Microbial interference and colonization of the murine gastrointestinal tract by Listeria monocytogenes

Abstract

Two strains of Listeria monocytogenes, one that formed smooth colonies on agar surfaces and a variant of it that formed rough colonies, colonized the gastrointestinal tracts of germfree mice. Within 24 h after mice were inoculated orally with about 100 bacteria, the population levels per gram (wet weight) of tissue of both strains were 105 to 107 in the stomach and ileum and 108 to 109 in the cecum and colon, respectively. As detected in Gram-stained histological sections, in such gnotobiotes, the bacteria colonized the lumen in all areas of the tract and much of the mucus layer on the epithelial surface in the proximal colon. The strain that formed smooth colonies did not colonize the tracts of specificpathogen-free mice, but did colonize, to the same levels as in germfree mice, the stomachs and bowels of ex-germfree mice previously associated with two members of the indigenous flora (Bacteroides and Clostridium). In the latter animals, however, the listeria did not form layers on the colonic epithelium as efficiently as they did in monoassociated gnotobiotes.

Effect of acid-adaptation on Listeria monocytogenes survival and translocation in a murine intragastric infection model

“…One day after inoculation, when a 4 log 10 decrease of the bacterial population levels had occurred, this di¡erence was no longer observed (data not shown). This last result probably re-£ects the fact that L. monocytogenes does not colonize the intestinal epithelium of speci¢c pathogen-free mice [12]; combination of rapid transit and expulsion in the feces, intraluminal multiplication during the transit and competition with the bacteria of the intestinal £ora [12] may Table 1 Acid-adaptation results in higher L. monocytogenes population level in the lower intestine account for the transient character of the initial di¡erence in bacterial population levels between acid-adapted and neutral-grown bacteria. Acid-adaptation and reduction of gastric acid pH thus led to a better survival to the intragastric transit and to a higher live bacterial load reaching the next intestinal compartments.…”

Commensal microbes provide first line defense against Listeria monocytogenes infection

“…Previous studies have suggested, although never conclusively proven, that gut commensals can protect the host from L. monocytogenes infection. In the 70s, Zachar and Savage (1979) reported that GF mice, in contrast to SPF mice, were highly susceptible to L. monocytogenes infection, and their colon would become rapidly colonized by L. monocytogenes after low intra-gastric inocula. The authors hypothesized that the rich microbiota carried by SPF mice might account for their resistance to infection, but were unable to prevent intestinal growth of L. monocytogenes by gavage of selected bacterial species, even though this treatment reduced penetration of L. monocytogenes into intestinal tissue, as assessed by microscopy (Zachar and Savage, 1979).…”

Systemic Dissemination by Intrarectal Infection with Listeria monocytogenes in Mice

“…However, it is difficult to explain how Listeriae spread from the large intestine to these organs when mice were infected intrarectally. Although the bacterium is able to multiply in the intestinal epithelial cells in vitro (4) and in germfree mice and rats in vivo (1,13), it could not reportedly grow there in specific-pathogen-free or conventional rodents. In our studies (9, Fig.…”