A Listeria adhesion protein-deficient Listeria monocytogenes strain shows reduced adhesion primarily to intestinal cell lines.

Abstract

Listeria monocytogenes adheres and penetrates intestinal cell linings for systemic infection. A 104-kDa Listeria adhesion protein (LAP) from L. monocytogenes was previously demonstrated to be responsible for adhesion to intestinal enterocyte-like Caco-2 cells. We investigated the adhesion and invasion characteristics of a LAP-deficient mutant L. monocytogenes strain (A572) to various human intestinal and non-intestinal cell lines to assess the possible target host cells. Among the intestinal cell lines, A572 showed significantly reduced adhesion than the wild type (WT) strain to the cells of ileum-cecum (HCT-8) and colon (Caco-2 and HT-29), whereas A572 and WT did not show any significant differences in adhesion to other intestinal cell lines from duodenum (HuTu-80) or jejunum (Int-407). Differences in adhesion between A572 and WT were little or none in non-intestinal cell lines from liver, kidney, bladder, ovary, cervix, breast, larynx, or skin. Invasion data showed that A572 was invasive but the invasion efficiency was proportional to its adhesion characteristics to respective cell lines. In mouse bioassay, A572 was not found in liver following oral administration, suggesting that LAP mutant was possibly unable to pass through intestinal cell linings. Immuno-electron microscopy revealed that the LAP is localized in the bacterial surface as well as the cytoplasm. In summary, this study indicated that the LAP-mediated adhesion is associated with the intestinal cells originating from the lower part of small intestine and from the upper part of large intestine, and possibly plays an important role during the intestinal phase of infection.