Flagella-driven motility is a target of human Paneth cell defensin activity.

In the mammalian intestine, flagellar motility can provide microbes competitive advantage, but also threatens the spatial segregation established by the host at the epithelial surface. Unlike microbicidal defensins, previous studies indicated that the protective activities of human α-defensin 6 (HD6), a peptide secreted by Paneth cells of the small intestine, resides in its remarkable ability to bind microbial surface proteins and self-assemble into protective fibers and nets. Given its ability to bind flagellin, we proposed that HD6 might be an effective inhibitor of bacterial motility.

Characterization of an intelectin-1 () knockout mouse model.

Intelectins are carbohydrate-binding proteins implicated in innate immunity and highly conserved across chordate evolution, including both ascidians and humans. Human intelectin-1 (ITLN1) is highly abundant within the intestinal mucosa and binds microbial but not host glycans. Genome-wide association studies identified SNPs in that are linked to susceptibility for Crohn's disease.

Flagella at the Host-Microbe Interface: Key Functions Intersect With Redundant Responses.

Many bacteria and other microbes achieve locomotion flagella, which are organelles that function as a swimming motor. Depending on the environment, flagellar motility can serve a variety of beneficial functions and confer a fitness advantage. For example, within a mammalian host, flagellar motility can provide bacteria the ability to resist clearance by flow, facilitate access to host epithelial cells, and enable travel to nutrient niches.