Atopy, asthma, and the mycobacteria

• Published in: Thorax 2000-06, Vol.55 (6), p.443-445
• Main Author: HOPKIN, J M
• Format: Article
• Language: English
• Subjects: Age; Allergies; Antibiotics; Antigens; Asthma; Asthma - epidemiology; Asthma - immunology; BCG Vaccine - immunology; Cytokines; Epidemiology; Humans; Hypersensitivity, Immediate - epidemiology; Hypersensitivity, Immediate - immunology; Immunoglobulin E - immunology; Interleukins - immunology; Mycobacteriaceae - immunology; Studies; T-Lymphocytes, Helper-Inducer - immunology; Tuberculin - immunology; Tuberculosis; Tumor necrosis factor-TNF
• ISSN: 0040-6376; 1468-3296
• DOI: 10.1136/thorax.55.6.443

The acknowledged rapid rise in the atopic disorders in developed communities points to important environmental determinants of overactive Th2 immunity and to the likelihood that these are related to socioeconomic development. 19 Dietary change and greater pollution by indoor allergens or noxious agents more generally have been considered candidate mechanisms, but change in the patterns of microbial exposure is a potential mechanism which crucially relates to immune development. 6 20 One temporal association with the increase in atopy in developed communities has been a significant fall in exposure to many microbes including the helminths already referred to and Mycobacterium tuberculosis. [...]there is a link between increased atopy and small sibships in which there may be less sharing of various microbial exposures than in larger sibships. 21 Some data indicate that fetal and neonatal allergen specific responses are naturally Th2 in the first instance, and that these need conversion towards a Th1 type to produce the non-atopic state of clinical tolerance to allergens; Th1 promoting microbial exposures are the natural candidates for delivering such tolerance. 22 Experimental animal data suggest that commensal organisms in the gut are essential for the tolerance to allergen that usually results from oral exposure. 23-25 It is therefore interesting that two epidemiological studies have linked early life treatment with antibiotics, potent reducers of gut commensals, with subsequent atopic disorder. 26 27 Other epidemiological studies have related less atopy with early life exposure to measles, mycobacteria, and a range of orofecal pathogens. 28-30 A putative link between exposure to mycobacteria and less atopy was illustrated in a study of Japanese children 30 in whom strongly positive tuberculin responses in early life were associated significantly with less asthma, rhinoconjunctivitis, and eczema in later childhood.