zoom RSS 妊娠中に微生物に曝された母親から生まれた子どもはアレルギーになりにくい

<<   作成日時 : 2009/12/09 00:41   >>

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 妊娠マウスに納屋周囲の庭にいる微生物を吸入させると、子どもマウスがアレルギー抵抗性を獲得すると証明した。微生物暴露により軽度の炎症反応がおこり、微生物感受性のToll-like receptors (TLRs)とサイトカインが増加する。母親のTLRsシグナルが子どもに伝えられ、子どもマウスがアレルギー抵抗性を持つという。
Mom's Exposure to Microbes Lowers Allergies in Kids
Study found pregnant mice that inhaled barnyard air passed protection to offspring
-- Robert Preidt

画像Study found pregnant mice that inhaled barnyard air passed protection to offspring.

MONDAY, Dec. 7 (HealthDay News) -- Children born to mothers exposed to microbes during pregnancy may be less likely to develop allergies, German researchers say.

They found that pregnant mice exposed to inhaled barnyard microbes gave birth to allergy-resistant offspring. The microbe exposure triggered a mild inflammatory response in the mothers. This response was characterized by increased expression of microbe-sensing Toll-like receptors (TLRs) and the production of immune molecules called cytokines.

The study was published online Dec. 7 in the Journal of Experimental Medicine.

The researchers said the mothers' TLRs are essential for transmitting allergy protection to their offspring, but it's not known how the TLR signals translate into allergy resistance in the mice pups.

In addition, further investigation is needed to determine whether this mother-to-offspring protection applies to a wide range of allergens, including those found in food, said the team at the Phillips-University of Marburg.

Previous research has shown that children raised on farms -- which teem with environmental microbes -- develop fewer allergies than those raised in cities or in non-farming rural areas. One theory is that early-life exposure to microbes conditions a young child's developing immune system to tolerate microbes and allergens later in life.

But it may not be a child's exposure to microbes that protects against allergies. Studies have found that children of farming mothers are also less susceptible to allergies, regardless of the child's own exposure to microbes. This new study reveals a biological mechanism that helps explain this phenomenon.

More information

The Asthma and Allergy Foundation of America has more about allergies.
SOURCE: Journal of Experimental Medicine, news release, Dec. 7, 2009

Copyright (c) 2009 ScoutNews, LLC. All rights reserved.

Published online December 7, 2009
The Journal of Experimental Medicine
The Rockefeller University Press, 0022-1007 $30.00
(c) 2009 Conrad et al.

Brief Definitive Report

Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78

Melanie L. Conrad1, Ruth Ferstl2, Rene' Teich1, Stephanie Brand1, Nicole Blu"mer1, Ali O". Yildirim1, Cecilia C. Patrascan1, Anna Hanuszkiewicz3, Shizuo Akira4, Hermann Wagner2, Otto Holst3, Erika von Mutius5, Petra I. Pfefferle1, Carsten J. Kirschning6, Holger Garn1, and Harald Renz1

1 Department of Clinical Chemistry and Molecular Diagnostics, Philipps-University of Marburg, 35043 Marburg, Germany
2 Institute of Medical Microbiology, Immunology, and Hygiene, Technical University Munich, 81675 Munich, Germany
3 Division of Structural Biochemistry, Research Center Borstel, Leibniz-Center for Medicine and Biosciences, 23845 Borstel, Germany
4 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan
5 University Children's Hospital, Ludwig-Maximilians University Munich, 80337 Munich, Germany
6 Institute of Medical Microbiology, University Duisburg-Essen, 45147 Essen, Germany

CORRESPONDENCE Harald Renz: renzh@med.uni-marburg.de

The pre- and postnatal environment may represent a window of opportunity for allergy and asthma prevention, and the hygiene hypothesis implies that microbial agents may play an important role in this regard. Using the cowshed-derived bacterium Acinetobacter lwoffii F78 together with a mouse model of experimental allergic airway inflammation, this study investigated the hygiene hypothesis, maternal (prenatal) microbial exposure, and the involvement of Toll-like receptor (TLR) signaling in prenatal protection from asthma. Maternal intranasal exposure to A. lwoffii F78 protected against the development of experimental asthma in the progeny. Maternally, A. lwoffii F78 exposure resulted in a transient increase in lung and serum proinflammatory cytokine production and up-regulation of lung TLR messenger RNA. Conversely, suppression of TLRs was observed in placental tissue. To investigate further, the functional relevance of maternal TLR signaling was tested in TLR2/3/4/7/9--/-- knockout mice. The asthma-preventive effect was completely abolished in heterozygous offspring from A. lwoffii F78--treated TLR2/3/4/7/9--/-- homozygous mother mice. Furthermore, the mild local and systemic inflammatory response was also absent in these A. lwoffii F78--exposed mothers. These data establish a direct relationship between maternal bacterial exposures, functional maternal TLR signaling, and asthma protection in the progeny.

M.L. Conrad, R. Ferstl, R. Teich, C.J. Kirschning, H. Garn, and H. Renz contributed equally to this paper.

Abbreviations used: BAL, bronchoalveolar lavage; BMDM, BM-derived macrophage; MCh, β-methacholine; PAS, periodic acid-Schiff; PRR, pattern recognition receptor; TLR, Toll-like receptor.

(c) 2009 Conrad et al.
This article is distributed under the terms of an Attribution--Noncommercial--Share Alike--No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution--Noncommercial--Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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