African-American women who experience racism at increased risk for adult-onset asthma

Main Category: Respiratory / Asthma
Also Included In: Women's Health / Gynecology;  Psychology / Psychiatry
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
African-American women who experience racism at increased risk for adult-onset asthma

According to a new study from the Slone Epidemiology Center (SEC) at Boston University, African-American women who reported more frequent experiences of racism had a greater likelihood of adult-onset asthma compared to women who reported less frequent experiences.

The study, which currently appears on-line in the journal Chest, was led by Patricia Coogan, DSc, senior epidemiologist at SEC and research professor of epidemiology at Boston University School of Public Health.

This study followed 38,142 African-American women, all of whom are participants in the Black Women's Health Study (BWHS), between 1997 and 2011. They completed health questionnaires every two years. In 1997 and 2009 they provided information on their experiences of "everyday" racism, like poor service in stores or restaurants, and "lifetime" racism, which was discrimination encountered on the job, in housing and by police.

The results indicate that as experiences of everyday and lifetime racism increased, the incidence of adult-onset asthma also rose, up to a 45 percent increase in women in the highest compared to the lowest category of the racism measures. Furthermore, the incidence of asthma was increased even more in women who were in the highest category of everyday racism in both 1997 and 2009, and who may have had more consistent experiences of racism over time.

"This is the first prospective study to show an association between experiences of racism and adult-onset asthma," said Coogan. "Racism is a significant stressor in the lives of African American women, and our results contribute to a growing body of evidence indicating that experiences of racism can have adverse effects on health." The hypothesized mechanism linking experiences of racism to asthma incidence is stress and its physiological consequences, particularly effects on the immune system and the airways. "Given the high prevalence of both asthma and of experiences of racism in African Americans, the association is of public health importance," she added.

BWHS is the largest follow-up study of the health of African American women in the United States. Led by researchers at the Slone Epidemiology Center, the BWHS has followed 59,000 African-American women through biennial questionnaires since 1995 and has led to a better understanding of numerous health conditions that disproportionately affect African-American women.

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Experiences of Racism and the Incidence of Adult-Onset Asthma in the Black Women’s Health Study, Chest. 2013. doi:10.1378/chest.13-0665

Boston University Medical Center Funding for this study was provided by the National Institutes of Health's National Heart, Lung, and Blood Institute (grant award #HL107314) and the National Cancer Institute (grant award #CA058420).

Boston University Medical Center

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The relationship between proteinases and asthma

Main Category: Respiratory / Asthma
Article Date: 18 Aug 2013 - 0:00 PDT Current ratings for:
The relationship between proteinases and asthma

Dr. David Corry compares the allergic response to a computer.

"The core of a computer is its CPU (central processing unit) or chip. We are looking for the chip that drives allergic disease," said the professor of medicine, chief of the section of immunology, allergy and rheumatology in Baylor College of Medicine's department of medicine and director of the Biology of Inflammation Center at BCM. In a report that appears online in the journal Science, he and colleagues at BCM describe an important component of that chip - a molecule called toll-like receptor 4 that plays a key role in prompting the innate or immediate response that drives allergic disease and asthma.

Asthma is part of a battle that takes place as the immune system marshals its forces to fight off an invading organism-or what mimics such invaders. The ensuing fight takes a significant toll on the human airway and lungs, often generating a violent and itself potentially deadly reaction - asthma.

In 2002, Corry and his colleagues found that proteinases, enzymes that chop up other proteins, are important in initiating the adaptive immune response that prompts generation of the critical T-cells and B-cells that populate the adaptive immune system. The adaptive immune system specifically targets allergens, and Corry knew that the more immediate innate immune system also played an important role in asthma and allergy.

"If you take many proteinases and give them to mice, they will induce an allergic disease that resembles asthma," he said.

With that key finding in the adaptive immune system, the researchers turned their attention to the puzzle presented by the innate immune system.

"What is the relationship between proteinases and asthma?" he said. Other work in the field pointed to another immune molecule called toll-like receptor 4 that was believed to play a role in activating T-helper type 2 (Th2) cells.

Instead, he and his colleagues found that the proteinases carve up a protein known as fibrinogen, leaving behind fragments that signal through the crucial toll-like receptor 4 to activate the cells of the innate immune system - the macrophages of the airway and airway epithelia.

