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Infants colonized with enterotoxin‐producing staphylococci at 3 months display a decreased frequency of interferon‐γ‐producing CD45RO lymphocytes upon stimulation with staphylococcal enterotoxin A at birth but not at 6 months of age
Author(s) -
Schauer Uwe,
Thurau Anja,
Seitz Miriam,
Nowak Lars,
Petri Holger,
Leinhaas Claudia,
Rieger Christian
Publication year - 1999
Publication title -
pediatric allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.269
H-Index - 89
eISSN - 1399-3038
pISSN - 0905-6157
DOI - 10.1034/j.1399-3038.1999.00035.x
Subject(s) - enterotoxin , cytokine , medicine , immunology , superantigen , colonization , microbiology and biotechnology , biology , immune system , t cell , escherichia coli , gene , biochemistry
The aim of the study was to elucidate the relationship between the cytokine response to staphylococcal enterotoxin A (SEA) at birth and subsequent staphylococcal colonization in the first months of life. In a cohort of 45 newborns, cord blood lymphocytes were stimulated with SEA (10 ng/ml) in vitro , re‐stimulated with PMA (phorbol myristate acetate) and ionomycin at day 3 and assessed for CD45RO expression and cytokine generation by flow cytometry. The infants were classified into three groups according to nasal staphylococcal colonization and enterotoxin generation at 3 months: There were 16 infants with either no colonization or non‐enterotoxin‐producing staphylococci, 16 infants with enterotoxins B, C, D and E, and 13 infants colonized with SEA‐producing staphylococci. At birth, the group without subsequent colonization displayed a significantly higher frequency of CD45RO‐positive interferon‐γ‐producing cells (1.7%; range 0.0–9.3%) in comparison to the SEA‐positive group (0.1%; range 0.0–0.4%) and also to the group positive for other enterotoxins (0.50%; range 0.0–2.5%). Comparable but less pronounced results were found for interleukin‐5 but not for interleukins 2 and 4. At 6 months, no differences in cytokine generation were detected between the three groups. The results provide evidence that a non‐specific immunologic immaturity at birth is a risk factor for early bacterial colonization. Furthermore, it is remarkable that this immaturity is similar to that seen in infants destined to be atopic with respect to disequilibrium of interferon‐γ to interleukin‐4 generation. Thus the link between early staphylococcal colonization and subsequent atopy requires further investigation.