Category Archives: Allergy

Believe me, it ‘s not hygiene

I have written earlier about the hygiene hypothesis and my doubts that more or less “hygiene” influences the development of allergy (blog | paper). As we are further swamped with regular statements like Continue reading Believe me, it ‘s not hygiene

Allergy immigrant studies

I am starting here a thread of immigrant studies – seems that there are now ~100 available in the medical literature. This could be the nice question for a meta-analysis: Does the move to a high prevalence country lead to more allergy, e.g. do your peers matter? Continue reading Allergy immigrant studies

The third largest problem in epidemiology

-moblog- In my view, epidemiology is not very flexible to adjust to new methods and new techniques. Following some discussion that I had today with STW about eQTLs (quantitative traits derived by RNA microarrays or metabolome profiles) and JMA about system biology, it is likely that we are facing huge changes. Phenotypes may no more called intermediary and we may soon forget old controversies of disease definition. We will instead use new system-terms like NonImm076Trig31Ste0098 or TLR9-096321-Auto5337. Yea, yea.

Lactase variants in Europe – any connection to allergy?

I will present this poster next Monday in San Francisco at the Annual Conference of the American Thoracic Society. Continue reading Lactase variants in Europe – any connection to allergy?

Why we didn´t find the asthma gene

The J Int Med has a symposium series about the “origins of the developmental origins theory” scienceblog:doi:10.1111/j.1365-2796.2007.01809.x or the so called “Barker hypothesis” Continue reading Why we didn´t find the asthma gene

Osteopontin bridging air pollution and immunology of allergic inflammation

Ostepopontin (OPN) is a remarkable substance. The many aliases already point towards a multitude of biological functions: SPP1=secreted phosphoprotein 1, BSPI 1=bone sialoprotein-1, CIT, ETA-1, GC110940, nephropontin, osteoprotegerin, uropontin, bone sialoprotein I, early T-lymphocyte activation among others. Continue reading Osteopontin bridging air pollution and immunology of allergic inflammation

Asthma no more a disease but a symptom

There already some rumors – an earlier Lancet perspective named asthma a symptom “like fever” (scienceblog:doi:10.1016/S0140-6736(06)69271-4:). A new editorial now compares it to “diarrhea” Continue reading Asthma no more a disease but a symptom

Ca2+ and IgE

Two decades ago, 10% calcium gluconate had been recommended for the treatment of anaphylaxis (couldn’t find any explanation for that but renember one of my teachers saying it will stabilize the membranes). There is now an update in scienceblog:doi:10.1038/ni1441: Continue reading Ca2+ and IgE

Hubs and superhubs in asthma: low activity

Here comes the reference to a first molecular system biology paper on asthma – something on my to-do list for 3 years. The authors constructed a biological interaction network using a database of curated molecular interactions. Continue reading Hubs and superhubs in asthma: low activity

Does my partner cause my allergy?

A funny question answered in Allergy.

After adjustment for age, sex, parental predisposition and social status, the risk of hay fever was more than double in subjects who lived together with a partner having the same disease (odds ratio 2.4 […]). If subjects lived together with an affected partner, the risk of developing the disease increased with the time the partners lived together (1-11 years, OR 1; 12-23 years, OR 1.8; 24-35 years, OR 7.4; 36-54 years, OR 13.7).

Whatever that means – improved recall, shared doctor, non random mating, shared food, transmissible agent in descending order – it has been noticed already 40 years ago by Montgomery Smith and Lloyd Knowler in the Am Rev Resp Dis 1965; 92:16:

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Filaggrin makes its way

A 3rd paper in nature genetics details the filaggrin gene structure: exon 3 has 10 repeats (as well as three variants FLG8+, FLG10+, FLF8+10+) and 15 SNPs – one of the few success stories in allergy research. In the discussion section, they ask the rhetoric question:

This study raises questions of interest to the complex trait field. Would SNP tagging of these multiple, relatively rare alleles, with frequencies no greater than 0.013, have readily identified this particularly strong susceptibility gene?

Nay, nay.

When are we being sensitized?

JACI has a paper in press that addresses this important question. The background is that allergen induced T-cell reactivitiy has been shown in cord blood – a strong argument that sensitization occurs transplacentally. Genotyping of these cells confirmed their fetal origin. It is unclear, however, if this is only a transient (normal?) reaction – and mothers want to know if they need to avoid for example peanuts during pregnancy. Rowe et al. now arrive at a clear conclusion Continue reading When are we being sensitized?