Multifaceted Defense against Listeria monocytogenes in the Gastro-Intestinal Lumen

Simone Becattini,Eric Pamer

doi:10.3390/pathogens7010001

Abstract

Listeria monocytogenes is a foodborne pathogen that can cause febrile gastroenteritis in healthy subjects and systemic infections in immunocompromised individuals. Despite the high prevalence of L. monocytogenes in the environment and frequent contamination of uncooked meat and poultry products, infections with this pathogen are relatively uncommon, suggesting that protective defenses in the general population are effective. In the mammalian gastrointestinal tract, a variety of defense mechanisms prevent L. monocytogenes growth, epithelial penetration and systemic dissemination. Among these defenses, colonization resistance mediated by the gut microbiota is crucial in protection against a range of intestinal pathogens, including L. monocytogenes. Here we review defined mechanisms of defense against L. monocytogenes in the lumen of the gastro-intestinal tract, with particular emphasis on protection conferred by the autochthonous microbiota. We suggest that selected probiotic species derived from the microbiota may be developed for eventual clinical use to enhance resistance against L. monocytogenes infections.

Highlights

Listeria monocytogenes is a gram-positive pathogen that infects humans and animals by ingestion of contaminated food, and is associated with high rates of mortality [1,2]
Treatment with cephalosporins was shown to worsen the effect of immune-suppressant drugs administered prior to oral L. monocytogenes inoculation, by increasing both intestinal expansion and systemic spread of intragastrically inoculated bacteria [89]. Consistent with this previous work, we recently showed that perturbation of the microbiota through antibiotic treatment dramatically increases luminal expansion of L. monocytogenes in mice, rendering doses as low as 100 CFUs capable of colonizing the entire intestinal tract and leading to systemic spread [28]
Luminal expansion of L. monocytogenes in the gut increases the risk of systemic dissemination and the development of severe disease, and classic and more recent experimental studies using animal models are revealing that host defense is multifaceted, involving the epithelial barrier, innate and adaptive immune defenses and, perhaps least appreciated but extremely important, the commensal microbial populations that inhabit the mammalian GI tract

Summary

Introduction

Listeria monocytogenes is a gram-positive pathogen that infects humans and animals by ingestion of contaminated food, and is associated with high rates of mortality [1,2]. Pathogens 2018, 7, 1 environment and frequently contaminates foods, making encounter with this pathogen a relatively common event for humans It is not widely appreciated, Listeria monocytogenes transiently and asymptomatically colonizes a sizable percentage of the human population, with estimates varying between 1 and. A more likely possibility is that despite frequent passages through the GI tract of human beings, L. monocytogenes rarely progresses to systemic infection This would suggest that efficient resistance mechanisms are in place to prevent expansion of this pathogen following ingestion. The mechanisms of Listeria invasion and spread within the mammalian host have been elucidated by elegant experimental studies mapping the trafficking of genetically tagged bacteria upon inoculation into mice and guinea pigs [26,27] These studies have demonstrated that L. monocytogenes replicates in intestinal villi and is shed into the gut lumen, generating a second wave of penetration that results in. Intra-rectal administration of Listeria results in systemic infection of mice following dissemination via caudal lymph nodes [29,32], supporting the notion that the large intestine serves as a likely invasion portal

Host-Derived Factors

Host Immune Defenses

Gut Microbiota

Findings

Conclusions