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Neonatal exposure to staphylococcal superantigen improves induction of oral tolerance in a mouse model of airway allergy.

Artikel i vetenskaplig tidskrift
Författare Anna Lönnqvist
Sofia M Östman
Nina Almqvist
Susanne Hultkrantz
Esbjörn Telemo
Agnes E Wold
Carola Rask
Publicerad i European journal of immunology
Volym 39
Nummer/häfte 2
Sidor 447-56
ISSN 1521-4141
Publiceringsår 2009
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 447-56
Språk en
Länkar dx.doi.org/10.1002/eji.200838418
Ämnesord Animals, Animals, Newborn, immunology, Disease Models, Animal, Enterotoxins, immunology, metabolism, Immune Tolerance, immunology, Immunity, Mucosal, Lung, immunology, metabolism, Mice, Mice, Inbred BALB C, Mouth Mucosa, immunology, microbiology, Ovalbumin, immunology, Respiratory Hypersensitivity, immunology, microbiology, Staphylococcus, immunology, Superantigens, immunology, metabolism, T-Lymphocytes, Regulatory, immunology, metabolism
Ämneskategorier Bakteriologi, Medicinsk mikrobiologi, Allergologi, Immunbiologi

Sammanfattning

The hygiene hypothesis suggests that lack of microbial stimulation in early infancy may lead to allergy, but it has been difficult to identify particular protective microbial exposures. We have observed that infants colonised in the first week(s) of life with Staphylococcus aureus have lower risk of developing food allergy. As many S. aureus strains produce superantigens with T-cell stimulating properties, we here investigate whether neonatal mucosal exposure to superantigen could influence the capacity to develop oral tolerance and reduce sensitisation and allergy. BALB/c mice were exposed to staphylococcal enterotoxin A (SEA) as neonates and fed with OVA as adults, prior to sensitisation and i.n. OVA challenge. Our results show that SEA pre-treated mice are more efficiently tolerised by OVA feeding, as shown by lower lung-cell infiltration and antigen-specific IgE response in the SEA pre-treated mice, compared with sham-treated mice. This was not due to deletion or anergy of lymphocytes by SEA treatment, because the SEA pre-treated mice that were fed with PBS showed similar inflammatory response as the sham-treated PBS-fed mice. Our results suggest that strong T-cell activation in infancy conditions the mucosal immune system and promotes development of oral tolerance.

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