Aggregation and Dispersal on Mucosal Surfaces

Abstract

This chapter considers two additional facets of adherence: (i) that in addition to adhering to a surface, bacteria often adhere to each other; and (ii) that colonization is sometimes promoted by relinquishing adherence. It focuses on bacterial aggregation. Bacteria adhering to mucosal surfaces commonly exhibit interbacterial aggregation or agglutination, perhaps with relatively few points of anchorage to the substratum. On the mucosa, interbacterial aggregation presumably plays the same biophysical role as it does on abiotic substrata, although data to this effect are few. Recent studies demonstrated that Escherichia coli aggregation mediated by antigen 43 (Ag43) protects bacteria from H2O2-dependent killing. The study of aggregation and biofilm formation by staphylococcal species continues to represent the paradigm for bacterial infections. Bacterial aggregation and microcolony formation are considered to be an initial stage of biofilm formation. Biofilms of Pseudomonas aeruginosa represent bacteria embedded in an alginate polysaccharide matrix. Instead of a shortening and thickening of the fimbriae as seen with enteropathogenic E. coli (EPEC), meningococci (MC) shed their fimbriae completely and initiate a complex signal transduction cascade within the cell. Dispersin mutants are deficient in colonization of the streptomycin-treated mouse model, suggesting that enteroaggregative E. coli (EAEC) mutants exhibiting collapsed fimbriae and hyperaggretation are not able to establish colonization of the intestine. Although each bacterium interacting with a mucosal surface must modify its colonization approach to fit its particular life-style and survival strategy, comparative biology continues to indentify new conserved general functions such as aggregation and its counterpoint, dispersal.