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Departments of
*
Physiology and
Comparative Medicine, East Carolina University School of Medicine, Greenville, NC 27858;
Department of Biology, Southern Adventist University, Collegedale, TN 37315; and
§
Myrvik Enterprises, Southport, NC 28461
Previous studies showed that local macrophages phagocytose
nonantigenic chitin particles (1–10 µm polymers of
N-acetyl-D-glucosamine) through mannose
receptors and produce IL-12, IL-18, and TNF-
. These cytokines lead
to the production of IFN-
by NK cells. To determine whether chitin
could down-regulate Th2 responses, chitin was given orally (8 mg/day
for 3 days before and 13 days during ragweed allergen immunization) in
BALB/c and C57BL/6 mice. These ragweed-immunized mice were given
ragweed intratracheally on day 11. Three days after the challenge, the
immunized mice with saline (controls) showed increases in serum IgE
levels and lung eosinophil numbers. The chitin treatment resulted in
decreases of these events in both strains. To dissect the inhibitory
mechanisms of Th2 responses, spleen cells (4 x 106
cells/ml) isolated from the ragweed-immunized mice (controls) were
cultured in the presence of ragweed and/or chitin for 3 days (recall
responses). Ragweed alone stimulated the production of IL-4 (0.6
ng/ml), IL-5 (20 U/ml), and IL-10 (3.2 ng/ml), but not IFN-.
Ragweed/chitin stimulation resulted in significant decreases of IL-4,
IL-5, and IL-10 levels and the production of IFN- (48 U/ml).
Moreover, spleen cells isolated from the chitin-treated mice showed
ragweed-stimulated IFN- production (15 U/ml) and significantly lower
levels of the Th2 cytokines, suggesting that the immune responses were
redirected toward a Th1 response. Collectively, these results indicate
that chitin-induced innate immune responses down-regulate
Th2-facilitated IgE production and lung eosinophilia in the allergic
mouse.
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