Differential expression of chemokines and their receptors in adult and neonatal macrophages infected with human or avian influenza viruses.
In 1997, avian influenza virus H5N1 was transmitted directly from chicken to human and resulted in a severe disease that had a higher mortality rate in adults than in children. The characteristic mononuclear leukocyte infiltration in the lung and the high inflammatory response in H5N1 infection prompted us to compare the chemokine responses between influenza virus-infected adult and neonatal monocyte-derived macrophages (MDMs). The effects of avian influenza virus A/Hong Kong/483/97 (H5N1) (H5N1/97), its precursor A/Quail/Hong Kong/G1/97 (H9N2) (H9N2/G1), and human influenza virus A/Hong Kong/54/98 (H1N1) (H1N1/98) were compared. Significantly higher expression of CCL2, CCL3, CCL5, and CXCL10 was induced by avian influenza viruses than by human influenza virus. Moreover, the increase in CCL3 expression in H5N1/97-infected adult MDMs was significantly higher than that in neonatal MDMs. Enhanced expression of CCR1 and CCR5 was found in avian virus-infected adult MDMs. The strong induction of chemokines and their receptors by avian influenza viruses, particularly in adult MDMs, may account for the severity of H5N1 disease.
Zhou
Jianfang
J
Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Law
Helen K W
HK
Cheung
Chung Yan
CY
Ng
Iris H Y
IH
Peiris
J S Malik
JS
Lau
Yu Lung
YL
D000328:Adult; D000367:Age Factors; D000818:Animals; D001717:Birds; D002478:Cells, Cultured; D018925:Chemokines / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D005312:Fetal Blood / Q000166:cytology; D015967:Gene Expression Regulation, Viral / Q000276:immunology; D006801:Humans; D007231:Infant, Newborn; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology* / Q000472:pathogenicity / Q000502:physiology; D053124:Influenza A Virus, H5N1 Subtype / Q000276:immunology* / Q000472:pathogenicity / Q000502:physiology; D053127:Influenza A Virus, H9N2 Subtype / Q000276:immunology* / Q000472:pathogenicity / Q000502:physiology; D005585:Influenza in Birds / Q000276:immunology; D007251:Influenza, Human / Q000276:immunology; D008264:Macrophages / Q000166:cytology / Q000276:immunology* / Q000821:virology; D009698:Nucleoproteins / Q000378:metabolism; D019707:Receptors, Chemokine / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D013997:Time Factors; D015854:Up-Regulation / Q000276:immunology; D014779:Virus Replication
D018925:Chemokines; D009698:Nucleoproteins; D019707:Receptors, Chemokine