Resolvin D1 regulates epithelial ion transport and inflammation in cystic fibrosis airways

Ringholz, Fiona; Higgins, Gerard; Hatton, Aurélie; Sassi, Ali; Moukachar, Ahmad; Fustero-Torre, Coral; Hollenhorst, Monika I.; Sermet‐Gaudelus, Isabelle; Harvey, Brian; McNally, Paul; Urbach, V.

doi:10.1016/j.jcf.2017.11.017

Cited by 26 publications

(39 citation statements)

References 31 publications

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“…The NTEPD data suggest that exogenous RvD1 stimulates chloride secretion through a channel other than CFTR while simultaneously inhibiting ENaC. Ringholz et al also evaluated the impact of RvD1 on host defenses . When CF alveolar macrophages were treated with RvD1, there was increased phagocytosis of labeled beads compared to vehicle treated alveolar macrophages.…”

Section: Characteristics Of the Cystic Fibrosis Inflammatory Responsementioning

confidence: 79%

“…The ratio of RvD1/IL‐8 positively correlated with FEV 1 , indicating that an imbalance between RvD1 and the pro‐inflammatory mediator it down‐regulates may associate with progressive lung deterioration . Ringholz et al evaluated the impact of RvD1 on airway surface liquid (ASL) height and innate defense in CF . Application of RvD1 to primary CF bronchial epithelial cells and to CF cell lines increased ASL height in a dose‐dependent fashion, likely through the inhibition of the epithelial sodium channel (ENaC) and other ion transport pathways, rather than through a direct effect on cystic fibrosis transmembrane conductance regulator (CFTR).…”

Section: Characteristics Of the Cystic Fibrosis Inflammatory Responsementioning

confidence: 99%

“…Ringholz et al also evaluated the impact of RvD1 on host defenses. 17 When CF alveolar macrophages were treated with RvD1, there was increased phagocytosis of labeled beads compared to vehicle treated alveolar macrophages. There was also a significant reduction in intracellular viable P aeruginosa in CF alveolar macrophages that were pre-treated with RvD1 compared to those pre-treated with vehicle, thereby demonstrating the importance of RvD1 in host defense.…”

mentioning

confidence: 97%

“…16 Ringholz et al evaluated the impact of RvD1 on airway surface liquid (ASL) height and innate defense in CF. 17 Application of RvD1 to primary CF bronchial epithelial cells and to CF cell lines increased ASL height in a dose-dependent fashion, likely through the inhibition of the epithelial sodium channel (ENaC) and other ion transport pathways, rather than through a direct effect on cystic fibrosis transmembrane conductance regulator (CFTR). In nasal transepithelial electrical potential difference (NTEPD) studies, application of RvD1 to the nasal mucosa was associated with reduced amiloride-sensitive NTEPD in CF mice but not WT mice.…”

mentioning

confidence: 99%

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Inflammation in cystic fibrosis: An update

Roesch

Nichols

Chmiel

2018

Pediatric Pulmonology

198

221

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Inflammation plays a critical role in cystic fibrosis (CF) lung pathology and disease progression making it an active area of research and important therapeutic target. In this review, we explore the most recent research on the major contributors to the exuberant inflammatory response seen in CF as well as potential therapeutics to combat this response. Absence of functional cystic fibrosis transmembrane conductance regulator (CFTR) alters anion transport across CF airway epithelial cells and ultimately results in dehydration of the airway surface liquid. The dehydrated airway surface liquid in combination with abnormal mucin secretion contributes to airway obstruction and subsequent infection that may serve as a trigger point for inflammation. There is also evidence to suggest that airway inflammation may be excessive and sustained relative to the infectious stimuli. Studies have shown dysregulation of both pro-inflammatory mediators such as IL-17 and pro-resolution mediators including metabolites of the eicosanoid pathway. Recently, CFTR potentiators and correctors have garnered much attention in the CF community. Although these modulators address the underlying defect in CF, their impact on downstream consequences such as inflammation are not known. Here, we review pre-clinical and clinical data on the impact of CFTR modulators on inflammation. In addition, we examine other cell types including neutrophils, macrophages, and T-lymphocytes that express CFTR and contribute to the CF inflammatory response. Finally, we address challenges in developing anti-inflammatory therapies and highlight some of the most promising anti-inflammatory drugs under development for CF.

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Section: Characteristics Of the Cystic Fibrosis Inflammatory Responsementioning

confidence: 79%

Section: Characteristics Of the Cystic Fibrosis Inflammatory Responsementioning

confidence: 99%

mentioning

confidence: 97%

mentioning

confidence: 99%

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Inflammation in cystic fibrosis: An update

Roesch

Nichols

Chmiel

2018

Pediatric Pulmonology

198

221

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“…RvE2 has a biological effect that is similar to that of RvE1; it regulates neutrophil chemotaxis and activates phagocytosis and synthesis of anti-inflammatory cytokines. The anti-inflammatory mechanism of RvD action in bronchopulmonary pathology is under study [119,120]. Lipoxin A4 receptor (ALX) and G protein-coupled receptor 32 (GPR32) have been identified as receptors for RvD1.…”

Section: Ppar Researchmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptors as a Therapeutic Target in Asthma

et al. 2020

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The complexity of the pathogenetic mechanisms of the development of chronic inflammation in asthma determines its heterogeneity and insufficient treatment effectiveness. Nuclear transcription factors, which include peroxisome proliferatoractivated receptors, that is, PPARs, play an important role in the regulation of initiation and resolution of the inflammatory process. The ability of PPARs to modulate not only lipid homeostasis but also the activity of the inflammatory response makes them an important pathogenetic target in asthma therapy. At present, special attention is focused on natural (polyunsaturated fatty acids (PUFAs), endocannabinoids, and eicosanoids) and synthetic (fibrates, thiazolidinediones) PPAR ligands and the study of signaling mechanisms involved in the implementation of their anti-inflammatory effects in asthma. This review summarizes current views on the structure and function of PPARs, as well as their participation in the pathogenesis of chronic inflammation in asthma. The potential use of PPAR ligands as therapeutic agents for treating asthma is under discussion.

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