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Inflammatory cytokines TNF-alpha and IL-17 enhance the efficacy of cystic fibrosis transmembrane conductance regulator modulators
Journal article   Open access   Peer reviewed

Inflammatory cytokines TNF-alpha and IL-17 enhance the efficacy of cystic fibrosis transmembrane conductance regulator modulators

Tayyab Rehman, Philip H. Karp, Ping Tan, Brian J. Goodell, Alejandro A. Pezzulo, Andrew L. Thurman, Ian M. Thornell, Samantha L. Durfey, Michael E. Duffey, David A. Stoltz, …
The Journal of clinical investigation, Vol.131(16), e150398
08/16/2021
DOI: 10.1172/JCI150398
PMCID: PMC8363270
PMID: 34166230
url
https://doi.org/10.1172/JCI150398View
Published (Version of record) Open Access

Abstract

Without cystic fibrosis transmembrane conductance regulator-mediated (CFTR-mediated) HCO3- secretion, airway epithelia of newborns with cystic fibrosis (CF) produce an abnormally acidic airway surface liquid (ASL), and the decreased pH impairs respiratory host defenses. However, within a few months of birth, ASL pH increases to match that in non-CF airways. Although the physiological basis for the increase is unknown, this time course matches the development of inflammation in CF airways. To learn whether inflammation alters CF ASL pH, we treated CF epithelia with TNF-alpha and IL-17 (TNF-alpha+IL-17), 2 inflammatory cytokines that are elevated in CF airways. TNF-alpha+IL-17 markedly increased ASL pH by upregulating pendrin, an apical Cl- /HCO3- exchanger. Moreover, when CF epithelia were exposed to TNF-alpha+IL-17, clinically approved CFTR modulators further alkalinized ASL pH. As predicted bythese results, in vivo data revealed a positive correlation between airway inflammation and CFTR modulator-induced improvement in lung function. These findings suggest that inflammation is a key regulator of HCO3- secretion in CF airways. Thus, they explain earlier observations that ASL pH increases after birth and indicate that, for similar levels of inflammation, the pH of CF ASL is abnormally acidic. These results also suggest that a non-cell-autonomous mechanism, airway inflammation, is an important determinant of the response to CFTR modulators.
Life Sciences & Biomedicine Medicine, Research & Experimental Research & Experimental Medicine Science & Technology

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