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Published on: June 3, 2012
Influenza virus hemagglutinin stimulates the protein kinase C activity of human polymorphonuclear leucocytes
Abstract:
Human polymorphonuclear leukocytes (PMNL) incubated with influenza virus, A/USSR/90/77 (H1N1) or its hemagglutinin produced a significant increase in their PKC activity when compared with untreated PMNL. The activated kinase translocated from cytosol to cellular membrane. The calcium-dependent enzyme activity was inhibited by a specific inhibitor suggesting that alpha and/or beta isoforms of PKC were involved.
Insights
Influenza virus and its hemagglutinin activate protein kinase C (PKC) in human polymorphonuclear leukocytes (PMNL). This enzyme activation involves translocation and suggests the involvement of specific PKC isoforms.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human polymorphonuclear leukocytes (PMNL) play a crucial role in the innate immune response.
- Influenza virus infections can modulate immune cell function.
Purpose of the Study:
- To investigate the effect of influenza virus on protein kinase C (PKC) activity in human PMNL.
- To determine the cellular localization and potential isoforms of PKC involved.
Main Methods:
- Incubation of human PMNL with influenza virus (A/USSR/90/77 H1N1) or its hemagglutinin.
- Measurement of PKC activity and assessment of enzyme translocation.
- Use of specific inhibitors to probe PKC isoform involvement.
Main Results:
- Influenza virus and hemagglutinin significantly increased PKC activity in PMNL.
- Activated PKC translocated from the cytosol to the cellular membrane.
- Calcium-dependent activity and inhibition by a specific inhibitor indicated involvement of alpha and/or beta PKC isoforms.
Conclusions:
- Influenza virus modulates human PMNL function through PKC activation.
- PKC activation is associated with kinase translocation and calcium-dependent signaling.
- Alpha and/or beta PKC isoforms are likely involved in the cellular response to influenza virus.
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