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Relationships among specific viral pathogens, virus‐induced interleukin‐8, and respiratory symptoms in infancy
Author(s) -
Gern James E.,
Martin Matthew S.,
Anklam Kelly A.,
Shen Kunling,
Roberg Kathy A.,
CarlsonDakes Kirstin T.,
Adler Kiva,
GilbertsonWhite Stephanie,
Hamilton Rebekah,
Shult Peter A.,
Kirk Carol J.,
Da Silva Douglas F.,
Sund Sarah A.,
Kosorok Michael R.,
F. Lemanske Robert
Publication year - 2002
Publication title -
pediatric allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.269
H-Index - 89
eISSN - 1399-3038
pISSN - 0905-6157
DOI - 10.1034/j.1399-3038.2002.01093.x
Subject(s) - rhinovirus , medicine , respiratory system , immunology , virus , nasal lavage , asthma , influenza a virus , virology , allergy
Both virus‐mediated damage to airway tissues and induction of pro‐inflammatory cytokines such as interleukin‐8 (IL‐8) could contribute to symptom severity during viral respiratory infections in children. To test the hypothesis that IL‐8 contributes to the pathogenesis of respiratory symptoms during naturally acquired respiratory viral infections in children, nasal wash samples collected from infants with acute viral infections (n = 198) or from healthy uninfected infants (n = 31) were analysed for IL‐8. Nasal wash IL‐8 was positively related to age in uninfected children ( r s = 0.36, p < 0.05). Respiratory syncytial virus (RSV) infection caused more severe respiratory symptoms compared to infections with influenza A, parainfluenza viruses, or rhinoviruses. In addition, RSV, parainfluenza and rhinovirus infections increased levels of IL‐8 in nasal lavage fluid, and there were some differences in the ability of the viruses to induce IL‐8 production (RSV>influenza, p < 0.05). Finally, there were significant correlations between nasal wash IL‐8 levels and symptom scores during infections with rhinovirus ( r s = 0.56, p < 0.001) or influenza A ( r s = 0.45, p < 0.05), but not with parainfluenza virus or RSV. These findings provide evidence of a close relationship between the generation of IL‐8 and symptoms during acute community‐acquired infections with rhinovirus or influenza A. In contrast, for RSV and parainfluenza infections, factors in addition to IL‐8 production appear to contribute to the generation of clinical symptoms.