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Updated: Dec 24, 2025
Antigen-Capture Enzyme-Linked Immunosorbent Assay for Specific Detection of Mycoplasma pneumoniae
Published on: February 24, 2023
Mycoplasma polysaccharide protects against complement
Jeffrey R Bolland1, Warren L Simmons2, James M Daubenspeck2
1Department of Microbiology, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Abstract:
Although they lack a cell wall, mycoplasmas do possess a glycocalyx. The interactions between the glycocalyx, mycoplasmal surface proteins and host complement were explored using the murine pathogen Mycoplasma pulmonis as a model. It was previously shown that the length of the tandem repeat region of the surface lipoprotein Vsa is associated with susceptibility to complement-mediated killing. Cells producing a long Vsa containing about 40 repeats are resistant to complement, whereas strains that produce a short Vsa of five or fewer repeats are susceptible. We show here that the length of the Vsa protein modulates the affinity of the M. pulmonis EPS-I polysaccharide for the mycoplasma cell surface, with more EPS-I being associated with mycoplasmas producing a short Vsa protein. An examination of mutants that lack EPS-I revealed that planktonic mycoplasmas were highly susceptible to complement killing even when the Vsa protein was long, demonstrating that both EPS-I and Vsa length contribute to resistance. In contrast, the mycoplasmas were resistant to complement even in the absence of EPS-I when the cells were encased in a biofilm.
Insights
Mycoplasma pulmonis resistance to host complement involves both surface protein Vsa length and EPS-I polysaccharide. Biofilm formation confers complement resistance independently of these factors.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Mycoplasmas lack cell walls but possess a glycocalyx.
- Surface protein Vsa length influences susceptibility to complement-mediated killing in Mycoplasma pulmonis.
- Long Vsa variants (approx. 40 repeats) confer resistance, while short variants (≤5 repeats) are susceptible.
Purpose of the Study:
- To explore interactions between the mycoplasma glycocalyx, surface proteins, and host complement.
- To investigate the role of Vsa protein length and EPS-I polysaccharide in complement resistance.
- To determine the contribution of biofilm formation to mycoplasma survival.
Main Methods:
- Utilized Mycoplasma pulmonis as a model organism.
- Analyzed the effect of Vsa protein length on EPS-I polysaccharide affinity.
- Examined complement susceptibility in EPS-I deficient mutants and biofilm-encased cells.
Main Results:
- Vsa protein length modulates EPS-I polysaccharide association with the cell surface.
- Mycoplasmas producing short Vsa exhibit higher EPS-I association.
- EPS-I is crucial for complement resistance in planktonic cells, even with long Vsa.
- Biofilm formation confers complement resistance independent of EPS-I and Vsa length.
Conclusions:
- Both EPS-I polysaccharide and Vsa protein length are key contributors to Mycoplasma pulmonis complement resistance.
- Biofilm matrix provides a protective mechanism against complement-mediated killing.
- Understanding these mechanisms is vital for controlling mycoplasma infections.
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