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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. Only a minority of individuals exposed to
these Ags develops disease, suggesting that host factors are important
for the expression of HP. We compared the expression of HP in a
sensitive strain of mice, C57BL/6, and in a resistant strain of mice,
DBA/2. They were exposed to the thermophilic bacteria
Saccharopolyspora rectivirgula (SR) or to saline alone for
3 consecutive days/week for 3 wk. After exposure to Ag, C57BL/6 mice,
but not DBA/2 mice, developed granulomatous inflammation with an
increase in lung index (lung weight). Both strains had similar amounts
of Ag delivered to the lungs after intranasal installation, as
determined with 14C-labeled Ag. Both also had similar
increases in total bronchoalveolar cells after Ag exposure, but the
C57BL/6 mice had more lymphocytes. Compared with the resistant strain,
the sensitive strain had a significantly greater Ag-induced increase in
IL-12 and IFN-
gene expression. DBA/2 mice resembled sensitive,
C57BL/6 mice if they received IL-12 augmentation therapy at the time of
Ag exposure. These findings were not limited to lung, since both
unstimulated and SR-stimulated spleen cells from C57BL/6 mice released
significantly more IL-12 than cells from DBA/2 mice. However, spleen
cells from DBA/2 mice made more IFN- when exposed to IL-12, than
cells from C57BL/6 mice. These results suggest that the IL-12 response
to Ag may modulate in part the expression of HP.
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