Parasite-specified phagocytosis of Chlamydia psittaci and Chlamydia trachomatis by L and HeLa cells

Abstract

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 siiheres. 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 parasitespecified 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.

Rac interacts with Abi-1 and WAVE2 to promote an Arp2/3-dependent actin recruitment during chlamydial invasion

“…Because chlamydiae absolutely require an intracellular niche for replication, they have evolved very efficient means of entering host eukaryotic cells (Byrne and Moulder, 1978). The precise molecular mechanisms of chlamydial attachment and entry have not been defined.…”

Propagation of Ovine and Bovine Abortion Strains of Chlamydia psittaci in Suspension Cultures of L‐cells

“…The efficiency with which the B577 and the EBA-59-795 chlamydial strains infected the L-cells resembles the efficient parasite-specified endocytosis observed with the 6BC laboratory strain of Cpsittaci (BYRNE and MOULDER, 1978). Similarly, the process of cellular uptake is also preceded by an attachment step which can be demonstrated by adsorption at 4°C (BYRNE, 1978).…”

Binding, ingestion, and growth of Chlamydia trachomatis (L2 serovar) analyzed by flow cytometry

“…Previous analyses of host cell-chlamydia interactions have been unable to assess quantitatively both the number of cells interacting with bacteria and the relative number of bacteria interacting with cells. To monitor binding and ingestion of chlamydia, radiolabeled bacteria are usually incubated with target cell populations, and the amount of associated radioaqtivity is measured (3)(4)(5)(8)(9)(10)14,15). This method permits quantitative determination of relative numbers of bacteria interacting with cell populations, but not the number of cells actively involved in these associations.…”

“…Interactions between chlamydiae and host cells have been studied previously using radiolabaeled bacteria and analyses of whole cell populations (total radioactivity associated with cells) (3)(4)(5)(8)(9)(10)14,15). Fluorescent antibody techniques have been used qualitatively to detect intracellular inclusions (organelles containing proliferating bacteria) (19); these methods have not been adapted to study quantitative interactions between chlamydiae and eukaryotic cells.…”