A new study published in the Journal of Inflammation shows that the cystic fibrosis transmembrane conductance regulator (CFTR) plays an important role in regulating intestinal inflammatory responses. The research team hypothesized that genetic depletion of CFTR plays a significant role in the inflammatory status of human intestinal epithelial cell lines. In order to test this, the researchers induced inflammatory conditions by adding the human recombinant tumor necrosis factor (TNF) or Interleukin-1? (IL-1?) and genetically depleted CFTR expression from cell lines using short hairpin RNA interference (shRNAi).
shRNAi is a post-transcriptional process triggered by the introduction of double-stranded RNA (dsRNA) that induces gene silencing in a sequence-specific manner. The Lung Disease News report notes that the researchers observed that the CFTR gene and protein deficiency induced a significant increase in basal secretion of IL-8 as well as in IL-1?-induced secretion of IL-6 and -8, while the levels of the anti-inflammatory cytokine, IL-10, were unaffected by CFTR deficiency. The results from animal models also confirmed the in vitro findings.
According to Lung Disease News, the results call attention to the role played by CFTR in the regulation of intestinal inflammatory responses. The data also supported the hypothesis that CFTR appears to play functions that go further than its role as a chloride channel, and its disruption may prevent cells from optimally responding to exogenous or endogenous stimuli.
The researchers conclude that this study may be of particular relevance to cystic fibrosis patients who have changes in their intestinal microbiota, making them susceptible to pathogens that could induce exaggerated inflammatory responses, as noted on the Lung Disease News report.
Source: Lung Disease News
