ABSTRACT
Lipid metabolism of monkey kidney (LLC-MK-2) cells and cells infected with a Chlamydia trachomatis strain lymphogranuloma venereum (LGV) was studied. The protein-to-lipid ratio of normal MK-2 cells was found to increase linearly over a 60-h period of incubation. The protein-to-lipid ratio of the infected cells was similar to that in normal cells until 36 h after infection, when a plateau in the ratio was observed. Lipid synthesis of the infected cells was found to be inhibited after 48 h of infection. Turnover of host lipids did not appear to be markedly altered by infection with LGV over a 48-h period of incubation. An anteiso branched chain of 15:0 fatty acid was found in infected cells but not in normal cells. The appearance of this fatty acid, correlated with a rise in the infectivity of LGV, suggests that synthesis of specific lipids was associated with the infection.
Subject(s)
Granuloma Inguinale/metabolism , Kidney/metabolism , Lipid Metabolism , Acetates/metabolism , Animals , Carbon Radioisotopes , Cell Line , Chlamydia/isolation & purification , Culture Media , Culture Techniques , Esters , Fatty Acids/analysis , Fatty Alcohols , Granuloma Inguinale/microbiology , Haplorhini , Lipids/isolation & purification , Proteins/analysis , Viral Plaque Assay , Virus CultivationABSTRACT
The cell population kinetics of the transmissible venereal tumour of the dog was studied at two different stages of tumour growth using the labelled mitoses technique. At the first stage the tumours were growing with a doubling time of about 4 days; at the second stage their growth rate was limited, probably by an immune reaction on the part of the host, to a doubling time greater than 20 days.Labelling of the tumour cells was found to be extremely heterogeneous throughout the tumour. Mitotic figures, however, were present in well labelled as well as in poorly labelled fields, suggesting that thymidine did not reach all regions of the tumour nodules. The data were therefore analysed assuming that the cells in well labelled areas were representative of the total cell population in the neoplasm. The timing of the cell cycle was found to be similar in the rapidly growing tumours and in those growing more slowly. It is concluded that the slowing of growth was due to a considerable increase in the rate of cell loss as a result of the immune reaction.
