English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Susceptibility to  Bordetella pertussis  infection varies widely. These differences can partly be explained by genetic host factors. HcB-28 mice are more resistant to  B. pertussis  infection than C3H mice, which could partially be ascribed to the  B .  pertussis susceptibility locus-1  ( Bps1 ) on chromosome 12. The presence of C57BL/10 genome on this locus instead of C3H genome resulted in a decreased number of bacteria in the lung. To further elucidate the role of host genetic factors, in particular in the  Bps1  locus, in  B. pertussis  infection, and to identify candidate genes within in this region, we compared expression profiles in the lungs of the C3H and HcB-28 mouse strains following  B. pertussis  inoculation. Twelve and a half percent of the genomes of these mice are from a different genetic background.    Results  Upon  B. pertussis  inoculation 2,353 genes were differentially expressed in the lungs of both mouse strains. Two hundred and six genes were differentially expressed between the two mouse strains, but, remarkably, none of these were up- or down-regulated upon  B. pertussis  infection. Of these 206 genes, 17 were located in the  Bps1  region. Eight of these genes, which showed a strong difference in gene expression between the two mouse strains, map to the immunoglobulin heavy chain complex ( Igh ).    Conclusion  Gene expression changes upon  B. pertussis  infection are highly identical between the two mouse strains despite the differences in the course of  B. pertussis  infection. Because the genes that were differentially regulated between the mouse strains only showed differences in expression before infection, it appears likely that such intrinsic differences in gene regulation are involved in determining differences in susceptibility to  B. pertussis  infection. Alternatively, such genetic differences in susceptibility may be explained by genes that are not differentially regulated between these two mouse strains. Genes in the  Igh  complex, among which  Igh-1a/b , are likely candidates to explain differences in susceptibility to  B. pertussis . Thus, by microarray analysis we significantly reduced the number of candidate susceptibility genes within the  Bps1  locus. Further work should establish the role of the  Igh  complex in  B. pertussis  infection.

Comparative gene expression profiling in two congenic mouse strains following Bordetella pertussis infection