Previous Article | Next Article ![]()
Journal of Bacteriology, January 2009, p. 411-421, Vol. 191, No. 1
0021-9193/09/$08.00+0 doi:10.1128/JB.01306-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Valério Monteiro-Neto,1,2
Zeus Saldaña,1
Maria A. Ledesma,1
Jose Luís Puente,3 and
Jorge A. Girón1*
Department of Immunobiology, University of Arizona, 15101 N. Campbell Ave., Tucson, Arizona,1 Centro de Ciências da Saúde, Centro Universitário do Maranhão, São Luís, Maranhão, Brazil,2 Departamento de Microbiología Molecular, Instituto de Biotecnología, Universidad Nacional de México, Cuernavaca, México3
Received 16 September 2008/ Accepted 16 October 2008
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 produces long bundles of polar type 4 pili (T4P) called HCP (for hemorrhagic coli pili) that form physical bridges between bacteria associating with human and animal epithelial cells. Here, we sought to further investigate whether HCP possessed other pathogenicity attributes associated with T4P production. Comparative studies performed with wild-type EHEC EDL933 and an isogenic hcpA mutant revealed that HCP play different roles in the biology of this organism. We found that in addition to promoting bacterial attachment to host cells, HCP mediate (i) invasion of epithelial cells, (ii) hemagglutination of rabbit erythrocytes, (iii) interbacterial connections conducive to biofilm formation, (iv) specific binding to host extracellular matrix proteins laminin and fibronectin but not collagen, and (v) twitching motility. Nonadherent laboratory E. coli strain HB101 complemented with hcpABC genes on plasmid pJX22, which specifies for HCP overproduction in EDL933, became hyperadherent and invasive and produced a thick biofilm, suggesting that the presence of HCP confers HB101(pJX22) new attributes otherwise not exhibited by HB101. Analogous to other bacteria in which T4P are involved in the pathogenesis of several infectious diseases, our data strongly suggest that HCP display multiple functions that may contribute to EHEC colonization of different hosts and to virulence, survival, and transmission of this food-borne pathogen.
Published ahead of print on 24 October 2008.
Present address: Departamento de Bacteriología Intestinal, Hospital Infantil de México Federico Gómez, Ciudad de México, México.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»