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The amyloidogenic peptide human amylin augments the inflammatory activities of eosinophils
Author(s) -
Horn Joanne T.,
Estridge Tom,
Pechous Penni,
Hyslop Paul A.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.5.526
Subject(s) - amylin , amyloid (mycology) , inflammation , biology , peptide , cytokine , endocrinology , medicine , immunology , biochemistry , diabetes mellitus , islet , botany
The amyloidogenic peptides, amyloid‐β (Aβ) and human amylin, are the major constituents of amyloid deposits found in patients with the chronic degenerative disorders Alzheimer's disease (AD) and type 2 diabetes, respectively. Recent studies have shown that a variety of inflammatory proteins such as cytokines are associated with the amyloid deposits of AD brain tissues. Therefore, in the present study, we sought to determine whether Aβ and/or human amylin could modulate the various inflammatory activities of eosinophils. We observed that human amylin but not Aβ peptides inhibited the in vitro interleukin‐5 (IL‐5)–mediated survival of cord blood–derived eosinophils (CBEs) in a concentration‐dependent manner. By contrast, rat amylin, a nonamyloidogenic peptide that is highly homologous to human amylin, failed to affect the IL‐5–mediated survival of CBEs. Similar inhibitory effects of human amylin were observed for peripheral blood eosinophils. Human amylin also enhanced the release of the cytokine granulocyte‐macrophage colony‐stimulating factor by CBEs that were stimulated with the calcium ionophore A23187 but was incapable of directly stimulating CBEs to release cytokines. In addition, the A23187‐induced release of the inflammatory lipid mediator leukotriene C 4 by CBEs was augmented by human amylin. These results suggest that the amyloidogenic peptide human amylin is capable of amplifying the various inflammatory activities of eosinophils.