Revisiting the steps of Salmonella gut infection with a focus on antagonistic interbacterial interactions Original paper

What was studied?

This review explores the complex process of Salmonella gut infection, emphasizing the role of antagonistic interbacterial interactions between the pathogen and commensal microbiota. The authors detail how Salmonella manipulates the gut environment to promote its own survival while disrupting the normal microbiota. They discuss the pathogen’s strategies, such as using type III secretion systems to trigger inflammation, which leads to shifts in the intestinal niche that favor its growth. The review also examines how Salmonella competes with commensal bacteria through mechanisms like bacteriocins, microcins, and type six secretion systems, linking these processes to the pathogen’s ability to persist and infect the host.

Who was studied?

The review synthesizes data from various animal models, including gnotobiotic and antibiotic-treated mice, to explore how Salmonella interacts with the microbiota. It focuses on commensal strains such as Escherichia coli Nissle 1917, Enterobacter cloacae, and Lactobacillus species, which produce bacteriocins and microcins that influence Salmonella colonization. The authors also examine pathogenic strains like Salmonella Typhimurium and other Enterobacteriaceae to understand how they engage in direct competition for resources in the gut. Genomic and transcriptomic studies of these bacteria provide insights into the specific loci involved in bacteriocin production, type six secretion systems, and other competitive strategies that shape the gut environment during infection.

Most important findings

The review highlights how Salmonella infection alters the gut microbiota, causing inflammation that disrupts butyrate-producing Firmicutes and increases luminal oxygen. This shift in the gut environment favors Salmonella’s growth and creates new opportunities for competition. Salmonella uses type III secretion system effectors to induce this inflammatory state, creating conditions that support its own metabolism while inhibiting other bacteria. The review also describes how commensals like Escherichia coli deploy bacteriocins and microcins, which target and kill Salmonella, while Salmonella itself produces colicins and microcins to counteract these competitors. In addition, the authors highlight the role of type six secretion systems in both Salmonella and other Enterobacteriaceae, which can target and kill competitor bacteria. These findings suggest that microbiome-based strategies, such as promoting beneficial bacterial interactions, can influence Salmonella infection dynamics.

Key implications

For clinicians, this review reframes Salmonella infection as a process heavily influenced by the gut microbiota and microbial competition. The authors suggest that microbiome signatures should include not only shifts in bacterial communities but also the presence of functional traits like colicins, microcins, and type six secretion systems, which can inform the risk of Salmonella colonization and infection. The presence of specific commensal strains, like Escherichia coli Nissle 1917, that produce competitive antimicrobial factors could be leveraged in clinical settings as a probiotic treatment to reduce Salmonella colonization. The review also points to the potential for developing narrow-spectrum antimicrobial therapies that exploit natural interbacterial competition mechanisms, such as targeting siderophore receptors, while preserving the broader gut microbiome.