Journal
JOURNAL OF IMMUNOLOGY
Volume 172, Issue 6, Pages 3766-3774Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.6.3766
Keywords
-
Categories
Ask authors/readers for more resources
Avian schistosomes are the primary causative agent of cercarial dermatitis in humans, but despite its worldwide occurrence, little is known of the immune mechanism of this disease. Using a murine model, hosts were exposed to primary (I X) and multiple (4 x) infections of Trichobilharzia regenti via the pinna. Penetration of larvae into the skin evoked immediate edema, thickening of the exposure site, and an influx of leukocytes, including neutrophils, macrophages, CD4(+) lymphocytes, and mast cells. A large proportion of the latter were in the process of degranulating. After 1 x infection, inflammation was accompanied by the release of IL-1beta, IL-6, and IIL-12p40. In contrast, in 4 x reinfected animals the production of histamine, IL-4, and IL-10 was dramatically elevated within 1 h of infection. Analysis of Ag-stimulated lymphocytes from the skin-draining lymph nodes revealed that cells from 1 X infected mice produced a mixed Th1/Th2 cytokine response, including abundant IFN-gamma, whereas cells from 4 x reinfected mice were Th2 polarized, dominated by IL-4 and IL-5. Serum Abs confirmed this polarization, with elevated levels of IgG1 and IgE after multiple infections. Infection with radiolabeled cercariae revealed that almost 90% of larvae remained in the skin, and the majority died within 8 days after infection, although parasites were cleared more rapidly in 4x reinfected mice. Our results are the first demonstration that cercarial dermatitis, caused by bird schistosomes, is characterized by an early type I hypersensitivity reaction and a late phase of cutaneous inflammation, both associated with a polarized Th2-type acquired immune response.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available