"Toll-like receptor 4 is not required for the Th2 response itself," said Corry. "But, the Th2 response is proteinase dependent."

"When the macrophages are activated by fibrinogen cleavage products in culture, you get beautiful activation," said Corry.

In the airway, the same fibrinogen fragments that are part of the blood clotting process can cause clotting that is a barrier to breathing, said Corry.

In his studies, he used proteinase-producing fungi as the environmental trigger for asthma. Laboratory mice that lacked toll-like receptor 4 did not mount a robust allergic airway disease when challenged by proteinase, viable fungi or other triggers but did have a normal Th2 immunity.

"Why do our bodies do this?" said Corry. The answer is both simple and complicated. The system developed to allow organisms to survive infection with deadly organisms such as fungi. How it achieves that is complicated. In this "survival mode," the immune system generates symptoms that can themselves create disease.

Against the insidious onslaught of organisms such as fungi, which can kill if left unchecked, asthma may be a better alternative, said Corry.

"If you don't fight fungi off, they will get you," he said.

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Funding for this work came from the U.S. National Institutes of Health (Grants HL75243, AI057696 and AI070973 and CA125123) and the C.N. and Mary V. Papadopoulos Charitable Fund from the Biology of Inflammation Center.

Corry holds the Cullen Trust for Health Care Endowed Chair in Immunology.

Cleavage of Fibrinogen by Proteinases Elicits Allergic Responses Through Toll-Like Receptor 4

Others who took part in this research include Valentine Ongeri Millien, Wen Lu, Joanne Shaw, Xiaoyi Yuan, Garbo Mak, M.D., Luz Roberts, Li-Zhen Song J. Morgan Knight, Chad J. Creighton, Amber Luong, and Farrah Kheradmand, all of BCM. Kheradmand and Corry are also with the Michael E. DeBakey Veterans Affairs Medical Center in Houston; Shaw and Creighton are also with the Dan L. Duncan Cancer Center at BCM.

Science 16 August 2013: Vol. 341 no. 6147 pp. 792-796; DOI: 10.1126/science.1240342

Baylor College of Medicine

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Small protein plays big role in asthma severity

Main Category: Respiratory / Asthma
Also Included In: Immune System / Vaccines;  Ear, Nose and Throat
Article Date: 05 Aug 2013 - 1:00 PDT Current ratings for:
Small protein plays big role in asthma severity

A new culprit has been identified that likely plays a big role in the severity of asthma - a small protein chemokine called CCL26. These findings were published in the Journal of Leukocyte Biology and represent the first demonstration that CCL26 is a potent regulator of the migration of asthmatic eosinophils, commonly observed in asthmatic airways. Results from this discovery may lead to new drug targets for the treatment of asthma.

"We hope that these studies will help to develop a new treatment that would specifically abrogate bronchial inflammation and provide a specific, efficacious and well-tolerated alternative to the current therapy," said Michel Laviolette, M.D., a researcher involved in the work from the Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, Faculté de Médecine, Université Laval, Québec, Canada.

Specifically, data from the report suggest that the chemokine CCL26 plays a crucial role in asthma pathogenesis and its severity by supporting the recruitment of eosinophils early in the development of the disease, and possibly later in severe asthma associated with persisting lung eosinophilia. To make this discovery, scientists used blood from healthy and asthmatic subjects to isolate eosinophils and measure their migration response to CCL26 in vitro. Researchers also assessed their response to other chemokines, CCL11 and CCL24, and showed that only CCL26 induced an amplified eosinophil migration of asthmatic eosinophils compared to healthy cells. Interestingly, this additional migration occurred after a 6-hour incubation and, in contrast to the migration induced by the other chemokines, was not eradicated by blocking the chemokine receptor CCR3 shared by these three chemokines.

"The control of eosinophils is central to asthmatic diseases and the underlying mechanisms are prime targets for treatments for the debilitating and sometimes life-threatening symptoms of asthma and allergy," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "This report shows that CCL26 could be a novel drug target to regulate eosinophils in these diseases."

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The Journal of Leukocyte Biology publishes peer-reviewed manuscripts on original investigations focusing on the cellular and molecular biology of leukocytes and on the origins, the developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes and other cells involved in host defense and inflammation. The Journal of Leukocyte Biology is published by the Society for Leukocyte Biology.

