In:
The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 37.8-37.8
Abstract:
The parasitic nematode Nippostrongylus brasiliensis (Nb) third-stage larvae (L3) migrate to the host lung at about 24 to 48 hrs after infection, causing lung damage, inflammation and a potent Th2-type response. Yet, little is known about the mechanism causing lung damage and whether components of the Th2-type immune response contribute to acute lung wound repair. In this study we report that migrating Nb larvae (L3) induce lung inflammation that results in increased hemorrhaging in addition to mechanical damage in the lung. Neutrophil depletion reduced lung hemorrhage and both hemorrhaging and neutrophil infiltration were decreased in Nb-infected IL-17R KO mice. Resolution of acute hemorrhage and inflammation was dependent on either IL-4 or IL-13 as IL-4Rα KO mice, but not IL-13Rα or IL-4 deficient mice, induced significantly higher hemorrhaging, neutrophil influx, and IL-17 expression. Elevations in Arg1, IGF-1, and IL-10 were also inhibited in IL-4RαKO mice. In IL-10KO mice, resolution of inflammation was also blocked, control of hemorrhaging was partly suppressed, and Arg1 and IGF-1 elevations were not affected. These data suggest that the Th2-type immune response mediates acute wound healing and control of IL-17-dependent inflammation during helminth infection.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.184.Supp.37.8
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2010
detail.hit.zdb_id:
1475085-5
Permalink