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.

Two-dimensional gel electrophoresis analysis in simultaneous influenza pneumonia and bacterial infection in mice

“…We found that MIP-2 was also increased significantly in incubated BAL cells from co-infected lungs compared with either single-infected lungs or non-infected lungs, as reported previously [9]. These results also suggested the important roles of these cytokines/chemokines and neutrophils in the pathogenesis of severe pneumonia because of influenza virus and bacteria co-infection [27,28]. Braun et al reported elevated A1AT concentrations despite decreases of the NE and MPO concentrations in BALF from acute pneumonia patients, and suggested the importance of the balance between aggressive factors (NE, MPO, lysozyme and MIP-2) and protective factors (e.g.…”

Acute infection with influenza virus enhances susceptibility to fatal pneumonia followingStreptococcus pneumoniaeinfection in mice with chronic pulmonary colonization withPseudomonas aeruginosa

“…Reduced MPO activity in influenza virus infection was also observed in the whole lungs of mice with chronic P. aeruginosa infection. Influenza virus has been demonstrated to have direct effects on neutrophil functions in vitro, including inhibition of chemotaxis, oxidative function and lysosome-phagosome fusion [19,20]. Pang et al [16] reported that sputum neutrophils obtained from patients with bronchiectasis showed a significantly reduced capacity to secrete lysozyme, but not MPO by influenza virus infection.…”

Pathogenesis of Borna Disease Virus: Granulocyte Fractions of Psychiatric Patients Harbor Infectious Virus in the Absence of Antiviral Antibodies

“…Whether granulocytes are productively infected or whether they have simply taken up infected cells or free virus remains to be determined. Polymorphonuclear leukocytes can harbor viruses (2,43,46,49), although it has rarely been shown that viruses infect these cells directly (reviewed in reference 1). On the other hand, it has been demonstrated that granulocytes take up virions; alternatively, infected cells or cell debris might be ingested by phagocytosing cells.…”