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REVIEW article
Front. Cell. Infect. Microbiol.
Sec. Microbes and Innate Immunity
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1566495
This article is part of the Research Topic Cell Migration and Tissue Remodeling in Infectious Diseases View all 3 articles
Wound Repair and Immune Function in the Pseudomonas infected CF Lung: Before and After Highly Effective Modulator Therapy
Provisionally accepted
Emma Lea Matthews 1,2
Meghan Hirsch 1,2
Federico Prokopczuk 3
Luke I Jones 1 Eriel MartÃnez 3
Jarrod Wesley Barnes 1,2
Stefanie Krick 1,2*- 1 Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States
- 2 Cystic Fibrosis Research Center, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States
- 3 Department of Microbiology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States
The leading cause of death for people with cystic fibrosis (pwCF) continues to be due to respiratoryrelated illnesses. Both wound repair and immune cell responses are dysregulated in the CF airways, creating a cycle of unresolved injury and perpetuating inflammation. PwCF are predisposed to colonization and infections with opportunistic bacteria like Pseudomonas aeruginosa (Pa), the most common adult pathogen in CF. Pa possesses key virulence factors that can exacerbate chronic inflammation and lung injury. With the approval of highly effective modulator therapies like elexacaftor/tezacaftor/ivacaftor (ETI), pwCF eligible for ETI have seen drastic improvements in lung function and clinical outcomes, including an increased life expectancy. While modulator therapies are improving bronchial epithelial cellular processes in wound repair and some areas of immunity, many of these processes do not reach a non-CF baseline state or have not been thoroughly studied. The effect of modulator therapy on Pa may lead to a reduction in infection, but in more longitudinal studies, there is not always eradication of Pa, and colonization and infection frequency can return to pre-modulator levels over time. Finally, in this review we explore the current state of additional treatments for CF lung disease, independent of CFTR genotype, including anti-inflammatories, phage-therapies, and Pa vaccines.
Keywords: wound repair1, Pseudomonas aeruginosa2, cystic fibrosis3, bronchial epithelium4, Immune System5, modulator therapy6, elexacaftor/tezacaftor/ivacaftor(ETI)7
Received: 24 Jan 2025; Accepted: 04 Apr 2025.
Copyright: © 2025 Matthews, Hirsch, Prokopczuk, Jones, MartÃnez, Barnes and Krick. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Stefanie Krick, Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, 35294, Alabama, United States
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