ENTRY OF COXIELLA-BURNETII INTO HOST-CELLS

The attachment to and entry into L mouse fibroblast cells of viable phase I and phase II Nine Mile Coxiella burnetii was investigated. The use of P-32-labelled rickettsiae showed that phase II C. burnetii attached more readily to L cells than phase I organisms; this probably accounts for the more rapid establishment of infection of host cells by the phase II agents. Two lines of evidence indicated that C burnetii plays a passive role in both attachment and entry into host cells: (1) inactivation of rickettsiae by either heat or glutaraldehyde did not affect either process, and (2) metabolic inhibitors of L cell phagocytic function - NaF and cytochalasin B and D - abolished rickettsiae uptake. These results indicate that it is an endocytotic event. While the presence of purified phase I lipopolysaccharide (LPS) did not interfere with attachment of rickettsiae to the surface of host cells, it markedly impaired entry of C burnetii in both phases. This suggests that LPS is not an adhesin and that it is toxic to the host cell. Treatment of L cells with either pronase, subtilisin or subtilopeptidase A significantly reduced the number of C. burnetii that adhered to the host cell surface; this result suggests that proteins are either proximate to or components of the C. burnetii attachment site.