress of gastric passage. Previous studies show that adhesion of EHEC 0157:H7 to human epithelial cells is increased if EHEC was pre-exposed to acid. Whole genome array analysis of EHEC reveals that the putative fimbrial gene yadK is significantly upregulated after EHEC exposure to acid treatments. In this study, a YadK deficient mutant (△yadK) in EHEC 0157:H7 wild-type (WT) strain 85-170 was constructed and phenotyped. The results of this study demonstrate that △yadK exposed to acid stress showed no acid-induced increase in bacteria-host cell adhesion observed in similarly acid-induced wild type cells. This study concludes that YadK plays a role in acid-induced host adhesion of EHEC 0157:H7. It also indicates that acid stress, which is a part of the host’s natural assault to resist invasion, may regulate factors responsible for enhanced bacteria-host attachment, resulting in increased EHEC virulence.

Characterization of the role of yadK in the pathogenesis of enterohaemorrhagic E. coli O157:H7

Enterohaemorrhagic Escherichia coli (EHEC) O157:H7 can use serious diarrhea and haemolytic uremic syndrome. Various factors including adhesins contribute to pathogenesis of EHEC. Previous studies suggested that yadK gene, which encodes a putative fimbrial adhesin in EHEC, may be involved in response of EHEC to acid stress. To characterize role of yadK protein in the pathogenesis of EHEC, recombinant yadK protein was generated and used to immunize rabbit to obtain anti-yadK antiserum, which was able to specifically recognize over-expressed yadK protein in EHEC. Western blotting with anti-yadK revealed a higher level of yadK expression in EHEC under acid adapted-acid stress compared to EHEC under unstressed conditions, which confirmed earlier yadK mRNA studies and indicated that yadK is upregulated in EHEC under acid stress. Finally, we observed that anti-yadK antiserum was able to specifically reduce adhesion of acid stressed EHEC to human epithelial cells compared to adhesion level of unstressed EHEC.

Characterization of the role of yadK in the pathogenesis of enterohaemorrhagic E. coli O157:H7

Enterohaemorrhagic Escherichia coli (EHEC) O157:H7 can use serious diarrhea and haemolytic uremic syndrome. Various factors including adhesins contribute to pathogenesis of EHEC. Previous studies suggested that yadK gene, which encodes a putative fimbrial adhesin in EHEC, may be involved in response of EHEC to acid stress. To characterize role of yadK protein in the pathogenesis of EHEC, recombinant yadK protein was generated and used to immunize rabbit to obtain anti-yadK antiserum, which was able to specifically recognize over-expressed yadK protein in EHEC. Western blotting with anti-yadK revealed a higher level of yadK expression in EHEC under acid adapted-acid stress compared to EHEC under unstressed conditions, which confirmed earlier yadK mRNA studies and indicated that yadK is upregulated in EHEC under acid stress. Finally, we observed that anti-yadK antiserum was able to specifically reduce adhesion of acid stressed EHEC to human epithelial cells compared to adhesion level of unstressed EHEC.

Promising Approach to Inhibit E. coli FimH Adhesion by C-Linked Mannosides

Antagonists of the uropathogenic Escherichia coli type-1 fimbrial adhesin (FimH) are recognized as attractive alternatives for antibiotic therapies and prophylactic strategies against acute and recurrent bacterial infections. [...]

A food-grade fimbrial adhesin FaeG expression system inLactococcus lactisandLactobacillus casei

Enterotoxigenic Escherichia coli (ETEC) infection is the major cause of diarrhea in neonatal piglets. The fimbriae as colonizing factor in the pathogenesis of ETEC constitute a primary target for vaccination against ETEC. Lactic acid bacteria (LAB) are attractive tools to deliver antigens at the mucosal level. With the safety of genetically modified LAB in mind, a food-grade secretion vector (pALRc or pALRb) was constructed with DNA entirely from LAB, including the replicon, promoter, signal peptide, and selection marker alanine racemase gene (alr). To evaluate the feasibility of the system, the nuclease gene (nuc) from Staphylococcus aureus was used as a reporter to be expressed in both Lactococcus lactis and Lactobacillus casei. Subsequently, the extracellular secretion of the fimbrial adhesin FaeG of ETEC was confirmed by Western blot analysis. These results showed that this food-grade expression system has potential as the delivery vehicle for the safe use of genetically modified LAB for the development of vaccines against ETEC infection.