Priming Of Leukocytes Research Articles

The Ability of Polymorphonuclear Leukocyte Priming Agents to Overcome Influenza A Virus-Induced Cell Dysfunction

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 IAV-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 IAV-induced cell dysfunction and the potential of these compounds as therapeutic agents to treat secondary bacterial infections are discussed.

Chemiluminescence response and endothelial cell damage following lipopolysaccharide priming of polymorphonuclear leukocytes

Neutrophils can be directly stimulated by endothelial cell suspensions, an observation that has also been made by experiments with nylon fiber, as an artificial model for PMNL/EC interactions [5]. As shown by experiments with endothelial cell suspensions a further amplification of this process following LPS-priming up to 10 ng/ml blood has been demonstrated.

Priming of leukocytes selectively increases the level of some interferon-α subtypes and not others

The effect of pretreatment with interferon (IFN) (‘priming’) on the production of individual IFN subtypes was studied in subpopulations of human peripheral blood mononuclear cells and in the myeloid cell line KG-1. It was found that priming had a selective enhancing effect on the production of certain IFN-α subtypes (IFN-α20K and IFN-α21K) and not on others. KG-1 cells produce both IFN-α and -β; however, only the production of IFN-α was enhanced by priming with either IFN-α,β or γ.