The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)-induced bronchiolitis.
Neutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasopharyngeal aspirates (NPA) (n = 19) and peripheral blood (PB) of infants with RSV bronchiolitis (n = 11) and PB from healthy controls (n = 9) was investigated. Monoclonal antibody against CD95 (Fas) and a binding protein Annexin V were used to determine the apoptosis of neutrophils. The expression of CD11b and CD18 on neutrophils was also detected with flow cytometry. The mean fluorescence intensity (MFI) of CD95 on neutrophils from RSV+ NPA was increased compared with cells from control PB (73.6 +/- 7.6 versus 31.5 +/- 4.3); the MFI of Annexin V, CD11b and CD18 on neutrophils from RSV+ NPA was up-regulated compared with cells from both control PB (105.3 +/- 18.1 versus 11.8 +/- 1.5; 1683 +/- 153.3 versus 841.1 +/- 72.3; 517 +/- 50.5 versus 147 +/- 8.7, respectively) and RSV+ PB (105.3 +/- 18.1 versus 35.8 +/- 4.1; 1683 +/- 153.3 versus 818 +/- 141.2; 517 +/- 50.5 versus 260 +/- 25.8, respectively). Furthermore, the percentage of neutrophils expressing Annexin V and the MFI of CD18 on neutrophils from RSV+ PB were increased compared with neutrophils from control PB. In addition, both CD11b (MFI) and CD18 (MFI) correlated with Annexin V (MFI) on neutrophils. We conclude that neutrophil apoptosis in RSV bronchiolitis is accelerated; and CD11b/CD18 may play an important role in RSV infection by influencing neutrophil apoptosis.
Wang
S Z
SZ
Department of Paediatrics, Flinders Medical Centre, Flinders University, Bedford Park, SA, Australia.
Smith
P K
PK
Lovejoy
M
M
Bowden
J J
JJ
Alpers
J H
JH
Forsyth
K D
KD
D017304:Annexin A5 / Q000096:biosynthesis; D017209:Apoptosis; D001988:Bronchiolitis / Q000276:immunology* / Q000821:virology; D018821:CD18 Antigens / Q000096:biosynthesis; D006801:Humans; D007223:Infant; D016177:Macrophage-1 Antigen / Q000096:biosynthesis; D009504:Neutrophils / Q000378:metabolism*; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology*; D018113:Respiratory Syncytial Virus, Human; D019014:fas Receptor / Q000096:biosynthesis
D017304:Annexin A5; D018821:CD18 Antigens; D016177:Macrophage-1 Antigen; D019014:fas Receptor