Abstract
In humans of all ages, the cell wall-less and genome-reduced species Mycoplasma pneumoniae can cause infections of the upper and lower respiratory tract. The well-documented occurrence of major peaks in the incidence of community-acquired pneumonia cases reported world-wide, the multifaceted clinical manifestations of infection and the increasing number of resistant strains provide reasons for ongoing interest in the pathogenesis of mycoplasmal disease. The results of recent studies have provided insights into the interaction of the limited virulence factors of the bacterium with its host. In addition, the availability of complete M. pneumoniae genomes from patient isolates and the development of proteomic methods for investigation of mycoplasmas have not only allowed characterization of sequence divergences between strains but have also shown the importance of proteins and protein parts for induction of the immune reaction after infection. This review focuses on selected aspects of the humoral host immune response as a factor that might influence the clinical course of infections, subsequent protection in cases of re-infections and changes of epidemiological pattern of infections. The characterization of antibodies directed to defined antigens and approaches to promote their induction in the respiratory mucosa are also preconditions for the development of a vaccine to protect risk populations from severe disease due to M. pneumoniae.
Highlights
Specialty section: This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology
This review focuses on selected aspects of the humoral host immune response as a factor that might influence the clinical course of infections, subsequent protection in cases of re-infections and changes of epidemiological pattern of infections
The characterization of antibodies directed to defined antigens and approaches to promote their induction in the respiratory mucosa are preconditions for the development of a vaccine to protect risk populations from severe disease due to M. pneumoniae
Summary
Use of C-terminal protein part Full-length characterization using 15 recombinant proteins, construction of a chimeric protein of C-terminal P1 part and P30 Construction of a chimeric protein of C-terminal P1 region and parts of P30 and MPN456 (unknown function) C-terminal protein part Conserved C-terminal and variable part of repMP4 of P1-types 1 and 2 C-terminal protein part Immunodominant COOH epitope Full-length characterization by using four recombinant proteins Full-length protein Fragment of P30 (without N-terminus) Fragment of P90 (aa 751–1088) Fragment of P200 (aa 641–678) Full-length protein Full-length protein Protein fragment (53 kDa). Despite the fact that 76% of the p1 sequence can be assigned to both RepMP copies, the divergence between the amino acid sequences of P1 adhesins of types 1 and 2 strains (1,628 and 1,635 aa) is only about 5% These distinct differences in amino acid sequence may influence the immune response of a colonized host. The reasons for the shift of genotypes remain unclear since it seems unlikely that the small sequence variations in the p1 gene of type 2 and type 2 variant strains will influence the immune response of infected patients. Further studies should be performed to give more insight into the role of the time-variable occurrence of genotype-specific antibodies (host-dependent) and the consequences of sequence differences in the P1 protein for the adherence process (pathogen-dependent) in the epidemiology of infections
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