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Suppression of endocytosis in neutrophils by influenza A virus in vitro
Abstract:
The effect of influenza A virus on the endocytic pathway in polymorphonuclear leukocytes (PMNLs) and the relationship of altered endocytic activity to virus-induced inhibition of other PMNL functions were examined with virus that caused decreased phagosomelysosome fusion and bacterial killing (depressing virus [DV]) and virus that did not (non-DV). Binding of both viruses to PMNL surface receptors was similar, but uptake of DV into PMNLs was decreased compared with that of non-DV. Both viruses were associated with the PMNL plasma membrane and were in endosomes. DV caused less stimulation of pinocytosis than did non-DV. The rate of exocytosis of fluoresceinated-dextran (FL-dextran) from cells stimulated with DV was significantly less than for non-DV. When PMNLs were pretreated with buffer, DV, or non-DV and then exposed to FL-dextran and N-formylmethionylleucylphenylalanine, the pinocytosis of FL-dextran was significantly less in cells pretreated with DV as compared with non-DV or buffer.
Insights
Influenza A virus impacts polymorphonuclear leukocyte (PMNL) endocytosis, with a "depressing virus" (DV) reducing phagosome-lysosome fusion and bacterial killing. This DV impairs PMNL functions more than non-depressing virus.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Polymorphonuclear leukocytes (PMNLs) are crucial for innate immunity.
- Influenza A virus can modulate immune cell functions.
- The endocytic pathway is vital for PMNL effector functions.
Purpose of the Study:
- To investigate how influenza A virus affects the endocytic pathway in PMNLs.
- To determine the relationship between altered endocytic activity and virus-induced inhibition of PMNL functions.
Main Methods:
- Comparison of a "depressing virus" (DV) and a "non-depressing virus" (non-DV) in PMNLs.
- Analysis of virus binding, uptake, and association with PMNLs.
- Assessment of pinocytosis and exocytosis rates using fluoresceinated-dextran (FL-dextran).
Main Results:
- Both DV and non-DV bound similarly to PMNLs, but DV uptake was reduced.
- DV led to decreased stimulation of pinocytosis compared to non-DV.
- Exocytosis of FL-dextran was significantly lower in cells exposed to DV.
Conclusions:
- Influenza A virus, particularly DV, impairs PMNL endocytic functions.
- Altered endocytosis by DV correlates with reduced PMNL bactericidal activity.
- DV interferes with key PMNL processes like phagosome-lysosome fusion and bacterial killing.