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Interactions of virulent and avirulent Legionella pneumophila with human polymorphonuclear leukocytes
J T Summersgill1, M J Raff, R D Miller
1Department of Microbiology and Immunology, University of Louisville School of Medicine, Kentucky 40292.
Abstract:
Isogenic virulent/avirulent variants of Legionella pneumophila (Lp) were examined in vitro for their effect on PMN function as determined by measurement of peak chemiluminescence and superoxide anion production. When exposed to virulent/avirulent strains of Lp, PMN function was less than that seen following exposure to E. coli, the reduction of the oxidative burst being more pronounced with virulent Lp strains in both assays. To determine whether differences in reduced PMN function correlate with differences in complement component C3 binding by virulent and avirulent Lp, four pairs of organisms were incubated in normal human serum and examined by quantitative immunofluorescence. All strains of Lp bound less C3 than E. coli, although each to different degrees. Avirulent isogenic strains bound more C3 than their virulent counterparts with one exception. Depressed PMN function following exposure to Lp may be due to reduced C3 binding, although other virulence-associated factors may be involved.
Insights
Legionella pneumophila (Lp) impairs neutrophil (PMN) function, reducing oxidative burst more with virulent strains. This may be linked to lower complement C3 binding by Lp.
Area of Science:
- Immunology
- Microbiology
- Bacterial Pathogenesis
Background:
- Neutrophils (PMNs) are critical immune cells for combating bacterial infections.
- Legionella pneumophila (Lp) is an opportunistic pathogen that can cause severe pneumonia.
- Understanding Lp's interaction with host immune cells is vital for developing effective treatments.
Purpose of the Study:
- To investigate the impact of virulent and avirulent Legionella pneumophila strains on neutrophil function.
- To determine if differences in complement component C3 binding correlate with observed alterations in PMN function.
Main Methods:
- In vitro analysis of isogenic virulent/avirulent Lp strains.
- Measurement of PMN chemiluminescence and superoxide anion production.
- Quantitative immunofluorescence to assess complement C3 binding to Lp.
Main Results:
- Exposure to both virulent and avirulent Lp reduced PMN function compared to E. coli.
- Virulent Lp strains caused a more pronounced reduction in the oxidative burst.
- Lp strains exhibited lower C3 binding than E. coli, with avirulent strains generally binding more C3 than virulent ones.
Conclusions:
- Reduced PMN function upon Lp exposure may be attributed to decreased C3 binding.
- Other virulence factors likely contribute to Lp's pathogenicity.
- Further research is needed to elucidate the complex interplay between Lp and the host immune system.