Pathophysiology of Mycoplasma pneumoniae Infection in Human Fetal Tracheal Organ Culture

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Nycoplasma pneumoniae-host cell interactions have been difficult to analyze: natural disease is limited to man, and low mortality provides little pathologic material. Data from experimental models suggest that the ciliated respiratory epithelium is the target cell of M. pneumoniae. Evaluation was made of fetal tracheal organ culture as a means of providing organized differentiated human epithelial cells for studies in vitro. Tracheas were removed from 15–20-week fetuses, obtained aseptically by hysterotomy for psychiatric indications; transverse sections were maintained in Hayflick's medium with Hepes buffer at 36°C in 5% CO2. The effects of M. pneumoniae were studied by observations of ciliary function, light microscopy and immunofluorescence. Ciliary motion (which could be quantitated stroboscopically) slowed, became disorganized and ceased by 96 h. Microscopic changes included epithelial cytoplasmic vacuolization and nuclear swelling, followed by loss of cilia. Immunofluorescence identified organisms among the cilia, between cells, and in surface microcolonies. No comparable changes were produced by 4 other human mycoplasma species which were tested. These findings suggest the patho-physiology of M. pneumoniae disease by revealing both functional and structural changes in parasitized human respiratory epithelium. The nature of this interaction may explain many general features of M. pneumoniae disease, particulary the frequency of tracheo-bronchitis with protracted paroxysmal cough which commonly occurs in childhood infections.