Soferman R, Bar-Zohar D, Jurgenson U, Fireman E. Ann Allergy Asthma Immunol. 2004;92:545–548
Purpose of the Study.
To investigate the relationship between the serum level of soluble CD14 (sCD14) in children hospitalized because of respiratory syncytial virus (RSV)–induced bronchiolitis and the subsequent development of recurrent wheezing.
Twenty-one infants aged 2 to 14 months who were hospitalized because of RSV bronchiolitis in the winter of 2001–2002. All were at least 37 weeks’ gestation without any neonatal complications or prior illness.
sCD14 was measured on admission to the hospital. RSV infection was documented by direct immunofluorescence. Children were assessed every 2 months for 1 year after discharge for the development of recurrent wheezing.
Nineteen patients completed the study. Six children did not have recurrent wheezing in the 12-month follow-up period (group A), and 13 had recurrent wheezing (group B). There was no significant difference in birth weight, male-to-female ratio (1:1), or age at hospitalization (group A: 6.3 ± 5.3 months; group B: 4.2 ± 3.3 months) between groups. There was a trend for children in group A to have been breastfed more than those in group B (83% vs 46%; P = .18). Similarly, children in group A tended to have higher birth weight than those in group B (3303 ± 647 vs 2864 ± 486 g; P = .15). Children in group A (nonwheezers) had significantly higher sCD14 levels on hospital admission than those in group B (wheezers) (14521 ± 1773 vs 11243 ± 3264 pg/mL; P < .05). sCD14 levels correlated with age at hospitalization (P < .01). The sCD14 level was >11 000 pg/mL in 5 of 6 (83%) children in group A and 6 of 13 (46%) children in group B. This level was chosen as the one felt to be the best predictor for subsequent recurrent wheezing.
In infants hospitalized for RSV bronchiolitis, high serum sCD14 levels correlate with protection from subsequent recurrent wheezing and may modulate the influence of RSV development of lower airway disease.
Membrane-bound CD14 on monocytes and macrophages binds lipopolysaccharide (LPS) and transfers it from LPS-binding protein to Toll-like receptors (TLRs). CD14/TLR activation by LPS enhances interleukin 12 and interleukin 18 synthesis, TH1 differentiation, and inhibition of the atopic phenotype. It is not clear from this study if increased sCD14 levels are the result of a differential responsiveness to RSV in group A or if sCD14 levels predated acquisition of the RSV infection. Nonetheless, this study adds another layer to our understanding of the early role of innate immune responsiveness and the subsequent risk of development of atopic disease.