Grant: Travel Awards - Institute Community Support
Direct Payment
$1,400.00
PLUNCs as potential modifier genes in Cystic Fibrosis
FY 2011-12
Summary
Cystic fibrosis (CF) is an inherited disease causing a build-up of thick, sticky mucus in the lung, digestive tract, and other areas of the body. This increases susceptibility to bacterial infection in the lung, leading to early death due to chronic lung disease. CF patients who have the same alteration in the primary causal gene may have a very different clinical course. One CF patient may have very mild lung disease and infrequent lung infections, while another with the same alteration may have frequent lung infections accompanied by great decreases in lung function. In our previous studies we performed a comprehensive search through all of the human chromosomes for genes (known as modifier genes) that cause some CF patients to become sicker faster than others. Particular regions of specific chromosomes were identified as influencing lung function but these regions each contain a handful of genes and the specific genes responsible for modifying disease severity remain to be determined.
One region of the human chromosome 20 which has been identified as being potentially relevant to CF contains the SPLUNC1 (BPIFA1) and LPLUNC1 (BPIFB1) genes. Both genes are thought to be involved in fighting bacterial infection in the lungs. Genetic variants in these genes have been associated with milder lung disease in CF patients. These variants may result in higher levels of SPLUNC1 and LPLUNC1 which could help rid the lungs of bacterial infection. To test this hypothesis, we measured SPLUNC1 and LPLUNC1 levels in CF and non-CF individuals with different genetic variants. We found that a genetic variant in the SPLUNC1 gene was associated with higher levels of the gene. We also found that both SPLUNC1 and LPLUNC1 have higher levels of expression in CF lung samples when compared to non-CF samples.
If PLUNCs are shown to be protective against bacterial infection in the lung, aerosolized forms of these molecules could be extremely useful in CF therapy.
Department
Program
Travel Awards - Institute Community Support
Recipient
Location
British Columbia, Canada
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
253082
Name
Saferali Aabida
Region
British Columbia
Country
Canada
Orgtype
Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Institute of Circulatory and Respiratory Health
Projecttitle
PLUNCs as potential modifier genes in Cystic Fibrosis
Programtype2
Undefined
Orgnameinp2
Direct Payment
Cihramount2
$1,400
Cihrequipment2
$0
Programname2
Travel Awards - Institute Community Support
Keyworddelim
Cystic Fibrosis; Modifier Genes; Pluncs
Abstract
Cystic fibrosis (CF) is an inherited disease causing a build-up of thick, sticky mucus in the lung, digestive tract, and other areas of the body. This increases susceptibility to bacterial infection in the lung, leading to early death due to chronic lung disease. CF patients who have the same alteration in the primary causal gene may have a very different clinical course. One CF patient may have very mild lung disease and infrequent lung infections, while another with the same alteration may have frequent lung infections accompanied by great decreases in lung function. In our previous studies we performed a comprehensive search through all of the human chromosomes for genes (known as modifier genes) that cause some CF patients to become sicker faster than others. Particular regions of specific chromosomes were identified as influencing lung function but these regions each contain a handful of genes and the specific genes responsible for modifying disease severity remain to be determined.
One region of the human chromosome 20 which has been identified as being potentially relevant to CF contains the SPLUNC1 (BPIFA1) and LPLUNC1 (BPIFB1) genes. Both genes are thought to be involved in fighting bacterial infection in the lungs. Genetic variants in these genes have been associated with milder lung disease in CF patients. These variants may result in higher levels of SPLUNC1 and LPLUNC1 which could help rid the lungs of bacterial infection. To test this hypothesis, we measured SPLUNC1 and LPLUNC1 levels in CF and non-CF individuals with different genetic variants. We found that a genetic variant in the SPLUNC1 gene was associated with higher levels of the gene. We also found that both SPLUNC1 and LPLUNC1 have higher levels of expression in CF lung samples when compared to non-CF samples.
If PLUNCs are shown to be protective against bacterial infection in the lung, aerosolized forms of these molecules could be extremely useful in CF therapy.
Competitiondate
201201
Approvedterm2
0 yr 1 mth
Pinamesdelim
Saferali, Aabida
Approvedterm
0 an 1 mois
Cihrcontribution2
Inst of Circ &Respiratory Hlth~ $1,400~ $0~