International Archives of Allergy and Immunology
Original Paper
Diesel Exhaust Particulates Enhance Eosinophil Adhesion to Nasal Epithelial Cells and Cause DegranulationTerada N.a · Maesako K.-i.a · Hiruma K.a · Hamano N.a · Houki G.a · Konno A.a · Ikeda T.b · Sai M.baDepartment of Otorhinolaryngology, Chiba University, School of Medicine, Chiba, and bMorinaga Bio-Science Laboratories, Inc., Kanagawa, Japan
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Article / Publication Details
Received: September 02, 1996
Accepted: April 28, 1997
Published online: September 04, 2009
Issue release date: 1997
Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0
ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)
For additional information: https://www.karger.com/IAA
Abstract
Diesel exhaust particulates (DEP) are a common air pollutant from diesel-engine-powered car exhaust and are thought to cause chronic airway diseases. On the other hand, eosinophils are major components of allergic inflammatory disorders such as asthma, nasal allergy and atopic dermatitis. We examined the effects of DEP and DEP extract (extract of polyaromatic hydrocarbons) on eosinophil adhesion, survival rate and degranulation. Eosinophils, human mucosal microvascular endothelial cells (HMMECs) and human nasal epithelial cells (HNECs) were preincubated in the presence or absence of DEP and DEP extract. 35S-labeled eosinophils were allowed to adhere to monolayers of HMMECs and HNECs. After washing, 35S radioactivity was determined and numbers of adherent eosinophils were calculated using each standard curve. The effects of DEP and DEP extract on eosinophil survival rate and degranulation were also determined. Although neither DEP nor DEP extract affected the adhesiveness of HMMECs and HNECs to eosinophils, 5 ng/ml of DEP extract and 50 ng/ml of DEP extract each significancy increased eosinophil adhesiveness to HNECs (134 ± 9 and 143 ± 8%, respectively; p < 0.01 vs. control), but neither effected eosinophil adhesiveness to HMMECs. DEP extract also induced eosinophil degranulation without changing the eosinophil survival rate. Given that eosinophil-derived lipid mediators and toxic proteins play important roles in the development of nasal allergy, the above findings strongly suggest that DEP plays an important role in promoting the nasal hypersensitivity induced by enhanced eosinophil infiltration of epithelium and eosinophil degranulation.
© 1997 S. Karger AG, Basel
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Article / Publication Details
Received: September 02, 1996
Accepted: April 28, 1997
Published online: September 04, 2009
Issue release date: 1997
Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0
ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)
For additional information: https://www.karger.com/IAA
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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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