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Inflammatory responses in mice sequentially exposed to JP-8 jet fuel and influenza virus
To examine the hypothesis that Jet Propulsion Fuel (JP-8) inhalation potentiates influenza virus-induced inflammatory responses, we randomly divided female C57BL/6 mice (4-weeks old, weighing approximately 24.6 g) into the following groups: air control, JP-8 alone (1023 mg/m 3 of JP-8 for 1 h/day fo...
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Published in: | Toxicology (Amsterdam) 2004-04, Vol.197 (2), p.138-146 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | To examine the hypothesis that Jet Propulsion Fuel (JP-8) inhalation potentiates influenza virus-induced inflammatory responses, we randomly divided female C57BL/6 mice (4-weeks old, weighing approximately 24.6
g) into the following groups: air control, JP-8 alone (1023
mg/m
3 of JP-8 for 1
h/day for 7 days), A/Hong Kong/8/68 influenza virus (HKV) alone (a 10
μl aliquot of 2000 viral titer in the nasal passages), and a combination of JP-8 with HKV (JP-8 + HKV). The HKV alone group exhibited significantly increased total cell number/granulocyte differential in bronchoalveolar lavage fluid (BALF) compared to controls whereas the JP-8 alone group did not. The JP-8 + HKV group further exacerbated the HKV alone-induced response. However, increases in pulmonary microvascular permeability and pathological alterations in JP-8 + HKV just matched the sum of JP-8 alone- and HKV alone-induced response. Increases in BALF substance P in the JP-8 alone group and BALF leukotriene B
4 or total lung compliance in the HKV alone group, respectively were similar to the changes in the JP-8 + HKV group. These findings suggest that changes in the JP-8 + HKV group may be attributed to either JP-8 inhalation or HKV treatment and indicate the different physiological responses to either JP-8 or HKV exposure. Taken together, most of the data did not provide supporting evidence that JP-8 inhalation synergizes influenza virus-induced inflammatory responses. |
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ISSN: | 0300-483X 1879-3185 |
DOI: | 10.1016/j.tox.2003.12.015 |