Asthma/atopy and staph toxins

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This article says that in 1300 teenagers - a good statistical basis ! - the level of antibodies against staph toxins is correlated to atopy and to the asthma levels, and that this staph-reaction biaises the immunity towards a Th2-state. This adds another layer of suspicion against staph in asthma and atopy. Some of the researchers are those who already demonstrated the likely involvement of staph in polyps (not meaning that staph are the only cause of polyps, but that they likely play one of the star roles in the whole scenario).----------Eur Respir J.

2010 Jan 28. [Epub ahead of print]Th2-associated immunity to bacteria in asthma in teenagers and susceptibility to asthma.Hollams

E, Hales

B, Bachert

C, Huvenne

W, Parsons

F, de

Klerk N, Serralha

M, Holt

B, Ahlstedt

S,

W, Sly

P, Holt

PG.Centre for Child Health Research, The University of Western Australia, Perth, Australia.Bacterial colonisation of the airways is associated with increased risk for childhood asthma. IgE against bacterial antigens has been reported in some asthmatics, suggesting a role for bacterial-specific Type-2 immunity in disease pathogenesis. We aimed to investigate relationships between bacterial-specific IgE amongst teenagers and asthma susceptibility.We measured titres of IgE against Haemophilus influenzae(HI), Streptococcus pneumonia(SP) and Staphylococcus aureus(SA) in 1380 teenagers, and related these to asthma

symptomatology and immunophenotypes.IgE titres against SA-derived enterotoxins were highest amongst atopics and were associated with asthma risk. Surprisingly, IgE titres against HI and SP surface antigens

were higher and not stratified by atopy, and independently associated with decreased asthma risk.The positive association between Type-2 immunity to SA and asthma phenotypes likely reflects IgE-mediated effector cell activation via enterotoxin antigens which are secreted in soluble form. The contrasting benign nature of Type-2 immunity to HI and

SP antigens may reflect their lower availability in soluble forms that can crosslink IgE receptors. We theorise that they may instead be processed by antigen presenting cells and presented to Type-2 memory cells leading to mucosal secretion of IL-4/IL-13, a mechanism widely recognised in other tissues to attenuate Th1-associated bacterial-induced inflammation.