GeneSet Information

Tier II GS129089 • bronchial hyperresponsiveness 3 (Bhr3 Published QTL Chr 17)


QTL associated with bronchial hyperresponsiveness 3. The confidence interval is Chr17:3924615-48698388 bp,+strand


QTL-Bhr3-Mouse-Chr 17









Kleeberger SR


Genetic aspects of susceptibility to air pollution.


The European respiratory journal. Supplement May 2003, Vol 40, pp. 52s-56s


Inter-individual variation in human responses to air pollutants suggests that some subpopulations are at increased risk, and it is increasingly clear that genetic background is an important susceptibility factor. Genetically standardised animal models provide useful investigative tools. Linkage analyses using inbred mice identified chromosomal segments (quantitative trait loci (QTL)), with genes controlling susceptibility to the lung inflammatory (chromosome 17), injury (chromosome 11), and hyperpermeability (chromosome 4) responses to ozone (O3) exposure. An immune dysfunction response induced by exposure to sulphate-associated particles is linked to the identical chromosome 17 and 11 QTLs described for O3 susceptibility, thus similar genetic mechanisms may be controlling pulmonary responses to these pollutants. Candidate genes within the QTLs on chromosomes 4 and 17 include the toll-like receptor 4 and the pro-inflammatory cytokine, tumour necrosis factor-alpha, respectively. Functional analyses strongly support a role for these candidate genes in determining susceptibility to O3 and particulates. Because striking linkage homology exists between the human and mouse genomes, candidate susceptibility genes identified in the mouse are likely to aid research aimed at understanding human genetic factors that contribute to differential susceptibility. To date, no studies have examined the interaction between age and genetic background in the development of air pollution-induced lung disease. However, investigations have suggested an influence of age on genetic susceptibility to lung cancer and other diseases, which indicate that an interaction between age and genetic background may be important in air pollution disease pathogenesis. PUBMED: 12762575
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Annotation Information

Lung Diseases (D008171)
Animals (D000818)
Chromosomes (D002875)
Comprehension (D032882)
Models, Animal (D023421)
Neoplasms (D009369)
Wounds and Injuries (D014947)
Genetic Predisposition to Disease (D020022)
Chromosomes, Human, Pair 17 (D002886)
Insemination, Artificial, Heterologous (D007316)
Air Pollutants (D000393)
Air Pollution (D000397)
Lung Neoplasms (D008175)
Necrosis (D009336)
Research (D012106)
Toll-Like Receptors (D051193)
Toll-Like Receptor 4 (D051197)
Confidence Intervals (D016001)
pathogenesis (GO:0009405)
chromosome (GO:0005694)

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