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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.

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The obligately intracellular bacteria of the genus Chlamydia, which is only remotely related to other eubacterial genera, cause many diseases of humans, nonhuman mammals, and birds. Interaction of chlamydiae with host cells in vitro has been studied as a model of infection in natural hosts and as an example of the adaptation of an organism to an unusual environment, the inside of another living cell. Among the novel adaptations made by chlamydiae have been the substitution of disulfide-bond-cross-linked polypeptides for peptidoglycans and the use of host-generated nucleotide triphosphates as sources of metabolic energy. The effect of contact between chlamydiae and host cells in culture varies from no effect at all to rapid destruction of either chlamydiae or host cells. When successful infection occurs, it is usually followed by production of large numbers of progeny and destruction of host cells. However, host cells containing chlamydiae sometimes continue to divide, with or without overt signs of infection, and chlamydiae may persist indefinitely in cell cultures. Some of the many factors that influence the outcome of chlamydia-host cell interaction are kind of chlamydiae, kind of host cells, mode of chlamydial entry, nutritional adequacy of the culture medium, presence of antimicrobial agents, and presence of immune cells and soluble immune factors. General characteristics of chlamydial multiplication in cells of their natural hosts are reproduced in established cell lines, but reproduction in vitro of the subtle differences in chlamydial behavior responsible for the individuality of the different chlamydial diseases will require better in vitro models.

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One hour after suspensions of mouse fibroblasts (L cells) were exposed to 500 to 1,000 L-cell 50% infectious doses of Chlamydia psittaci (6BC), the L cells failed to attach to and spread out on solid substrates, phagocytosed polystyrene latex spheres at reduced rates, incorporated less [14C]isoleucine into protein, and had smaller soluble pools of nucleoside triphosphates. The infected L cells began to die at 8 h and were all dead by 20 h. Lower multiplicities of infection took correspondingly longer to kill the L cells. These effects of high multiplicities of C. psittaci on L cells will be referred to collectively as immediate toxicity. Similar effects were obtained with other strains of C. psittaci and C. trachomatis and with other cell lines. Ultraviolet-inactivated C. psittaci retained the ability to cause immediate toxicity, but heat-inactivated chlamydiae did not. C.psittaci cells had to be ingested by L cells before they were immediately toxic but, once they were phagocytosed, they did not need to multiply or to synthesize macromolecules in order to cause immediate injury to their hosts. Immediate toxicity was not the result of depression of energy metabolism, changes in the levels of intracellular cyclic nucleotides, or release of hydrolases from lysosomes. It was suggested that a lesion is produced in the plasma membrane of the L cell every time it ingests a chlamydial cell, that each act of ingestion produces an independent lesion, and that their injurious effects are additive. Thus, the more ingestion lesions there are, the faster the host cell dies. It was also suggested that induced phagocytosis, inhibition of lysosomal fusion, and death of mice and of cells in culture may all depend on a single activity of C. psittaci.