Analysis of the interaction of enteropathogenic bacteria with HLA B27 transfected murine fibroblasts showed a specific influence of HLA B27 on microbial invasiveness. This possible novel mechanism for the action of HLA B27 should be verified by using endogenous HLA B27 positive and negative human fibroblasts as a model for the direct interaction of arthritogenic bacteria and host cells.
Fibroblasts were obtained from healthy donors positive or negative for HLA B27; cultivated as monolayers; and infected with Salmonella enterica serovar enteritidis.
Invasion and survival of bacteria in human cells was not influenced by the presence of HLA B27. Enhancement of HLA class I molecule expression by treatment of cultures with interferon gamma decreased invasion and survival of bacteria in both HLA B27 positive and negative cells. After disappearance of live bacteria lipopolysaccharide antigens persisted within cells.
Endogenous HLA B27 does not modulate the direct interaction of Salmonella with human cells. Non-professional phagocytes are able to limit bacterial survival in cells, and interferon gamma accelerates killing of bacteria, but arthritogenic antigens persist after disappearance of live bacteria.