Responsible for O-acetylation at the C6-hydroxyl group of N-acetylmuramyl residues, forming the corresponding N,6-O-diacetylmuramic acid of the peptidoglycan. O-acetylation of the peptidoglycan is the major determinant for lysozyme resistance. Critical for virulence and escape from innate immune response of the host. Involved at both early and later stages of listeriosis in the mouse model of infection. Required for successful host colonization and for intracellular survival of bacteria in macrophages of the infected host. Controls the production of inflammatory mediators in the liver of the infected host. Confers resistance to host antimicrobial molecules and to cell wall-targeting molecules such as beta-lactam antibiotics and bacteriocins. Cells lacking this gene have no O-acetylated N-acetyl muramic acid residues on the cell wall. Sensitive to bacterial cell wall targeting antimicrobial molecules lysozyme, beta-lactam antibiotic cefotaxime and Staphylococcus gallinarum lantibiotic gallidermin. Impaired postinfection intracellular survival of bacteria inside human acute monocytic leukemia (THP-1) cells. Killed more efficiently and rapidly in mouse postinfection peritoneal-elicited macrophages (PEM) and bone marrow-derived macrophages (BMDM). Impaired ability of the bacteria to multiply in infected murine macrophage-like (RAW264.7) cells. Bacteria do not accumulate in vacuoles of the infected RAW264.7 cells, but reside in the cytosol and the infected cells are not forming protrusions. Virulence is drastically reduced in mice following intravenous infection as observed by the dramatic difference in LD(50) of the mutant (1100000 bacteria) compared to wild-type (700 bacteria). With sublethal infectious doses, has a reduced capacity to replicate in liver and spleen compared to wild-type. In the intestinal lumen of intragastrically infected human E-cadherin transgenic mice, which are permissive to Listeria oral infection, the number of bacteria is strongly decreased 24 hours postinfection. There are also significantly fewer bacteria in the small intestine tissue compared to wild-type. Triggers increased secretion of cytokines interleukin 2 (IL-2), IL-6, IL-12 and IL-5, and chemokines CCL2, CXCL9 and CCL3 from the liver cells of the infected mouse at 6 hours postinfection. At later time points of infection, the production of the inflammatory mediators is increased in case of IL-6, similar in case of IL-2, CXCL9 and IL-5, and lower in case of IL-12, CCL2 and CCL3 compared to the wild-type. The virulence of a double oatA/pgdA deletion mutant is more reduced than that of either single mutant as detected by lack of colonization in the bloodstream, liver and spleen of infected mouse 24 hours postinfection. Belongs to the acyltransferase 3 family.