Human seroreactivity to gut microbiota antigens - 06/11/15
Abstract |
Background |
Although immune responses directed against antigens from the intestinal microbiota are observed in certain diseases, the normal human adaptive immune response to intestinal microbiota is poorly defined.
Objective |
Our goal was to assess the adaptive immune response to the intestinal microbiota present in 143 healthy adults and compare this response with the response observed in 52 children and their mothers at risk of having allergic disease.
Methods |
Human serum was collected from adults and children followed from birth to 7 years of age, and the serum IgG response to a panel of intestinal microbiota antigens was assessed by using a novel protein microarray.
Results |
Nearly every subject tested, regardless of health status, had serum IgG that recognized a common set of antigens. Seroreactivity to the panel of antigens was significantly lower in atopic adults. Healthy infants expressed the highest level of IgG seroreactivity to intestinal microbiota antigens. This adaptive response developed between 6 and 12 months of age and peaked around 2 years of age. Low IgG responses to certain clusters of microbiota antigens during infancy were associated with allergy development during childhood.
Conclusions |
There is an observed perturbation of the adaptive response to antigens from the microbiota in allergic subjects. These perturbations are observable even in childhood, suggesting that optimal stimulation of the adaptive immune system by the microbiota might be needed to prevent certain immune-mediated diseases.
Le texte complet de cet article est disponible en PDF.Key words : Adaptive, atopy, allergy, childhood, IgG, microarray, microbiota, bacterial antigens, bacterial antibodies
Abbreviations used : ARC, NCBI
Plan
| Supported by National Institutes of Health grant DK071176; the Swedish Research Council (K2011-56X-21854-01-06); the Swedish Heart-Lung Foundation (20050514); the Ekhaga Foundation (210-53); the Research Council for the South-East Sweden; the Olle Engqvist Foundation; the Swedish Asthma and Allergy Association; the Vårdal Foundation for Health Care Science and Allergy Research, Sweden (B2007 042); and the University Hospital of Linköping, Sweden. |
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| Disclosure of potential conflict of interest: This study was supported by a National Institutes of Health grant (DK071176), the Swedish Research Council (K2011-56X-21854-01-06), the Swedish Heart-Lung Foundation (20050514), the Ekhaga Foundation (210-53), the Research Council for the South-East Sweden, the Olle Engqvist Foundation, the Swedish Asthma and Allergy Association, the Vårdal Foundation for Health Care Science and Allergy Research, Sweden (B2007 042), and the University Hospital of Linköping, Sweden. T. R. Abrahamsson has received consultancy fees from BioGaia, and his institution has received or has grants pending from BioGaia AB. C. N. Bernstein's institution has received funding from the Canadian Institutes of Health Research; has received or has grants pending from AbbVie, Takeda, Shire, Janssen; has received compensation for board membership from AbbVie, Shire, Takeda, Pfizer, Cubist Pharmaceuticals, and Theradiag; and has received payment for delivering lectures from AbbVie and Shire. M. C. Jenmalm has received consultancy fees from BioGaia. C. O. Elson has received consultancy fees from NovoNordisk, Ferring Research Institute, Theravance, ImmusanT, Ironwood Pharmaceuticals, Baxter Healthcare, Lumira Capital, and Bristol Myers Squibb; has received payment for delivering lectures from Janssen; and receives royalties from Prometheus. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 136 - N° 5
P. 1378 - novembre 2015 Retour au numéro
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