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Cystic Fibrosis: Pathogenesis01:23

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Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
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In addition to multiple alleles at the same locus influencing traits, numerous genes or alleles at different locations may interact and influence phenotypes in a phenomenon called epistasis. For example, rabbit fur can be black or brown depending on whether the animal is homozygous dominant or heterozygous at a TYRP1 locus. However, if the rabbit is also homozygous recessive at a locus on the tyrosinase gene (TYR), it will have an unshaded coat that appears white, regardless of its TYRP1...
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Cystic fibrosis (CF) is an autosomal recessive disorder that predominantly affects individuals of Northern European descent, occurring at a rate of 1 in 3500. It is caused by a genetic mutation in a gene on chromosome 7, most commonly the ΔF508 mutation, that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This results in thicker mucus secretions and obstruction pathologies in multiple organs, including the lungs and sinuses.
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Uncovering Cystic Fibrosis Carrier: Insights From a Heterozygous CFTR-F508del Rabbit Model.

Do-Yeon Cho1,2,3, Alexis E McFeely1, Daniel Skinner1

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Summary

Cystic fibrosis carriers with a single CFTR mutation show reduced sinonasal function and impaired Pseudomonas aeruginosa clearance. This rabbit model aids in understanding CRS in carriers and testing CFTR therapies.

Keywords:
CF carrierCFTRanimal modelcystic fibrosisphenotyperabbit modelrhinosinusitis

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Area of Science:

  • Otorhinolaryngology
  • Genetics
  • Infectious Disease

Background:

  • Chronic rhinosinusitis (CRS) is linked to impaired mucociliary clearance and bacterial infections.
  • Individuals with cystic fibrosis transmembrane conductance regulator (CFTR) mutations are at higher risk for CRS.
  • The sinonasal characteristics and host-pathogen interactions in CF carriers are not well understood.

Purpose of the Study:

  • To characterize the sinonasal phenotype and host-pathogen interactions in a rabbit model of heterozygous CFTR mutation.
  • To evaluate the potential of CFTR modulators in treating sinonasal dysfunction.

Main Methods:

  • Heterozygous ΔF508 CF rabbits and wild-type (WT) rabbits were compared.
  • Sinonasal structure, CFTR function (NPD, Ussing chamber), and response to Pseudomonas aeruginosa infection were assessed.
  • Computed tomography, histology, bacterial quantification, and RNA sequencing were utilized.

Main Results:

  • Heterozygous rabbits exhibited sinus hypoplasia and reduced CFTR-mediated chloride transport.
  • These rabbits showed increased bacterial burden, persistent radiographic opacification, and delayed recovery after P. aeruginosa infection.
  • A distinct transcriptional profile was observed in the heterozygous sinonasal environment.

Conclusions:

  • Heterozygous ΔF508 CF rabbits serve as a relevant model for CF carriers with sinonasal disease.
  • The model demonstrates reduced CFTR function, altered host defense, and impaired infection clearance.
  • This platform can be used to study CRS pathogenesis and test CFTR-targeted therapies in carriers.