Because classical agglutination mediated by immunoglobulin A (IgA) is inefficient at pathogen densities typically achieved during infection in the gut lumen, it remains unclear how IgA protects against bacterial pathogens in vivo. In Nature, Moor et al. show that high-affinity IgA-mediated cross-linking prevents daughter-cell separation after division and that such 'enchained growth' accelerates pathogen clearance. Oral vaccination in a mouse model of salmonellosis induces high-avidity, lipopolysaccharide-binding IgA antibodies that act protectively by inducing bacterial clumping in chain structures driven by bacterial growth rather than by collision. Enchained growth is density independent and drives clump formation at densities characteristic of natural infection with Salmonella typhimurium. IgA-induced enchainment into clonal clumps prevents horizontal gene transfer between plasmid-positive clones and plasmid-negative clones and thus diminishes pathogen evolution. Enchained growth is also observed for Escherichia coli strains, which indicates that this might represent an important mechanism of the control for pathogens and commensals.

Nature 544, 498–502 (2017)