Related Experiment Video

Updated: Feb 24, 2026

Visualization of Pseudomonas aeruginosa within the Sputum of Cystic Fibrosis Patients
07:25

Visualization of Pseudomonas aeruginosa within the Sputum of Cystic Fibrosis Patients

Published on: July 16, 2020

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PDE4 Inhibitor Apremilast Rebalances Inflammatory Responses to Pseudomonas aeruginosa Infection in CF Rats

Linto Antony1,2, Lawrence Rasmussen1,2, Denise Stanford1,2

  • 1Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA.

Biorxiv : the Preprint Server for Biology
|February 23, 2026
PubMed

Insights

Apremilast (Apr) shows promise in managing persistent airway inflammation in cystic fibrosis (CF) models. This phosphodiesterase 4 inhibitor rebalanced inflammation without increasing infection, suggesting it could complement CFTR modulator therapies.

Area of Science:

  • Pulmonology
  • Pharmacology
  • Immunology

Background:

  • Chronic airway inflammation persists in cystic fibrosis (CF) patients despite highly effective modulator therapy (HEMT).
  • Existing anti-inflammatory treatments for CF are limited by side effects or incompatibility with CFTR modulators.
  • Novel strategies are needed to rebalance inflammation without compromising host defense against infection.

Purpose of the Study:

  • To evaluate the efficacy of apremilast (Apr), a selective phosphodiesterase 4 (PDE4) inhibitor, in modulating airway inflammation in a humanized CF (G551D) rat model.
  • To assess the safety and compatibility of Apr with CFTR modulator therapy.

Main Methods:

  • Humanized CF (G551D) rats were treated prophylactically with Apr and subsequently challenged with *Pseudomonas aeruginosa*.
  • Lung function, lung injury, inflammatory markers (Th1/Th17 axes), bacterial burden, and CFTR expression/function were assessed.
  • In vitro studies examined the effect of Apr on G551D-CFTR phosphorylation.

Main Results:

  • Short-term prophylactic Apr treatment preserved lung function and reduced lung injury in CF rats.
  • Apr broadly modulated inflammatory responses, particularly Th1 and Th17 pathways.
  • Apr did not significantly increase bacterial burden or negatively impact CFTR expression.
  • Apr enhanced G551D-CFTR phosphorylation in vitro, indicating compatibility with HEMT.

Conclusions:

  • Apremilast demonstrates potential as an adjunct therapy to CFTR modulators for managing airway inflammation in CF.
  • Apr may help rebalance inflammation in CF without compromising host defense mechanisms.
  • Further investigation into Apr's role in CF treatment is warranted.

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