All you need to know about the house dust mite
For the Curious

The foetus, dust mites and a naughty asthma gene

Upon birth, almost all newborn's immune systems react to specific environmental factors transferred from mother to child during pregnancy. It is a form of maternal education into her 'world' and demonstrates that the child's immune system may be immature, but not inexperienced. In this article it is the genetically vulnerable foetus, continually exposed to maternal dust mite allergen Der p1 that is the focus of attention. The development of early asthma is the concern.
Early in life a developing foetus swallows amniotic fluid to test and absorb elements from the mother's diet and the air she breathes. Not all the encounters are helpful. For example exposure to nicotine from tobacco smoke, or, for those genetically predisposed to allergy, contact to proteins such as from birch tree pollen, timothy grass, a whey protein from cow or sheep's milk can lead to problems. Exposure to these and more potential allergens may set the foetus on a pathway towards allergy as unique genes switch on, then off again, to set patterns for life. Nicotine from tobacco is especially harmful as it can amplify immune reactions in the foetal environment.

The vulnerable foetus Genes and the environment present two distinct pathways towards immune tolerance or an 'early warning' reaction. In very early life scientists report that both genes and the environment can impact simultaneously, thus setting patterns for future life. Following birth, the immune testing of the environment continues and accelerates.

House dust mites Over 12 years ago doctors, investigating pregnant women who were continually exposed to dust mite allergens during pregnancy, reported the presence of the major mite allergen (Der p1) in foetal fluid at 16 to 17 weeks of gestation. The women had all undergone amniocentesis at that time and chose to continue their pregnancy to full term. At 22 weeks foetal immune response to Der p1 was detected. Continuing the study to full term, the doctors noted that, in some cases, Der p1 was found to be at higher levels in blood and urine of the newborn than in that of the mother. They were surprised to note in one case Der p1 was significantly (110%) higher in the newborn than in the mother's blood, whereas, in the amniotic fluid at 16 weeks gestation Der p1 can be barely detectable. This finding led the research team to speculate that foetal exposure to Der p1 can be accumulative. It is of interest to note that at full term the baby is swallowing 700 mL of amniotic fluid per day and is able to absorb 10% of the macromolecules within the fluid.

Der p1 is an active digestive enzyme considered small enough to cross the placenta into the amniotic fluid. The enzyme is known to 'cleave' important elements that bind cells together causing cell death and a breach in lung defences. What influence Der p1 has on a developing (genetically vulnerable) foetus has yet to be fully described, however performance of the gene ADAM33, so called 'asthma gene', can present a clue.

ADAM33 ??? the asthma gene Clusters of genes are associated with allergy and lung disease, but one of the most well studied and interesting is ADAM33. This gene (discovered in 2002) normally sits quietly as a connective tissue component tethered to cells such as in the smooth muscle located just underneath lung cells. However, if damaged by 'cleaving' it can turn into an active enzyme creating a tunnelling system of micro-blood vessels and thickening of the smooth muscle. The reason for the increase in blood vessels is to help deliver powerful immune defences that will swing into action upon invasion of pathogens, be they viral, bacterial or recognised allergens. Der p1 from dust mites can be considered in this grouping. Scientists suspect ADAM33 may be 'cleaved' before or shortly following birth thus creating a protective immune system primed to react to environmental insults later in life. In this scenario ADAM33 is not alone. There are other candidate genes such as Matrix metalloproteinase 12, but that's another story.

ADAM33 is a life long resident in lung tissue. Repeated morphing of the 'asthma gene' in its microenvironment may result in altered barrier function and disordered lung tissue, (known as remodelling) a syndrome of many respiratory diseases, in young and old alike.

Research findings Doctors report that a loss of lung-power can be detected as early as 4 weeks of age. However, recently a clinical study demonstrated that children, at high-risk from asthma, can be protected from the disease through environmental and dietary manipulation. The children were followed from infancy through to eighteen years of age. The report on the study states, 'early intervention within the first few months of life is likely to be crucial in preventing the remodelling of airways which is the hallmark of asthma'.


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'Developmental origins of asthma and related allergic disorders'. In: Developmental origins of health and disease. Warner JO, Editors, Gluckman P, Hanson M., Cambridge University Press 2006; p 349-369,

'Using genetics to predict the natural history of asthma? Mechanisms of allergic disease.', Holloway JW, Arshad SH, Holgate ST, J Allergy Clin Immunol 2010; 126:200-2009

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