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The Severity of Lethal H5N1 Viral Infection‐Induced Changes in Pulmonary Inflammation and Functions Is Age‐Dependent
Author(s) -
Zang Na,
Zhuang Jianguo,
Ye Chunyan,
Pollock Zemmie,
Tipper Jennifer,
Xu Fadi
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1030.4
Subject(s) - inflammation , hypoxemia , lung , medicine , juvenile , immunology , case fatality rate , viral load , bronchoalveolar lavage , virus , biology , physiology , genetics , epidemiology
H5N1 viral infection results in ~60% mortality with the highest rate in the juvenile (10‐19 years old). Our previous study has shown that all Balb/c mice at 4W age die 8‐9 days after lethal H5N1 viral (HK483) infection, in which a remarkable drop of body temperature (BT) is an indication of fatality (AJRCCM 2013). This study was undertaken to test the hypothesis that HK483 infection‐induced changes in pulmonary inflammation and function, and drop of BT and body weight (BW) were greater in juvenile (20W) than that in younger (4W) mice. The two age groups of mice were intranasally inoculated with HK483 virus (100 PFU). After measurement of BW and BT, they were anesthetized for collecting arterial blood and then euthanized for BALF, brain and lung tissue collections on days ‐1, 3, 5, and 7 postinfection. We found that the viral infection similarly increased BALF cells, and gradually decreased BW, BT, lung dry/wet ratios, and S a o 2 in the two groups without difference in lung H5N1 viral titers. At the early stage of infection the dominant increases of BALF cell types were neutrophils in 4W but lymphocytes in 20W mice. At late stage, 20W mice, compared to 4W mice, showed less severe BT/BW drops and a two‐day delay in the occurrence of hypoxemia and hypercapnemia (appeared on day 5 postinfection). Our data suggest that the impact of lethal H5N1 viral infection on pulmonary inflammation and function is age‐dependent, i.e., it is worse in younger than juvenile mice, which is somewhat different from the clinical observations in humans (Supported by HL119683).