Related Experiment Video
Updated: May 16, 2026

Opsono-Adherence Assay to Evaluate Functional Antibodies in Vaccine Development Against Bacillus anthracis and Other Encapsulated Pathogens
Published on: May 19, 2020
EPS-I polysaccharide protects Mycoplasma pulmonis from phagocytosis
Brandon M Shaw1, James M Daubenspeck, Warren L Simmons
1Department of Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Abstract:
Few mycoplasmal polysaccharides have been described and little is known about their role in pathogenesis. The infection of mice with Mycoplasma pulmonis has been utilized in many in vivo and in vitro studies to gain a better understanding of host-pathogen interactions during chronic respiratory infection. Although alveolar macrophages have a primary role in host defence, M. pulmonis is killed inefficiently in vitro. One antiphagocytic factor produced by the mycoplasma is the family of phase- and size-variable Vsa lipoproteins. However, bacteria generally employ multiple strategies for combating host defences, with capsular polysaccharide often having a key role. We show here that mutants lacking the EPS-I polysaccharide of M. pulmonis exhibit increased susceptibility to binding and subsequent killing by alveolar macrophages. These results give further insight into how mycoplasmas are able to avoid the host immune system and sustain a chronic infection.
Insights
Mycoplasma pulmonis uses EPS-I polysaccharide to evade immune cells. Mutants lacking this polysaccharide are more vulnerable to alveolar macrophages, revealing a new mechanism of mycoplasma pathogenesis.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Mycoplasma pulmonis is a common cause of chronic respiratory infections in mice.
- Alveolar macrophages are key immune cells in lung defense but inefficiently kill M. pulmonis.
- The role of mycoplasmal polysaccharides in pathogenesis is poorly understood.
Discussion:
- This study investigates the role of the EPS-I polysaccharide in M. pulmonis immune evasion.
- EPS-I deficient mutants showed increased susceptibility to alveolar macrophage binding and killing.
- This suggests that EPS-I is an antiphagocytic factor contributing to M. pulmonis survival.
Key Insights:
- Mycoplasma pulmonis utilizes the EPS-I polysaccharide as a mechanism to evade host immune responses.
- The absence of EPS-I significantly enhances the phagocytosis and killing of M. pulmonis by alveolar macrophages.
- This highlights the critical role of bacterial polysaccharides in host-pathogen interactions.
Outlook:
- Further research into EPS-I could reveal new therapeutic targets for M. pulmonis infections.
- Understanding polysaccharide-mediated immune evasion is crucial for combating chronic microbial persistence.
- Investigating other potential polysaccharide virulence factors in mycoplasmas is warranted.
Related Concept Videos
Inhibitors of Gram-positive Cell Wall Synthesis
Bacterial Phylum Tenericutes
Atypical Pneumonia
Defense Against Bacterial Pathogens
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
Outer Layers of the Cell Envelope
Formation of Lipopolysaccharides

