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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Sep 26, 2013

 

In children with asthma, diesel exposure was associated with more frequent
asthma symptoms and increased IL-17A blood levels.






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Asthma severity in children exposed to diesel exhaust

A new study shows exposure to diesel exhaust particles from traffic pollution leads to increased asthma severity in children. This is due to increased blood levels of IL-17A, a protein associated with several chronic inflammatory diseases, in children with high diesel exposure.

The research, conducted in mice and in humans, showed that neutralizing IL-17A prevented airway inflammation.


"Neutralization of IL-17A may be a useful potential therapeutic strategy to counteract the asthma-promoting effects of traffic-related air pollution, especially in highly exposed, severe allergic asthmatics."

Gurjit Khurana Hershey, MD, PhD, director of asthma research, Cincinnati Children's, senior author of the study


Dr. Hershey and her colleagues studied 235 children and teens with asthma. The researchers plotted each person's primary address and estimated their diesel exposure attributable to traffic based on where they lived. The researchers also studied mice exposed to diesel particles and dust mites, a common household allergen.

The study by researchers at Cincinnati Children's Hospital Medical Center is published online in the Journal of Allergy and Clinical Immunology.

In children with asthma, diesel exposure was associated with more frequent asthma symptoms and increased IL-17A blood levels.

Similarly, exposure to both diesel and dust mites resulted in more severe asthma in mice compared to dust mite exposure alone. When IL-17A was neutralized in mice, it alleviated airway inflammation induced by diesel exposure.


"Blocking IL-17A may be a useful strategy to counteract the effects of traffic-related air pollution, especially in highly exposed allergic asthmatic children," says Dr. Hershey.

Background
IL-17A has been implicated in severe forms of asthma. However, the factors that promote IL-17A production during the pathogenesis of severe asthma remain undefined. Diesel exhaust particles (DEPs) are a major component of traffic-related air pollution and are implicated in asthma pathogenesis and exacerbation.

Objective
We sought to determine the mechanism by which DEP exposure affects asthma severity using human and mouse studies.

Methods
BALB/c mice were challenged with DEPs with or without house dust mite (HDM) extract. Airway inflammation and function, bronchoalveolar lavage fluid cytokine levels, and flow cytometry of lung T cells were assessed. The effect of DEP exposure on the frequency of asthma symptoms and serum cytokine levels was determined in children with allergic asthma.

Results
In mice exposure to DEPs alone did not induce asthma. DEP and HDM coexposure markedly enhanced airway hyperresponsiveness compared with HDM exposure alone and generated a mixed TH2 and TH17 response, including IL-13+IL-17A+ double-producing T cells. IL-17A neutralization prevented DEP-induced exacerbation of airway hyperresponsiveness. Among 235 high DEP–exposed children with allergic asthma, 32.2% had more frequent asthma symptoms over a 12-month period compared with only 14.2% in the low DEP–exposed group (P = .002). Additionally, high DEP–exposed children with allergic asthma had nearly 6 times higher serum IL-17A levels compared with low DEP–exposed children.

Conclusions
Expansion of TH17 cells contributes to DEP-mediated exacerbation of allergic asthma. Neutralization of IL-17A might be a useful potential therapeutic strategy to counteract the asthma-promoting effects of traffic-related air pollution, especially in highly exposed patients with severe allergic asthma.

The study was supported by grants from the NIEHS (R21016830; T32 ES010957) and the NHLBI (R01HL097135).

About Cincinnati Children's
Cincinnati Children's Hospital Medical Center ranks third in the nation among all Honor Roll hospitals in U.S.News and World Report's 2013 Best Children's Hospitals ranking. It is ranked #1 for cancer and in the top 10 for nine of 10 pediatric specialties. Cincinnati Children's, a non-profit organization, is one of the top three recipients of pediatric research grants from the National Institutes of Health, and a research and teaching affiliate of the University of Cincinnati College of Medicine. The medical center is internationally recognized for improving child health and transforming delivery of care through fully integrated, globally recognized research, education and innovation. Additional information can be found at http://www.cincinnatichildrens.org. Connect on the Cincinnati Children's blog, via Facebook and on Twitter.

Original press releas: http://www.cincinnatichildrens.org/news/release/2013/protein-explains-asthma-severity-09-23-2013/