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Interaction of virulent Mycoplasma pneumoniae with hamster tracheal organ cultures
Abstract:
Exposure of hamster tracheal organ cultures to virulent Mycoplasma pneumoniae leads to alterations in ribonucleic acid (RNA) and protein biosynthesis and metabolism of the respiratory epithelium. An examination of the turnover rates of RNA and protein in infected tracheal organ cultures indicates that the rates of degradation of both prelabeled host cell RNA and protein are similar to those of uninfected controls. Infected tracheal organ cultures shifted to a nonpermissive medium within 24 h after infection and further incubated in the nonpermissive medium for 72 or 96 h behaved as normal uninfected cultures in terms of metabolic precursor uptake. Under these conditions, mycoplasmas remained attached to the respiratory epithelium. Cell membranes prepared from virulent mycoplasmas by several procedures neither attached to nor altered the metabolic activity of tracheal cultures. These data indicate that the intimate contact between virulent mycoplasmas and the respiratory epithelium does not alone account for the subsequent interruption of host cell metabolism but must be accompanied by continued multiplication and biochemical function of attached mycoplasmas.
Insights
Virulent Mycoplasma pneumoniae disrupts respiratory cell metabolism. Continued mycoplasma multiplication and function, not just attachment, are essential for this disruption in hamster tracheal organ cultures.
Area of Science:
- Microbiology
- Cell Biology
- Respiratory Medicine
Background:
- Mycoplasma pneumoniae infections can cause respiratory illness.
- The precise mechanisms by which M. pneumoniae affects host cell metabolism are not fully understood.
Purpose of the Study:
- To investigate the role of Mycoplasma pneumoniae in altering host cell metabolism.
- To determine if mycoplasma attachment alone or continued metabolic activity is responsible for host cell dysfunction.
Main Methods:
- Hamster tracheal organ cultures were exposed to virulent M. pneumoniae.
- RNA and protein turnover rates were measured.
- Cultures were transferred to non-permissive media to halt mycoplasma replication.
- Host cell metabolic precursor uptake was assessed.
Main Results:
- M. pneumoniae infection altered host cell RNA and protein metabolism.
- RNA and protein degradation rates were similar in infected and uninfected cultures.
- When mycoplasma replication was halted, host cell metabolism normalized despite mycoplasma attachment.
- Isolated mycoplasma membranes did not affect host cell metabolism.
Conclusions:
- Intimate contact between M. pneumoniae and respiratory epithelium is insufficient to explain host cell metabolic disruption.
- Continued multiplication and biochemical function of attached M. pneumoniae are necessary for altering host cell metabolism.