In order to survive in the host, mycoplasmas have to adhere to the host tissue, mostly the epithelium, to have access to the appropriate nutrients, and to avoid the defense system. Studies of myco-plasma-host cell adhesion have centered around M. pneumoniae and M. genitalium. Both organisms are of a characteristic flask-shape, with several proteins, so-called adhesins, which are involved in the adhesion process, clustered at specific tip organelles. These proteins have been identified in studies involving trypsin treatments, specific antibodies, and mutants and revertants which lost and regained the ability to cytadhere. The cellular receptor molecules for M. pneumoniae adhesins were identified as long-chain sialo-oligosaccharides of the Ii antigen type. This may contribute to the fact that high-titer cold agglutinin-type autoantibodies against this antigen are occasionally found after M. pneumoniae infections. According to findings in a mouse model, colonization of epithelia is related to hormonal status: estradiol promotes attachment to cervical and uterine epithelia, possibly by receptor induction.
As shown in animal models of mycoplasma infections, phagocytes which amass in infected tissue comprise the first line of defense against these organisms. However, in the absence of specific antibodies, mycoplasmas can survive neutrophil phagocytosis. This may be one of the mechanisms by which dissemination into unusual sites and persistence occurs in hypogammaglobulinemic patients. Interestingly, in vitro mycoplasmas can modulate class II major histocompatibility complex (MHC) expression by macrophages. Whether this influences the antigen-presenting function of these cells during an actual infection is still unclear. The fact that patients with hypogammaglobulinemia are more frequently colonized with mycoplasmas and ureaplasmas than persons with an intact immune system, and the finding that a significant fraction of those patients also suffer from mycoplasmal septic arthritis strongly suggest that antibodies protect the host from these bacteria. Secretory immunoglobulin A (IgA) appears to be important in preventing localized colonization, whereas systemic antibodies may protect from primary infection and secondary spread from localized colonization. Unlike other mycoplasma species, U. urealyticum possesses a host-specific IgA protease as a potential virulence factor. Moreover, urea-plasmas and many mycoplasmas, e.g. M. fermentans, M. hominis, M. hyorhinis and several others, have the facility to escape the humoral immune response by undergoing high-frequency antigenic variation of some of their surface antigens. The genetic mechanisms for this 'phase variation' were recently elucidated. There have been surprisingly few recent investigations into the involvement of T cells in a specific response to mycoplasmas, although early studies had shown that patients develop specifically proliferating T cells a few weeks after M. pneumoniae infection, and that this response may persist for several years. The importance of cellular immunity also became evident from studies in an animal model with nude mice. These animals, which are devoid of a functional T cell repertoire, could not be protected, as control animals, against vaginal colonization by M. pulmonis by prior oropharyngeal infection with the same organism.
In vitro effects of mycoplasmas and their products on various cells of the immune system are manifold. Occasionally an apparently mycoplasma-mediated inhibition of lymphocyte proliferation was recorded in experiments in which proliferation was measured by uptake of radioactive thymidine. However, this effect was found to be due to scavenging of thymidine by living mycoplasmas. On the other hand, stimulation of B or T cell proliferation by heat-killed mycoplasmas has been noted, as well as mycoplasma-mediated generation of cytotoxic T cells, and activation of macrophages to become cytolytic and to release proinflammatory cytokines, nitric oxide and arachidonate metabolites. Some of the effects on lymphocytes are indirect, and are due to a macrophage activator that is present to various extents in the membranes of many if not all mycoplasmas and ureaplasmas. This macrophage activator also modulates class II MHC expression. Recent biochemical data indicate that this material consists of mycoplasmal lipoproteins and lipopeptides derived from the former. M. arthritidis, a strain arthritogenic in mice and rats, is the only mycoplasma known so far which produces a superantigen. This protein was recently sequenced, and has been the subject of many studies that have elucidated its specific interaction with particular T cell receptor and class II MHC species.
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