Role of chemotaxis in the association of motile bacteria with intestinal mucosa: in vivo studies

Abstract

In vivo loops were prepared in the small intestine of rabbits and injected with mixtures of Vibrio cholerae and polystyrene spheres (1.1-tim diameter). The loops were removed and frozen after 15 min and then sectioned in a cryostat. The locations of particles and vibrios were determined microscopically. The vibrio/ particle ratio was unity in the lumen of the loops, but increased 10-fold in the deep intervillous spaces, indicating active invasion of the mucus gel by the chemotactic parent strain. Motile nonchemotactic mutants and nonmotile mutants of this strain invaded the mucus at the same rate as inert particles. Similar results were obtained with intestinal loops prepared in germfree mice. When germfree mice were diassociated with mixtures of chemotactic (parent or revertant) and nonchemotactic mutant vibrios in equal proportions, the chemotactic strain rapidly outgrew its nonchemotactic counterpart in the intestine. Nonchemotactic mutants introduced as monoassociates into germfree mice were rapidly overgrown by nonmotile mutants which apparently arose spontaneously in the gut. Motility was therefore beneficial to survival only when it was directed by chemotactic stimuli, whereas it was a liability in the absence of such stimuli. Growth of chemotactic vibrios in small intestinal loops of rabbits paralleled that of nonchemotactic mutants for the first 4 to 6 h. Thereafter, the growth rate of the chemotactic vibrios was significantly faster. This was correlated with a significantly higher degree of association with the mucosa on the part of the chemotactic vibrios.

Colonization resistance and microbial ecophysiology: using gnotobiotic mouse models and single-cell technology to explore the intestinal jungle

“…It has been demonstrated using FISH that growth of both commensal and pathogenic E. coli strains mainly takes place in the mucus layer of the large intestine (Poulsen et al, 1994;Moller et al, 2003). Other enteropathogens, such as Salmonella enterica serovar Typhimurium (S. Typhimurium), Citrobacter rodentium, and V. cholerae were shown to grow in the mucus layer (Freter et al, 1981;Stecher et al, 2004Bergstrom et al, 2010). Escherichia coli genes and pathways induced upon growth in cecal mucus include catabolism of the major mucin-derived sugars N-acetylglucosamine (NAG), N-acetylneuraminic (sialic) acid, glucosamine, fucose and ribose, tryptophan, threonine, serine, aspartate, and phosphatidylethanolamine (Chang et al, 2004).…”

Roles for motility in bacterial–host interactions

“…The presence of this organism in aquatic environments contributes to endemic disease, and the evolution of new pathogenic strains provides the potential for epidemic, and even pandemic, spread (Mel and Mekalanos, 1996). The relationship between V. cholerae motility and pathogenesis has been studied for many years (Fretter et al, 1981); however, a well-defined role for motility in this context still remains uncertain (Richardson, 1991;Gardel and Mekalanos, 1996). Some interesting links between the expression of virulence determinants and motility have been found recently.…”

Expression of flagella and motility by Shigella

“…However, these events are also viewed as virulence properties that may favour adherence to or penetration into eukaryotic cells (Finlay and Falkow, 1989;Salyers and Whitt, 1994;Allison et aL, 1992). In the intestine, these properties would seem crucial for enteric pathogens such as Vibrio cholerae, Campylobacter jejuni, Helicobacter pylori and Salmonella typhimurium to swim across the mucus layer in the gastrointestinal tract in order to reach suitable sites for colonization and invasion (Freter et aL, 1981;Carsiotis et aL, 1984;Guentzel and Berry, 1975;Hazell etaL, 1986;Weinstein et aL, 1984;Eaton et aL, 1992). However, other workers have shown that the lack of flagella and motility does not affect the virulence of mouse pathogens (McCormick et aL, 1990;Lockman and Curtis, 1990).…”