Parasite-specified phagocytosis of Chlamydia psittaci and Chlamydia trachomatis by L and HeLa cells.
Phagocytosis of the 6BC strain of Chlamydia psittaci and the lymphogranuloma venereum 440L strain of Chlamydia trachomatis by L cells and HeLa 229 cells occurred at rates and to extents that were 10 to 100 times greater than those observed for the phagocytosis of Escherichia coli and polystyrene latex spheres. Both species of Chlamydia were efficiently taken up by host cells of a type they had not previously encountered. Phagocytosis of chlamydiae was brought about by the interaction of parasite surface ligands with elements of the host cell surface. The chlamydial ligands were readily denatured by heat, were masked by antibody, and were resistant to proteases and detergents. The host cell components were reversibly removed by proteases. Chlamydial phagocytosis was inhibited when host cells were incubated for many hours with cycloheximide. It was suggested that the presence on the chlamydial cell surface of ligands with high affinity for normal, ubiquitously occurring structures on the surface of host cells is an evolutionary adaptation to intracellular existence. The term parasite-specified phagocytosis was used to describe the efficient phagocytosis of chlamydiae by nonprofessional phagocytes and to distinguish it from the host-specified immunological and non-immunological phagocytosis carried out by professional phagocytes.
D002692:Chlamydia trachomatis / Q000276:immunology*; D002691:Chlamydophila psittaci / Q000276:immunology*; D003513:Cycloheximide / Q000494:pharmacology; D004926:Escherichia coli / Q000276:immunology; D006367:HeLa Cells / Q000276:immunology*; D006358:Hot Temperature; D007106:Immune Sera / Q000494:pharmacology; D007739:L Cells / Q000276:immunology*; D007840:Latex; D008863:Microspheres; D010447:Peptide Hydrolases / Q000494:pharmacology; D010587:Phagocytosis / Q000187:drug effects; D013045:Species Specificity
D007106:Immune Sera; D007840:Latex; D003513:Cycloheximide; D010447:Peptide Hydrolases