The overall objectives of this project are to investigate the molecular pathogenesis of Mycoplasma pneumoniae disease and to develop a means for controlling this disease. This approach is based on our previous studies and can be summarized as follows. First, the specific attachment of virulent M. pneumoniae to the respiratory epithelium is a prerequisite for colonization of M. pneumoniae in the respiratory tract and subsequent disease development. An avirulent strain which is incapable of attachment to respiratory epithelim does not produce disease. Second, the attachment of M. pneumoniae to respiratory epithelim is via a specialized terminal structure and a protein (P1) localized on the surface of the terminal structure has been demonstrated to be the mediator responsible for the attachment. Third, monoclonal antibodies specific to P1 protein produced by hybridoma techniques inhibit the attachment of virulent M. pneumoniae to respiratory epithelium. Our recent work indicates that P1 is a major immunogen as antibodies specific to it can be demonstrated in sera and respiratory secretions of patients with natural infection. These findings strongly suggest that P1 protein can be a promising candidate as a useful vaccine. In the present research, we propose: 1) to develop methods for the mass production of P1 protein by recombinant DNA techniques; 2) to examine the antigenic composition of P1 protein; and 3) to develop rapid diagnosis procedures for the detection of antibodies to and antigens of M. penumoniae. Adequate quantities of P1 protein will allow us to study the molecular function of P1 and to test its efficacy as a vaccine. Antigenic analyses of P1 proteins prepared from both virulent and avirulent strains should enable us to establish the molecular """"""""reasoning"""""""" of attachment and other biological activities of this unique protein. The availability of rapid diagnostic procedures will help the clinicians in therapeutic decision-making.
