ABSTRACT
We report a study on the effect of herpes simplex virus 1 (HSV-1) infection on apoptosis of neutrophils from both adults and neonates and present evidence showing that HSV-1 enhances apoptosis in neonatal, but not adult, neutrophils. HSV-1 enhanced the expression of both Fas and Fas ligand on the surface of neonatal neutrophils. Treatments with anti-Fas antibody and a Fas ligand inhibitor significantly reduced the induction of apoptosis by HSV-1. Using an ELISA assay, it was found that HSV-1 infection also leads to increased release of soluble FasL from HSV-1-infected neonatal neutrophils. Increased neonatal neutrophil apoptosis following HSV-1 infection may represent an important mechanism by which HSV-1 may diminish the antiviral response of neonatal neutrophils and might explain, at least in part, the severity of infections that are caused in newborns by this herpesvirus.
Subject(s)
Apoptosis , Herpes Simplex/immunology , Herpesvirus 1, Human , Neutrophils/virology , Adult , Antibodies, Blocking/pharmacology , Fas Ligand Protein , Herpes Simplex/pathology , Herpes Simplex/virology , Humans , Infant, Newborn , Membrane Glycoproteins/antagonists & inhibitors , Membrane Glycoproteins/metabolism , Neutrophils/immunology , Tumor Necrosis Factor Inhibitors , Tumor Necrosis Factors/metabolism , fas Receptor/drug effects , fas Receptor/metabolismABSTRACT
We prospectively studied the levels of eicosanoids in intubated patients with severe bronchiolitis and compared them to electively intubated non-infected infants. LeukotrieneE(4) (LTE(4)), leukotrieneB(4) (LTB(4)), and prostaglandinE(2) (PGE(2)) levels were significantly increased (P <.01) from endotracheal (ET) aspirates of infants with bronchiolitis compared with controls, as were urinary LTE(4) levels (P <.001). We conclude that eicosanoids are increased in the tracheal aspirates and urine of children with bronchiolitis.