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Departments of
* Microbiology and Immunology and
Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China
In this study, we examine the effects of Dermatophagoides
farinae (Der f), a major source of airborne allergens, on
alveolar macrophages (AMs), and we also test its contribution to
allergic responses in mice. Der f activated NF-
B of AMs and, unlike
OVA or LPS stimulation, up-regulated IL-6, TNF-
, and NO. In
addition, it down-regulated antioxidants, but affected neither the
expression nor production of IL-12. Der f-stimulated AMs expressed
enhanced levels of costimulatory B7 molecules, supported T cell
proliferation, and promoted Th2 cell development. The enhanced
accessory function was suppressed by blockade mAbs to B7.2, IL-6, and
TNF- and by N-monomethyl-L-arginine, an
NO synthase inhibitor, and N-acetylcysteine, a thiol
antioxidant, whereas it was augmented by
(±)-S-nitroso-N-acetylpenicillamine, an NO
donor. Arg-Gly-Asp-Ser peptide and neo-glycoproteins galactose-BSA and
mannose-BSA inhibited the Der f-induced IL-6 and TNF- productions
and enhanced accessory function of AMs. Der f was more potent than OVA
for inducing pulmonary eosinophilic inflammation, NO, and serum
allergen-specific IgG1 Ab production in mice. AMs from Der f-challenged
mice expressed enhanced levels of B7 and augmented T cell proliferation
ex vivo. In Der f-challenged mice, respiratory syncytial virus
infection (5 x 105 pfu; 3 days before Der f
instillation) augmented Der f-specific Ab production, whereas
dexamethasone (50 mg/kg; 1 h before Der f instillation) diminished
the allergic airway inflammation and Ab response. We conclude that AMs
are sensitive targets for Der f and that the Der f-induced
proinflammatory responses may represent an important mechanism in
mediating the development of allergic sensitization and
inflammation.
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