The Vibrio cholerae O139 O-antigen polysaccharide is essential for Ca ²⁺ -dependent biofilm development in sea water

Abstract

Vibrio cholerae is both an inhabitant of estuarine environments and the etiologic agent of the diarrheal disease cholera. Previous work has demonstrated that V. cholerae forms both an exopolysaccharide-dependent biofilm and a Ca 2؉ -dependent biofilm. In this work, we demonstrate a role for the O-antigen polysaccharide of V. cholerae in Ca 2؉ -dependent biofilm development in model and true sea water. Interestingly, V. cholerae biofilms, as well as the biofilms of several other Vibrio species, disintegrate when Ca 2؉ is removed from the bathing medium, suggesting that Ca 2؉ is interacting directly with the O-antigen polysaccharide. In the Bay of Bengal, cholera incidence has been correlated with increased sea surface height. Because of the low altitude of this region, increases in sea surface height are likely to lead to transport of sea water, marine particulates, and marine biofilms into fresh water environments. Because fresh water is Ca 2؉ -poor, our results suggest that one potential outcome of an increase is sea surface height is the dispersal of marine biofilms with an attendant increase in planktonic marine bacteria such as V. cholerae. Such a phenomenon may contribute to the correlation of increased sea surface height with cholera.

Genetic determinants of biofilm development of opaque and translucent Vibrio parahaemolyticus

“…It is genetically distinct from the thick capsule (CPSA) locus (encoded by the cpsA-K locus; VPA1403-1413). In some respects, the phenotypes of mutants with potential O-ag defects resem-ble the recently described phenotypes of V. cholerae Oantigen mutants (Kierek and Watnick, 2003b); however, in V. parahaemolyticus, both putative O-antigen mutations cause significantly altered biofilm architecture in the context of CPSA production; whereas the importance of Oag mediated biofilm formation in V. cholerae is only seen under environmental conditions that eliminate the contribution of VPS to biofilm formation (Kierek and Watnick, 2003b).…”

Potential Novel Therapeutic Strategies in Cystic Fibrosis: Antimicrobial and Anti-Biofilm Activity of Natural and Designed α-Helical Peptides Against Staphylococcus aureus, Pseudomonas aeruginosa, and Stenotrophomonas maltophilia

“…For example EPSs from V. cholera containing the neutral sugars glucose and galactose are important architectural components of its biofilm [29][30][31]. On the other hand, EPSs from E. coli (group II capsular polysaccharide) [26], V. vulnificus (capsular polysaccharide) [32], P. aeruginosa (mainly extracellular polysaccharide) [27,33] and marine bacterium Vibrio sp.…”

Sticky Situations: Key Components That Control Bacterial Surface Attachment

“…These environmental signals have been identified as activators of vps gene transcription that are responsible for synthesis of the Vibrio polysaccharide (VPS) and biofilm formation (76). In contrast, Ca 2ϩ was found to enhance vps-independent biofilm formation, with removal of Ca 2ϩ (freshwater is calcium poor) resulting in the disintegration of V. cholerae biofilms as well as the biofilms of several other Vibrio species (77). The finding suggests that environmental activators of vps-dependent biofilm development are present in freshwater in association with arthropods while environmental activators of vps-independent biofilm development are present in calcium-rich seawater (76).…”

“…For example, loss of the group 1 capsular polysaccharide (CPS) in V. vulnificus is associated with increased attachment and, subsequently, reduced biofilm formation (23,73). V. cholerae O139 contains a locus with genes for CPS and lipopolysaccharide (LPS) O antigen biosynthesis that also plays a negative role in biofilm formation (77). A third example is a putative O antigen CPS locus of V. parahaemolyticus, VP0214-VP0237, whose loss increases attachment (43).…”