Interplay between mycoplasma surface proteins, airway cells, and the protean manifestations of mycoplasma-mediated human infections.

Adherence of mycoplasmas to specific tissue surfaces is a crucial step in the establishment of infection. Several pathogenic mycoplasmas are flask-shaped and possess specialized tips that permit a highly oriented surface parasitism of host target cells. Mycoplasma pneumoniae, which causes primary atypical pneumonia in humans, requires a network of interactive adhesins and accessory proteins to cytadhere. The adhesins must cluster at the mycoplasma tip organelle in close association with cytadherence-related accessory proteins and a naplike structure, which together appear to comprise a primitive cytoskeleton-like system. Proline-rich regions associated with these proteins play critical roles in the maintenance of the structural and functional integrity of the tip. Mycoplasma genitalium, originally isolated from the human urogenital tract of patients with nongonococcal urethritis, also colonizes airway cells along with M. pneumoniae. The molecular basis for cytadherence of these mycoplasmas is discussed in terms of the identification, cloning, and sequencing of the implicated mycoplasma genes, their common DNA and amino acid homologies and structural and functional domains, and the organizational similarities in their cytadherence-related operons. In addition, the multiorgan protean manifestations of mycoplasma infection are discussed in terms of the role that mycoplasma adhesins may play in molecular mimicry, postinfectious autoimmunity, and immune-mediated damage.