Adhesion properties of commensal bacteria mediate ROS stimulation in intestinal epithelial cells

The mammalian host maintains a mutually beneficial coexistence with a diverse intestinal microbiota, which can affect many aspects of gut homeostasis. However, how commensal bacteria can modulate host processes is largely unknown. Recently, we reported that commensal bacteria can induce reactive oxygen species (ROS) in gut epithelial cells and influence signaling by transient oxidative inactivation of regulatory pathways such as NF‐kappaB and ERK MAPK. Here we describe marked differences in the capacity of gut bacteria to induce ROS in cultured intestinal epithelial cells and the living mouse intestine. Commensal Lactobacilli (e.g. LGG) were potent ROS inducers, while other commensals or pathogens stimulated significantly less or no ROS. LGG spaC mutant has been shown to be a key factor for adhesion on human intestinal mucus. This mutant could not adhere to Caco‐2 cells and induced significantly lower amounts of ROS in Caco‐2 cells or in mouse jejunum, compared with isogenic WT Lactobacillus. These data indicate that distinct members of the microbiota or probiotics with high adhesion have an enhanced ability to induce ROS and mediate epithelial signaling. The relative abilities of distinct members of the microflora to stimulate ROS and affect host cell signaling may represent a parameter that defines a healthy intestinal bacterial community.