Role of Intestinal Flora in the Development of Allergy

Marko Kalliomäki, Erika Isolauri


Curr Opin Allergy Clin Immunol. 2003;3(1) 

In This Article

Abstract and Introduction

Purpose of Review: The frequency of allergic diseases is increasing worldwide. Experimental and clinical studies have linked a reduced number of early infections to this trend. The gastrointestinal system, which comprises the largest lymphoid tissue and microbial reservoir of the body, has received more attention during the last few years as a potential determiner in the development of atopic disease.
Recent Findings: Alterations in intestinal microbiota have been detected both in infants suffering from allergic disease and in those later developing the disorder. Delay in the compositional development of Bifidobacterium and Lactobacillus in gut microflora was a general finding in allergic children. In a subsequent study, perinatal administration of lactobacilli halved the later development of atopic eczema during the first 2 years of life. Specific strains of the healthy gut microbiota have been shown to induce the production of IL-10 and transforming growth factor- , which possess an important regulative role in the development of allergic type immune response. Probiotics also strengthen gut defence barrier mechanisms and reduce antigen load in the gut. Pattern recognition receptors in intestinal epithelial and antigen-presenting cells have been demonstrated to mediate a continuing dialogue between host and gut microbiota.
Summary: Despite several promising findings, the exact role of gut normal microbiota in the development of allergy remains to be elucidated. For successful interventions, more data concerning a communication between host and specific microbial species are needed.

Allergy, manifested in atopic eczema, allergic rhinoconjunctivitis and asthma, represents an epidemic of rising importance in both the developed and developing world.[1] Atopic eczema is typically the first manifestation of the disorder followed by the subsequent respiratory allergic diseases.[2] The immunological basis of allergy originates from the overexpression of type 2 T helper cells, secreting IL-4, IL-5 and IL-13, which results in allergic inflammation in affected organs.[3] The hygiene hypothesis of allergy has related a reduced early microbial exposure to the rising frequency of allergic diseases.[4] In this overview we present recent epidemiological and experimental data which have both renewed the bipolar Th1-Th2 concept in the development of allergy and extended the hygiene hypothesis more tightly to the gut microbiota.[5*,6*] The host-microbe crosstalk in the gut as a delicate immunomodulator of the immune system and a potential target for therapeutical interventions is also discussed.


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