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A critical role for eotaxin in experimental oral antigen-induced eosinophilic gastrointestinal allergy

Hogan, Simon P. and Mishra, Anil and Brandt, Eric B. and Foster, Paul S. and Rothenberg, Marc E. (2000) A critical role for eotaxin in experimental oral antigen-induced eosinophilic gastrointestinal allergy. Proceedings of the National Academy of Sciences of the United States of America, 97 (12). pp. 6681-6686. ISSN 0027-8424. PMCID PMC18701. doi:10.1073/pnas.97.12.6681.

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Despite marked advances in the understanding of allergic responses, the mechanisms regulating gastrointestinal allergy are not very well understood. We have developed a model of antigen-induced eosinophil-associated gastrointestinal allergy and characterized the role of eotaxin and IL-5. Challenge of allergen-sensitized mice with oral allergen, in the form of enteric-coated beads, resulted in marked allergen-specific IgG(1) and IgE, Th-2-type (IL-4 and IL-5) cytokine production, and eosinophil accumulation in the blood and small intestine. In the genetic absence of eotaxin, a chemokine constitutively expressed in the gastrointestinal tract, eosinophil recruitment into the small intestine was ablated, and these mice developed enhanced eosinophil accumulation in the blood compared with wild-type mice. Interestingly, in the absence of IL-5, allergen challenge promoted partial eosinophil accumulation into the small intestine and a decline in circulating eosinophil levels. Collectively, these results establish that the accumulation of gastrointestinal eosinophils is antigen induced, can occur independent of IL-5, and provides a molecular mechanism to explain the dichotomy between peripheral blood and tissue eosinophilia. Furthermore, eotaxin is identified as a critical regulator of antigen-induced eosinophilic inflammation in the gastrointestinal tract.

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Additional Information:© 2000 by the National Academy of Sciences. Edited by K. Frank Austen, Harvard Medical School, Boston, MA, and approved April 11, 2000 (received for review March 6, 2000). We thank Connie Lobas for excellent technical assistance and F. Finkelman, M. Cohen, A. Srikiatkhachorn, G. K. Hershey, S. Wert, N. Zimmermann, and L. Poulos for critical reading of the manuscript and helpful discussions. We thank A. Lippelman for secretarial assistance and Alicia Emly for graphic assistance.We also thank Robert Coffman for the anti-CCR3 serum and James and Nancy Lee for anti-MBP serum. This work was supported in part by the National Health Medical Research Council (Australia), C. J. Martin Postdoctoral Fellowship (S.P.H.), the Jaffe Family Fund of the American Academy of Asthma, Allergy, and Immunology (S.P.H.), National Institutes of Health grant R01AI45898–01 (M.E.R.), and the Human Frontier Science Program (M.E.R. and P.S.F.). This paper was submitted directly (Track II) to the PNAS office. The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Funding AgencyGrant Number
National Medical Research Council (Australia)UNSPECIFIED
C. J. Martin Postdoctoral FellowshipUNSPECIFIED
American Academy of Asthma, Allergy, and ImmunologyUNSPECIFIED
Human Frontier Science ProgramUNSPECIFIED
Issue or Number:12
PubMed Central ID:PMC18701
Record Number:CaltechAUTHORS:HOGpnas00
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:963
Deposited By: Tony Diaz
Deposited On:15 Nov 2005
Last Modified:08 Nov 2021 19:06

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