ArticleInfection and immunity2004
Resistance of Mycoplasma pulmonis to complement lysis is dependent on the number of Vsa tandem repeats: shield hypothesis.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Serum Resistance ofPathogens (Basel, Switzerland) · 2022Article
- Antibodies Specific to Membrane Proteins Are Effective in Complement-Mediated Killing of Mycoplasma bovis.Infection and immunity · 2019Article
- Identifying genome-wide immune gene variation underlying infectious disease in wildlife populations - a next generation sequencing approach in the gopher tortoise.BMC genomics · 2018Article
- The Role of Lipoproteins in Mycoplasma-Mediated Immunomodulation.Frontiers in microbiology · 2018Article
- Article
- Catalase Enhances Growth and Biofilm Production of Mycoplasma pneumoniae.Current microbiology · 2015Article
- EPS-I polysaccharide protects Mycoplasma pulmonis from phagocytosis.FEMS microbiology letters · 2013Article
- Mycoplasma polysaccharide protects against complement.Microbiology (Reading, England) · 2012Article
- Mycoplasma pulmonis Vsa proteins and polysaccharide modulate adherence to pulmonary epithelial cells.FEMS microbiology letters · 2012Article
- The Vsa shield of Mycoplasma pulmonis is antiphagocytic.Infection and immunity · 2012Article
- Occurrence, plasticity, and evolution of the vpma gene family, a genetic system devoted to high-frequency surface variation in Mycoplasma agalactiae.Journal of bacteriology · 2009Article
- Mycoplasma biofilms ex vivo and in vivo.FEMS microbiology letters · 2009Article
- Large-scale transposon mutagenesis of Mycoplasma pulmonis.Molecular microbiology · 2008Article
- Biofilms protect Mycoplasma pulmonis cells from lytic effects of complement and gramicidin.Infection and immunity · 2007Article
- A stochastic mechanism for biofilm formation by Mycoplasma pulmonis.Journal of bacteriology · 2007Article
- Distinctive repertoire of contingency genes conferring mutation- based phase variation and combinatorial expression of surface lipoproteins in Mycoplasma capricolum subsp. capricolum of the Mycoplasma mycoides phylogenetic cluster.Journal of bacteriology · 2006Article
- Resistance to antimicrobial peptides and stress response in Mycoplasma pulmonis.Antimicrobial agents and chemotherapy · 2005Article
- Avoidance of the host immune system through phase variation in Mycoplasma pulmonis.Infection and immunity · 2005Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Vsa proteins are associated with the virulence of the murine respiratory pathogen Mycoplasma pulmonis. The antigens consist of a conserved N-terminal region that is combined with one of several different variable C-terminal regions comprised of tandem repeats. M. pulmonis strains that produce VsaA with about 40 tandem repeats do not adhere to polystyrene or erythrocytes and are highly resistant to complement killing. Strains that produce VsaA with three tandem repeats adhere strongly to polystyrene and erythrocytes and are highly susceptible to complement killing. We report here that the resistance to complement lysis was not due to a lack of activation of the complement cascade. Isolation and analysis of M. pulmonis strains that produced Vsa proteins other than VsaA (VsaG and VsaI) with either long or short repeat regions indicated that adherence to polystyrene and resistance to complement were dependent on the length of the repeat region but not on the Vsa type. Furthermore, M. pulmonis Vsa variants were susceptible to the polypeptide pore-forming molecule gramicidin D, independent of the Vsa type and length. Collectively, the data indicate the Vsa proteins nonspecifically mediate M. pulmonis surface interactions and function to sterically hinder access of complement to the mycoplasma cell membrane while permitting access of smaller molecules.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.