Research Awards Nationwide 2010-2011
New York Recipients
Download the Research Awards Nationwide 2010-2011 PDF or search other states here.

KAISER MOHAMMAD BIJLI, PhD
University of Rochester, Rochester, NY
Biomedical Research Grant, Funded by the American Lung Association

Blocking Excess Protein Production May Lead to New Lung Injury Treatments

Regulation of Endothelial NF-kappaB Activity and ICAM-1 Expression by c-Src. Thrombin is an enzyme that promotes blood clotting. It is released during sepsis and tissue injury. Upon its release, it interacts with blood vessel wall cells called endothelial cells and activates these cells. This activation process increases the production of a protein called ICAM-1 on the surface of endothelial cells, which promotes the binding of circulating white blood cells to the endothelium, the layer of cells that line the blood vessels. This binding promotes the migration of white blood cells across the endothelium to the site of inflammation, a process which is implicated in the development of acute lung injury. Although scientists have come to realize that ICAM-1 plays a crucial role in acute lung injury, the precise way this protein is produced remains unclear. The researchers will study the regulation and the role of ICAM-1 in lung injury. This research may reveal ways to block excess production of ICAM-1, leading to new treatment targets for inflammatory diseases involving acute lung injury.

ANDREA COOPER, PhD
Trudeau Institute, Saranac Lake, NY
DeSouza Research Award, Funded by the American Lung Association of the Southwest

Examining Inflammatory Response In Lung Disease Caused By Environmental Bacterium

The Impact Of Antigen-Specific T Cells On The Immunopathologic Consequences In Mycobacterium Avium-Induced Lung Disease. Disease caused by Mycobacterium avium (M. avium) can occur in smokers, those with impaired lung function, aging women and people repeatedly exposed to aerosol clouds of this environmental bacterium. The disease consists of an inflammatory response in the lung and can progress and cause significant illness. To better understand this inflammatory response, the researchers will use a mouse model of the disease. They will use state-of-the-art techniques to examine the immune cell functions that occur following infection with M. avium and determine whether changing these functions alters disease development. The findings will highlight potential mechanisms that can be examined in targeted human studies and may suggest potential treatments.

BOUKE CATHERINE DE JONG, MD, PhD
New York University, New York,
Biomedical Research Grant, Funded by the American Lung Association

Studying Variant of TB Bacterium May Provide Insights to Fight the Disease

Defective ESAT-6 Secretion as a Mechanism of Attenuation of M. africanum. Only a small number of people who become infected with the bacterium that causes tuberculosis will get sick themselves. It is not understood why some people get sick while the majority stays healthy after infection. One way to increase the understanding of immunity to TB is to study differences in "behavior" between different strains of the TB bacterium and to search for bacterial genes that cause those differences. The researchers will study a variant of M. tuberculosis, called M. africanum, which is abundant in West Africa. M. africanum patients and their household members are less likely to mount an immune response to a protein called ESAT-6, which is produced by the TB bacteria and is essential to their causing disease. Preliminary findings suggest that M. africanum secretes less ESAT-6 than M. tuberculosis. The researchers will study the mechanism of defective ESAT-6 secretion in M. africanum by manipulating a bacterial gene that is thought to explain the difference. A better understanding of how the ESAT-6 protein works could form the basis for new drugs that would interrupt its secretion. ESAT-6 is part of a candidate TB vaccine, and this study will inform TB vaccine development, which aims to prevent lung disease caused by TB.

MATTHEW GIANNANDREA, PhD
University of Rochester, Rochester, NY
Senior Research Training Fellowship, Funded by the American Lung Association

Seeking Protection From Lung Infection in Babies Receiving Oxygen Treatment

Effects of Neonatal Oxygen Supplementation on the Response of CD8+ T -cells to Influenza Virus Infection. Currently, more than one out of every 10 babies born in the U.S. are premature. Premature infants with low birth weight often have under-developed lungs and require supplemental oxygen treatment in order to survive. While this life-saving treatment is effective, these infants are often diagnosed with a chronic lung disease called bronchopulmonary dysplasia (BPD). Infants that survive with BPD experience decreased lung function in addition to an increased susceptibility to respiratory infections, which is particularly dangerous during the flu season. In order to devise appropriate treatments, more information is needed to explain why babies with BPD have an increased risk of lung infection. The researchers previously studied how oxygen supplementation at birth affects susceptibility to a respiratory infection using a mouse model. Their preliminary data indicated that the production of immune cells called killer Tcells that are specific to the influenza virus are impaired in mice exposed to oxygen at birth. The researchers will further study how these killer T-cells in mice exposed to oxygen at birth work against virus-infected cells. The findings will help guide drug and vaccine design that could ultimately help limit susceptibility to infection in human survivors of BPD.