Details: Véronique Provost, Marie-Chantal Larose, Anick Langlois, Marek Rola-Pleszczynski, Nicolas Flamand, and Michel Laviolette. CCL26/eotaxin-3 is more effective to induce the migration of eosinophils of asthmatics than CCL11/eotaxin-1 and CCL24/eotaxin-2. J Leukoc Biol August 2013 94:213-222; doi:10.1189/jlb.0212074;

Federation of American Societies for Experimental Biology

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Summer holiday time-bomb facing children with asthma

Main Category: Respiratory / Asthma
Also Included In: Pediatrics / Children's Health
Article Date: 31 Jul 2013 - 2:00 PDT Current ratings for:
Summer holiday time-bomb facing children with asthma

Parents are being warned of an 'asthma attack time-bomb' potentially facing the 1.1 million children with asthma in the UK when they go back to school after the summer holidays.

Leading charity Asthma UK has today released alarming new data showing a dramatic surge in children's hospital admissions that coincides with their return to school.

In England, more children are rushed to hospital with an asthma attack in mid-September than any other week during the year. Over 4.6 times as many children in England were hospitalised because of their asthma in the third week of September 2011, compared with just six weeks previously when hospital admissions were at their lowest.[1]

The September spike in children's asthma hospital admissions occurs year after year in the UK and in many other countries, usually two to three weeks into the autumn term. Children aged six to seven years old are the most seriously affected.[2]

Asthma UK is tackling this worrying trend by launching a campaign targeting parents. The charity believes parents can help prevent back-to-school asthma attacks by making sure children carry on taking their preventer inhalers twice daily during the summer holidays. Studies suggest that children who have been forgetting to take their medicines over the break will be at a higher risk of having a serious asthma attack when they are exposed to common classroom asthma triggers in September, such as colds, flu and stress.[3]

Dr Samantha Walker, Deputy Chief Executive of Asthma UK, explains: "Normal routines can go out of the window during the summer break, which can effectively create a time-bomb for children with asthma. Those who forget to take their preventer inhalers over the summer will be less in control of their symptoms and therefore more vulnerable to asthma attacks come term-time."

On average, two children in every classroom have asthma, making it the most common long-term condition for children in the UK. More than 25,000 children were hospitalised because of their asthma in 2011-12 [4], and eighteen children under 14 died as a result of an asthma attack in 2011.[5] Children who have allergies on top of their asthma are thought to be particularly at risk.

According to Kate Jones, her son Jack's asthma always tends to flare up in the last week of September, and the 15-year-old from the Wirral is usually hospitalised as a result. She says: "Jack's been having attacks in September for as long as I can remember. He often gets them a few weeks after returning to school following the Easter holidays too.

"I can see how parents might become a bit lax with their child's medication over the summer. It's such a busy time, whether you're going on holiday or just trying to arrange for family members to look after them while you're at work. And that's another issue; often your relatives or friends are not as aware of what medication your child should be taking and when."

Asthma UK estimates that three quarters of asthma hospital admissions could be avoided with the right care and management. The charity is urging parents whose children have asthma to order a free 'My Asthma' pack, a child-friendly resource which helps under 12s develop a fun routine to manage their asthma over the summer, and as a result, reduce their risk of an attack in September.

Find out more about the 'Teach Asthma a Lesson Next Term!' campaign. Visit www.asthma.org.uk/backtoschool to order a My Asthma pack for your child.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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[1] Data source: Hospital Episode Statistics (HES), Health and Social Care Information Centre . Data acquired July 2013. In 2011-12, 582 children were hospitalised for their asthma in week 26 (w/c 19th September) compared with 125 children in week 20 (w/c 8th August).

[2] Sears MR, Johnston NW. Understanding the September asthma epidemic. McMaster University, Hamilton, Ontario, Canada. Journal of Allergy and Clinical Immunology, 10/2007; 120(3): 526-9

[3] Johnston NW, Johnston SL, Duncan JM, Greene JM, Kebadze T, Keith PK, Roy M, Waserman S, Sears MR. The September epidemic of asthma exacerbations in children: a search for etiology. J Allergy Clin Immunol. 2005 Jan;115(1):132-8.

