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Division of Cell Biology, Departments of
* Pediatrics and
Immunology, National Jewish Medical and Research Center, Denver, CO 80206; and
StressGen Biotechnologies, Collegeville, PA 19426
Microbial heat shock proteins (hsp) have been associated with the
generation and induction of Th1-type immune responses. We tested the
effects of treatment with five different microbial hsp
(Mycobacterium leprae, Streptococcus
pneumoniae, Helicobacter pylori, bacillus
Calmette-Guérin, and Mycobacterium tuberculosis)
in a murine model of allergic airway inflammation and airway
hyperresponsiveness (AHR). Mice were sensitized to OVA by i.p.
injection and then challenged by OVA inhalation. Hsp were administered
to each group by i.p. injection before sensitization and challenge.
Sensitized and challenged mice developed increased serum levels of
OVA-specific IgE with significant airway eosinophilia and heightened
responsiveness to methacholine when compared with nonsensitized
animals. Administration of M. leprae hsp prevented both
development of AHR as well as bronchoalveolar lavage fluid eosinophilia
in a dose-dependent manner. Treatment with M. leprae hsp
also resulted in suppression of IL-4 and IL-5 production in
bronchoalveolar lavage fluid, while IL-10 and IFN-
production were
increased. Furthermore, M. leprae hsp treatment
significantly suppressed OVA-specific IgE production and goblet cell
hyperplasia/mucin hyperproduction. In contrast, treatment with the
other hsp failed to prevent changes in airway responsiveness, lung
eosinophilia, or cytokine production. Depletion of /
T
lymphocytes before sensitization and challenge abolished the effect of
M. leprae hsp treatment on AHR. These results indicate
selective and distinctive properties among the hsp, and that M.
leprae hsp may have a potential therapeutic role in the
treatment of allergic airway inflammation and altered airway
function.
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