Bacterial Adhesins in Host-Microbe Interactions

Abstract

Most commensal and pathogenic bacteria interacting with eukaryotic hosts express adhesive molecules on their surfaces that promote interaction with host cell receptors or with soluble macromolecules. Even though bacterial attachment to epithelial cells may be beneficial for bacterial colonization, adhesion may come at a cost because bacterial attachment to immune cells can facilitate phagocytosis and clearing. Many pathogenic bacteria have solved this dilemma by producing an antiphagocytic surface layer usually consisting of polysaccharide and by expressing their adhesins on polymeric structures that extend out from the cell surface. In this review, we will focus on the interaction between bacterial adhesins and the host, with an emphasis on pilus-like structures.

Adhesion to the yeast cell surface as a mechanism for trapping pathogenic bacteria by Saccharomyces probiotics

“…Non-specific binding involves electrostatic and hydrophobic interactions of lower affinity than for specific binding. The localization and mechanisms of binding to the epithelial surface have been studied previously in enteropathogenic bacteria such as E. coli and Salmonella, and type I fimbriae are frequently involved in this adhesion, generally using mannose as a receptor (Kline et al, 2009). A number of different approaches have been taken over the years to inhibit adhesion of pathogenic bacteria, and addition of exogenous sugars and inhibition of fimbria assembly are two strategies that have been studied (Cusumano & Hultgren, 2009).…”

The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host–microbial interactions

“…Why distal colon is different is not understood, but one could speculate that this has to do with selection of the commensal flora. Bacteria often carry adhesins, usually at the tip of their fimbrie, that bind mucins (36). This was recently illustrated by the isolation of an adhesin from the commensal bacteria Lactobaccilus rhamnosus (37).…”

Mycobacterium tuberculosis adhesins: potential biomarkers as anti-tuberculosis therapeutic and diagnostic targets

“…However, the large number of different adhesin genes in an organism's genome suggests that there are multiple pathways for bacterial adherence (Brzuszkiewicz et al, 2006). This redundancy limits the use of adhesins as vaccine candidates (Kline et al, 2009). In addition, different adhesins are not produced simultaneously and continuously and require different environmental cues for expression, and many exist as antigenic variants (Klemm & Schembri, 2000).…”

“…A review by Kline et al (2009) highlighted adhesive proteins as protective antigens. These include: an E. coli FimH adhesin-based vaccine against cystitis in a primate model (Langermann et al, 2000), the E. coli Dr fimbrial antigen against urinary tract infection in mice (Goluszko et al, 2005), the Salmonella atypical fimbriae B chaperone (SafB) complexed with the SafD adhesin against invasive Salmonella enteritidis infection (Strindelius et al, 2004), a synthetic-peptide consensus-sequence vaccine (Cs1) against type IV pilus of P. aeruginosa in a mouse model (Kao et al, 2007) and a combination of three group B Streptococcus (GBS) pilus variants that mediate protection in mice against all tested GBS challenge strains (Margarit et al, 2009).…”

“…Invasion of host cells by bacteria is a complex process involving both bacterial and host cell determinants (Bermudez & Goodman, 1996;Danelishvili et al, 2003). Pathogenic bacteria, such as M. tuberculosis, must initially adhere to and invade eukaryotic cells as a survival mechanism, enabling host colonization and the evasion of host immune defences (Niemann et al, 2004;Pizarro-Cerdá & Cossart, 2006;Kline et al, 2009). Adherence and invasion mechanisms have been well studied in pathogenic bacteria and fungi (Finlay & Cossart, 1997;Pizarro-Cerdá & Cossart, 2006;Singh et al, 2012a;Monack & Hultgren, 2013;Foster et al, 2014).…”