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Published on: September 20, 2024
Biofilms protect Mycoplasma pulmonis cells from lytic effects of complement and gramicidin
Warren L Simmons1, Kevin Dybvig
1Department of Genetics, University of Alabama at Birmingham, KAUL 720, Birmingham, AL 35294-0004, USA. wsimmons@uab.edu
Abstract:
The length of the tandem repeat region of the Vsa protein of Mycoplasma pulmonis has previously been shown to modulate the susceptibility of mycoplasmas to killing by complement: cells that produce a short form of the Vsa protein are highly sensitive, and cells producing the long Vsa protein are resistant. In contrast to their differing susceptibilities to complement, the mycoplasmas were highly sensitive to gramicidin irrespective of the length of the Vsa protein produced. We show here that when encased within a biofilm, cells of M. pulmonis producing a short form of the Vsa protein were more resistant to complement and gramicidin than mycoplasmas that were dispersed. The resistance appeared to be localized to those mycoplasmas within tower structures of the biofilms. Biofilm formation may be a mechanism that protects mycoplasmas from host immunity.
Insights
Mycoplasma pulmonis biofilms protect against host immunity. Encased in biofilms, short Vsa protein variants showed increased resistance to complement and gramicidin, unlike dispersed cells.
Area of Science:
- Microbiology
- Immunology
- Biochemistry
Background:
- The Vsa protein length in Mycoplasma pulmonis influences complement susceptibility.
- Short Vsa variants are complement-sensitive, while long Vsa variants are resistant.
- Mycoplasmas are generally sensitive to gramicidin, regardless of Vsa protein length.
Purpose of the Study:
- To investigate the role of Mycoplasma pulmonis biofilms in protection against host immunity.
- To determine if biofilm formation alters susceptibility to complement and gramicidin.
Main Methods:
- Culturing Mycoplasma pulmonis with varying Vsa protein lengths.
- Encasing mycoplasmas in biofilms and assessing resistance.
- Comparing resistance of dispersed versus biofilm-encased mycoplasmas to complement and gramicidin.
Main Results:
- Biofilm-encased Mycoplasma pulmonis showed enhanced resistance to complement and gramicidin compared to dispersed cells.
- This resistance was observed in strains producing both short and long Vsa protein variants.
- Resistance was localized to mycoplasmas within the tower structures of biofilms.
Conclusions:
- Mycoplasma pulmonis biofilm formation is a potential mechanism for evading host immune responses.
- Biofilms confer protection against complement-mediated killing and antimicrobial agents like gramicidin.
- The structural organization within biofilms, specifically tower structures, may be crucial for this protective effect.
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