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Characterization of the effect of influenza virus on polymorphonuclear leukocyte membrane responses
Abstract:
Depressed chemotactic activity of polymorphonuclear leukocytes (PMNL) infected with influenza virus could be due to changes occurring at the plasma membrane. The present study examined the effect of unopsonized influenza virus on chemotaxis, adherence, receptor binding, shape change, membrane fluidity, and release of specific granules from PMNL. Chemotactic activity of PMNL under-agarose to the chemoattractants, zymosan-activated serum ( ZAS ) and N-formyl-methionyl-leucyl-phenylalanine (fMLP), and adherence of PMNL to a plastic surface were markedly decreased in virus-treated cells as compared to control cells. The binding of fMLP to the PMNL was increased in virus-treated cells compared with control cells. Exposure of cells to virus, ZAS , or fMLP caused 35%-50% of the cells to become bipolar in shape, whereas less than 5% of the cells exposed to buffer became bipolar. Influenza virus did not alter membrane fluidity as measured by electron spin resonance spectroscopy with the probe 5-doxyl stearate. Virus-treated PMNL stimulated with FMLP or Staphylococcus aureus exhibited a marked decrease in the amount of lactoferrin released into phagosomes, onto the cells' outer membrane, and into the extracellular medium as compared to control cells. The possible relationship between inhibition of lysosomal enzyme degranulation and decreased chemotactic activity and adherence of PMNL is discussed.
Insights
Influenza virus infection impairs polymorphonuclear leukocytes (PMNL) function, reducing their ability to move towards stimuli and adhere to surfaces. This study investigates the impact on PMNL
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Polymorphonuclear leukocytes (PMNL) are crucial for innate immunity.
- Influenza virus infection can compromise immune cell function.
- Changes in the PMNL plasma membrane may underlie impaired chemotaxis.
Purpose of the Study:
- To investigate the effects of influenza virus on PMNL chemotaxis, adherence, and degranulation.
- To explore the role of the PMNL plasma membrane in virus-induced functional deficits.
Main Methods:
- Under-agarose chemotaxis assay using zymosan-activated serum (ZAS) and N-formyl-methionyl-leucyl-phenylalanine (fMLP).
- Adherence assay to plastic surfaces.
- Fluorescence microscopy for cell shape analysis.
- Electron spin resonance spectroscopy for membrane fluidity.
- Lactoferrin release assay to measure degranulation.
Main Results:
- Influenza virus significantly decreased PMNL chemotaxis and adherence.
- fMLP binding to PMNL was increased post-virus exposure.
- Virus-treated PMNL showed reduced lactoferrin release upon stimulation.
- No alteration in PMNL membrane fluidity was observed.
Conclusions:
- Influenza virus impairs PMNL chemotaxis and adherence, potentially linked to altered degranulation.
- Plasma membrane changes may contribute to reduced PMNL function during viral infections.
- Further research is needed to elucidate the precise mechanisms of PMNL dysfunction.