ANDERS HAKANSSON, PhD
State University of New York at Buffalo, Buffalo, NY
Biomedical Research Grant, Funded by the American Lung Association

Protein Complex in Breast Milk May Fight Pneumonia

The Use of a Human Milk Protein Complex, HAMLET, to Treat Pneumococcal Pneumonia. Streptococcus pneumoniae (pneumococcus) is the most common cause of bacterial pneumonia and a common complication of influenza and measles virus infections. Pneumococci, like so many other bacterial pathogens, have become resistant to common antibiotics used to treat these infections and currently 30% of strains isolated in the U.S. are not susceptible to penicillin. During the researchers’ investigations of the antibacterial activity of breast milk, they discovered a protein complex called HAMLET with potent killing activity against S. pneumoniae and other respiratory tract pathogens that cause pneumonia. HAMLET kills pneumococci that are resistant to common antibiotics, and no resistance against HAMLET has been observed. The researchers will investigate the ability of HAMLET to kill bacteria growing in biofilms (the form of growth encountered during infection) and prevent and treat pneumococcal pneumonia in established mouse model systems, which closely resemble human disease. This research has the potential to lead to the development of more effective therapeutic agents against pneumococcal disease, with less risk for resistance development.

WLADIMIR LABEIKOVSKY, PhD
The Rockefeller University, New York, NY
Senior Research Training Fellowship, Funded by the American Lung Association

Sidestepping a Roadblock in Developing Treatments for Cystic Fibrosis

Structure and Mechanism of Bacterial ATPBinding Casette Proteins Resembling CFTR. Cystic fibrosis (CF) is a genetic disease that causes chronic bacterial infections and inflammation in the lung. CF is a rare but life-shortening disease; the average life expectancy of a person diagnosed with CF is around 35 years. To date, available therapies against CF are aimed almost exclusively at reducing symptoms, and there is no cure yet. CF is caused by mutations in the gene called CFTR. Most people with CF have a mutation in the CFTR gene that results in the misfolding and premature degradation of the protein encoding the gene. There are a number of research efforts underway to develop CF therapies, all of which would benefit from a thorough understanding of CFTR's molecular mechanism. Efforts in attaining this information have been hindered largely by the difficulties in obtaining sufficient amounts of stable, purified CFTR protein. The researchers aim to side-step this difficulty by studying bacterial proteins that resemble CFTR. This research should shed light on the structure and mechanism of CFTR.

MARINA REZNIK, MD
Montefiore Medical Center, Bronx, NY
Clinical Patient Research Grant, Funded by the American Lung Association

Can Home-Based Asthma Program Help Inner-City Children?

Health Worker Home-Based Asthma Intervention. Asthma disproportionately affects low-income African-American and Hispanic children living in inner cities. Not taking daily asthma medications as prescribed by the doctor has been implicated as one of the major factors in poor asthma outcomes in these communities. The researchers will evaluate the effectiveness of a home-based asthma education program called Wee Wheezers delivered by Community Health Workers, who share many of the experiences of the people in the community. The program is designed to improve adherence to medication and parental asthma knowledge, in order to reduce asthma symptoms and Emergency Department asthma visits. The study will include 250 children ages 2-7 being treated for persistent asthma, and their parents. They will be randomly assigned to routine care from their doctor, or the Wee Wheezers program. The researchers will determine whether the program is effective in decreasing the number of asthma symptom days, increasing adherence to taking prescribed asthma medication, and decreasing asthma-related Emergency Department visits. The study will also compare parental asthma knowledge and asthma management practices between the two groups.