Literature DB >> 23751771

Early life exposure to antibiotics and the risk of childhood allergic diseases: an update from the perspective of the hygiene hypothesis.

Chang-Hung Kuo1, Hsuan-Fu Kuo, Ching-Hua Huang, San-Nan Yang, Min-Sheng Lee, Chih-Hsing Hung.   

Abstract

The prevalence of allergic diseases has been growing rapidly in industrial countries during recent decades. It is postulated that growing up with less microbial exposure may render the immune system susceptible to a T helper type 2 (Th2)-predominant allergic response-also known as the hygiene hypothesis. This review delineates recent epidemiological and experimental evidence for the hygiene hypothesis, and integrates this hypothesis into the association between early life exposure to antibiotics and the development of allergic diseases and asthma. Several retrospective or prospective epidemiological studies reveal that early exposure to antibiotics may be positively associated with the development of allergic diseases and asthma. However, the conclusion is inconsistent. Experimental studies show that antibiotics may induce the Th2-skewed response by suppressing the T helper type 1 (Th1) response through inhibition of Th1 cytokines and disruption of the natural course of infection, or by disturbing the microflora of the gastrointestinal (GI) tract and therefore jeopardizing the establishment of oral tolerance and regulatory T cell immune responses. The hygiene hypothesis may not be the only explanation for the rapid increase in the prevalence of allergic diseases and asthma. Further epidemiological and experimental studies addressing the issue of the impact of environmental factors on the development of allergic diseases and the underlying mechanisms may unveil novel strategies for the prevention and treatment of allergic diseases in the future.
Copyright © 2013. Published by Elsevier B.V.

Entities:  

Keywords:  Allergic disease; Antibiotics; Asthma; Dendritic cells; Hygiene hypothesis

Mesh:

Substances:

Year:  2013        PMID: 23751771     DOI: 10.1016/j.jmii.2013.04.005

Source DB:  PubMed          Journal:  J Microbiol Immunol Infect        ISSN: 1684-1182            Impact factor:   4.399


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