BapA, a large secreted protein required for biofilm formation and host colonization of <i>Salmonella enterica</i> serovar Enteritidis

<jats:title>Summary</jats:title><jats:p>In environmental settings, biofilms represent the common way of life of microorganisms. <jats:italic>Salmonella enterica</jats:italic> serovar Enteritidis, the most frequent cause of gastroenteritis in developed countries, produces a biofilm whose matrix is mainly composed of curli fimbriae and cellulose. In contrast to other bacterial biofilms, no proteinaceous compound has been reported to participate in the formation of this matrix. Here, we report the discovery of BapA, a large cell‐surface protein required for biofilm formation by <jats:italic>S.</jats:italic> Enteritidis. Deletion of <jats:italic>bap</jats:italic>A caused the loss of the capacity to form a biofilm whereas the overexpression of a chromosomal copy of <jats:italic>bap</jats:italic>A increased the biofilm biomass formation. We provide evidence that overproduction of curli fimbriae and not cellulose can compensate for the biofilm deficiency of a <jats:italic>bap</jats:italic>A mutant strain. BapA is secreted through a type I protein secretion system (BapBCD) situated downstream of the <jats:italic>bap</jats:italic>A gene and was found to be loosely associated with the cell surface. Experiments with mixed bacterial populations positive or negative for BapA showed that BapA minus cells are not recruited into the biofilm matrix. The expression of <jats:italic>bapA</jats:italic> is coordinated with that of genes encoding curli fimbriae and cellulose, through the action of <jats:italic>csg</jats:italic>D. Studies on the contribution of BapA to <jats:italic>S.</jats:italic> Enteritidis pathogenesis revealed that orally inoculated animals with a <jats:italic>bap</jats:italic>A‐deficient strain survived longer than those inoculated with the wild‐type strain. Also, a <jats:italic>bap</jats:italic>A mutant strain showed a significantly lower colonization rate at the intestinal cell barrier and consequently a decreased efficiency for organ invasion compared with the wild‐type strain. Taken together, these data demonstrate that BapA contributes both to biofilm formation and invasion through the regular <jats:italic>Salmonella</jats:italic> infection route.</jats:p>