[4] Hospital Episode Statistics, Department of Health; Scottish Morbidity Record, Information Services Division, NHS Scotland; Health Services Wales; Hospital Inpatients System, Department of Health, Social Services & Public Safety Northern Ireland

[5] Office for National Statistics, General Register Office for Scotland, Northern Ireland Statistics & Research Agency

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Enzyme in airway lining cells could hold key for asthma sufferers

Main Category: Respiratory / Asthma
Article Date: 27 Jul 2013 - 0:00 PDT Current ratings for:
Enzyme in airway lining cells could hold key for asthma sufferers

An enzyme known for its role in heart disease may well be a promising target to treat asthma. Researchers from the University of Iowa have found that the enzyme, called CaMKII, is linked to the harmful effects of oxidation in the respiratory tract, triggering asthmatic symptoms. The finding could lead to the development of a drug that would target the CaMKII enzyme, the researchers say.

Asthma affects billions of people worldwide. In the United States, 8.5 percent of the population has asthma, which causes 3,000 deaths and more than $56 billion annually in medical and lost work costs, according to the federal Centers for Disease Control and Prevention. Despite its toll on health and productivity, treatment options remain confined to steroids, which have harmful, even life-threatening, side effects for those with severe cases.

Current treatments don't work well, noted Mark Anderson, professor and chair in internal medicine at the UI and a co-corresponding author on the paper, published in the journal Science Translational Medicine.

"It's a kind of an epidemic without a clear, therapeutic option," Anderson says. "The take-home message is that inhibiting CaMKII appears to be an effective anti-oxidant strategy for treating allergic asthma."

Anderson and co-corresponding author Isabella Grumbach knew from previous work that the CaMKII enzyme played a role in the oxidation of heart muscle cells, which can lead to heart disease and heart attacks. The scientists surmised the same enzyme may affect oxidation in the respiratory system as well.

The team first tested the enzyme in airway muscle cells, but to little effect. They then tried to block the enzyme in the airway lining (epithelial) cells. They noticed that mice with the blocked enzyme had less oxidized CaMKII, no airway muscle constriction and no asthma symptoms. Similarly, mice without the blocked enzyme showed high "oxidative stress," meaning lots of oxidized enzymes in the epithelial cells, a constricted airway and asthma symptoms.

"[The study] suggests that these airway lining cells are really important for asthma, and they're important because of the oxidative properties of CaMKII," says Anderson, whose primary appointment is in the Carver College of Medicine. "This is completely new and could meet a hunger for new asthma treatments. Here may be a new pathway to treat asthma."

"Ten years ago, not much was known about what CaMKII does outside of nerve cells and muscle cells in the heart," says Grumbach, associate professor in internal medicine at the UI. "My lab has worked on investigating its function mainly in blood vessels with the long-term goal to use blockers of CaMKII to treat common diseases. We are constantly finding that CaMKII is interesting and important."

The researchers also took tissue samples from the airways of patients with asthma. True to their hypothesis, they found more oxidized enzymes in those patients than in healthy individuals. Taking a step further, the team found that mild asthma patients who inhaled an allergen had a spike in oxidized CaMKII in the epithelial cells just a day later.

"We have this very compelling association," Anderson says, adding that more studies in patients are needed to validate the approach.

The researchers also plan to investigate inhaled drugs that could block the oxidation of theCaMKII enzyme, for treating heart disease and asthma. Anderson has a patent and is involved in a company, Allosteros Therapeutics, which is seeking to develop such a drug.

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The paper’s first author is Philip Sanders, a former postdoctoral student in Grumbach's lab, helped design the study and analyzed much of the data. Contributing authors from the UI include Olha Koval, Omar Jaffer, Anand Prasad, Thomas Businga, Jason Scott, Elizabeth Luczak, David Dickey, Francis Miller, Jr., Megan Dibbern, Joseph Zabner, Joel Kline, Chantal Allamargot, Alicia Olivier, David Meyerholz, Brett Wagner, Garry Buettner and Marshall Pope. Other contributing authors are Patrick Hayden from MatTek Corporation; Alfred Robison from the Mount Sinai School of Medicine in New York; Danny Winder, Timothy Blackwell and Ryszard Dworski from Vanderbilt University; Hans Michael Haitchi, David Sammut and Peter Howarth from the University of Southampton, United Kingdom; and Peter Mohler from Ohio State University.

The National Institutes of Health (grant numbers: K23 HL080030 02 and M01 RR-00095), the American Asthma Foundation and the Sandler Program for Asthma Research funded the work.

University of Iowa

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