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Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa College of Medicine and Veterans Administrations Medical Center, Iowa City, IA 52242
Hypersensitivity pneumonitis (HP) is a granulomatous, inflammatory
lung disease caused by inhalation of organic Ags, most commonly
thermophilic actinomycetes that cause farmer’s lung disease. The early
response to Ag is an increase in neutrophils in the lung, whereas the
late response is a typical Th1-type granulomatous disease. Many
patients who develop disease report a recent viral respiratory
infection. These studies were undertaken to determine whether viruses
can augment the inflammatory responses in HP. C57BL/6 mice were exposed
to the thermophilic bacteria Saccharopolyspora
rectivirgula (SR) for 3 consecutive days per wk for 3 wk. Some
mice were exposed to SR at 2 wk after infection with respiratory
syncytial virus (RSV), whereas others were exposed to SR after exposure
to saline alone or to heat-inactivated RSV. SR-treated mice developed a
typical, early neutrophil response and a late granulomatous
inflammatory response. Up-regulation of IFN-
and IL-2 gene
expression was also found during the late response. These responses
were augmented by recent RSV infection but not by heat-inactivated RSV.
Mice with a previous RSV infection also had a greater early neutrophil
response to SR, with increased macrophage inflammatory protein-2
(MIP-2, murine equivalent of IL-8) release in bronchoalveolar lavage
fluid. These studies suggest that viral infection can augment both the
early and late inflammatory responses in HP.
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