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The antigens participating in the macrophage micration inhibition to Mycoplasma pneumoniae
Abstract:
Recently the association of cellular immunity with pulmonary infiltrates in Mycoplasma pneumoniae infection has been suggested. Guinea pigs infected experimentally with M. pneumoniae developed a cellular hypersensitivity that could be demonstrated in vitro by the macrohage migration inhibition test. Peritoneal exudate cells obtained from guinea pigs sensitized with the organism were inhibited from migrating out of capillary tubes by the whole cell antigen. When the whole cells were extracted with aqueous acetone, the activity was found in the acetone insoluble (lipid-depleted) fraction, but not in lipid fraction. The activity was heat resistant, but diminished by treatment of 0.8 N HC1 at 100 degrees C for 30 min. The antigens responsible for the cellular immunity of M. pneumoniae were separated from the lipid, which had been considered the specific hapten associated with humoral immunity to this organism.
Insights
Cellular immunity in Mycoplasma pneumoniae infection involves specific antigens distinct from lipids. Researchers identified these antigens in lipid-depleted fractions, demonstrating their role in cellular hypersensitivity.
Area of Science:
- Immunology
- Microbiology
Background:
- Pulmonary infiltrates in Mycoplasma pneumoniae infections are increasingly linked to cellular immunity.
- Previous research suggested lipids were the primary antigens involved in humoral immunity.
Purpose of the Study:
- To investigate the nature of antigens responsible for cellular immunity in Mycoplasma pneumoniae infection.
- To differentiate cellular immunity antigens from those associated with humoral immunity.
Main Methods:
- Experimental infection of guinea pigs with Mycoplasma pneumoniae.
- In vitro macrophage migration inhibition test using whole cell antigen and extracted fractions.
- Biochemical analysis including aqueous acetone extraction, heat resistance, and acid hydrolysis tests.
Main Results:
- Guinea pigs infected with M. pneumoniae developed demonstrable cellular hypersensitivity.
- The cellular immunity activity was localized to the acetone-insoluble (lipid-depleted) fraction of the organism.
- The active antigen fraction was heat-resistant but sensitive to acid hydrolysis.
Conclusions:
- The antigens mediating cellular immunity in Mycoplasma pneumoniae infections are distinct from lipids.
- These findings separate the antigens responsible for cellular immunity from those previously identified as haptens for humoral immunity.