B cells oppose Mycoplasma pneumoniae vaccine enhanced disease and limit bacterial colonization of the lungs

Abstract

Development of an effective vaccine for Mycoplasma pneumoniae has been hindered by reports of Vaccine Enhanced Disease (VED) in test subjects vaccinated and challenged in studies conducted in the 1960s. The exact mechanism of disease exacerbation has yet to be fully described, but host immune responses to Lipid-Associated Membrane Proteins (LAMPs) lipoprotein lipid moieties have been implicated. LAMPs-induced exacerbation appears to involve helper T cell recall responses, due in part to their influence on neutrophil recruitment and subsequent inflammatory responses in the lung. Herein, we characterized the functions of host B cell responses to M. pneumoniae LAMPs and delipidated-LAMPs (dLAMPs) by conducting passive transfer and B cell depletion studies to assess their contribution to disease exacerbation or protection using a BALB/c mouse model. We found that antibody responses to M. pneumoniae LAMPs and dLAMPs differ in magnitude, but not in isotype or subclass. Passive transfer, dLAMP denaturation, and monoclonal antibody studies indicate that antibodies do not cause VED, but do appear to contribute to control of bacterial loads in the lungs. Depletion of B cells prior to LAMPs-vaccination results in significantly enhanced pathology in comparison to B cell competent controls, suggesting a possible regulatory role of B cells distinct from antibody secretion. Taken together, our findings suggest that B cell antibody responses to M. pneumoniae contribute to, but are insufficient for protection against challenge on their own, and that other functional properties of B cells are necessary to limit exacerbation of disease in LAMPs-vaccinated mice after infection.

Vimentin Is an Attachment Receptor for Mycoplasma pneumoniae P1 Protein

“…Attachment could be blocked by pretreatment with vimentin antibody, indicating that vimentin might be one of the receptors for M. pneumoniae adherence to host cells. Gavitt et al showed that monoclonal antibodies to P1 adhesion protein could interfere with the adhesion of Mycoplasma pneumoniae ( 57 ), and our study found that the change of vimentin expression and the blocking of vimentin would also affect the adhesion of rP1-C and Mycoplasma pneumoniae , which provided a new idea for the prevention and treatment of Mycoplasma pneumoniae infection.…”

Efficacy and Influencing Factors of Sangju Cough Mixture in the Adjuvant Treatment of Adult Patients with Mycoplasma pneumoniae Infection: A Retrospective Study

“… 3 , 4 MP lacks a cell wall and is sensitive to beta-lactams, glycopeptides, and fosfomycin. 5 , 6 Owing to the small size of MP, it can spread via droplets and lead to an epidemic. 7 …”

“…3,4 MP lacks a cell wall and is sensitive to betalactams, glycopeptides, and fosfomycin. 5,6 Owing to the small size of MP, it can spread via droplets and lead to an epidemic. 7 The medications for MP infection primarily include quinolones, macrolides, and tetracyclines.…”