High circulating immunoglobulin A levels in infants are associated with intestinal toxigenic Staphylococcus aureus and a lower frequency of eczema.
BACKGROUND
Intestinal bacteria trigger IgA production and delayed maturation of mucosal IgA response is linked to allergy development.


OBJECTIVE
Our aim was to investigate if plasma levels of IgA or APRIL (a proliferation inducing ligand), an important factor for IgA class switch recombination, in infancy correlates with intestinal colonization by any specific bacteria or yeast. We also examined if plasma IgA or APRIL levels are related to sensitization and the development of eczema.


METHODS
IgA was quantified in plasma obtained from infants at birth and at 4 and 18 months of age and APRIL was measured at 4 months of age. Colonization by major bacterial groups and yeast was followed in the first 8 weeks of life by quantitative culture of stool samples. A clinical evaluation regarding the presence of allergen-specific IgE or eczema and eosinophil counts in blood was performed at 18 months of age.


RESULTS
In multiple linear regression analysis, only colonization by Staphylococcus aureus strains producing toxins with superantigen function (SEA-D or TSST-1) made an independent contribution to plasma IgA levels at 4 months of age. Further, increased levels of APRIL in plasma at 4 months were negatively associated with sensitization while IgA plasma levels were inversely correlated to eczema development and blood eosinophil counts at 18 months of age.


CONCLUSIONS
Early intestinal colonization by toxigenic S. aureus strains seems to promote systemic IgA responses. Furthermore, high levels of APRIL and IgA in the circulation at 4 months of age seem to correlate negatively with allergy development.
Lundell
A-C
AC
Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden. annacarin.lundell@rheuma.gu.se
Hesselmar
B
B
Nordström
I
I
Saalman
R
R
Karlsson
H
H
Lindberg
E
E
Aberg
N
N
Adlerberth
I
I
Wold
A E
AE
Rudin
A
A
D000485:Allergens / Q000276:immunology; D004485:Eczema / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D004768:Enterotoxins / Q000276:immunology*; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D004926:Escherichia coli / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D007070:Immunoglobulin A / Q000097:blood*; D007073:Immunoglobulin E / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007223:Infant; D007422:Intestines / Q000276:immunology* / Q000382:microbiology; D016014:Linear Models; D013211:Staphylococcus aureus / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000097:blood; D053300:Tumor Necrosis Factor Ligand Superfamily Member 13 / Q000097:blood*
D000485:Allergens; D004768:Enterotoxins; D007070:Immunoglobulin A; D007075:Immunoglobulin M; C114631:TNFSF13 protein, human; D016212:Transforming Growth Factor beta; D053300:Tumor Necrosis Factor Ligand Superfamily Member 13; D007073:Immunoglobulin E