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The Ability of Polymorphonuclear Leukocyte Priming Agents to Overcome Influenza A Virus‐Induced Cell Dysfunction
Author(s) -
Abramson Jon S.,
Wagner M. Paige,
Ralston Elizabeth P.,
Wei Yu,
Wheeler J. Gary
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.50.2.160
Subject(s) - priming (agriculture) , virus , biology , granulocyte , immunology , influenza a virus , phorbol , orthomyxoviridae , guanosine , stimulation , respiratory burst , biochemistry , endocrinology , enzyme , protein kinase c , botany , germination
Abstract The major mortality and morbidity resulting from influenza virus infections are due to secondary bacterial infections which occur in association with virus‐induced inhibition of polymorphonuclear leukocyte (PMNL) function. The present study was undertaken to determine if compounds which prime PMNL function to subsequent stimulation with N‐formylmethionyl‐leucylphenylalanine (FMLP) or phorbol 12‐myristate 13‐acetate (PMA) can overcome influenza A virus (IAV)‐induced inhibition of the PMNL chemiluminescence response to these stimuli. Granulocyte‐macrophage colony stimulating factor (GM‐CSF), guanosine triphosphate (GTP), and 1‐oleoyl‐2‐acetylglycerol (OAG) were able to prime the PMNL response to FMLP and/or PMA and totally or partially overcome lAV‐induced PMNL dysfunction in cells stimulated with FMLP or PMA. A direct correlation was found between the extent of PMNL priming due to GM‐CSF, GTP, and OAG and the capacity of these compounds to overcome virus‐induced PMNL dysfunction. The implications of these findings in regard to the mechanism by which priming agents overcome lAV‐induced cell dysfunction and the potential of these compounds as therapeutic agents to treat secondary bacterial infections are discussed.