The Role of MicroRNAs in Innate Immunity & Cystic Fibrosis Lung Disease 🫁🧬 #pencis #researchawards

 

Introduction

Pulmonary disease in cystic fibrosis (CF) remains the leading cause of morbidity and mortality, driven by chronic infections and dysregulated immune responses. The innate immune system, which provides the first line of defense against bacterial, viral, and fungal pathogens, is profoundly altered in CF lung disease (CFLD). Both cellular components—such as airway epithelial cells, monocytes, macrophages, and neutrophils—and molecular mediators, including cytokines, chemokines, and transcription factors, display dysfunctional behavior. Emerging evidence highlights microRNAs (miRNAs) as key post-transcriptional regulators orchestrating immune and inflammatory pathways in CF. Understanding miRNA-mediated regulatory networks is therefore essential to unravel the complexity of CFLD pathogenesis and identify novel therapeutic and diagnostic strategies.

Dysregulation of Innate Immune Cells in CF Lung Disease

Innate immune cells in the CF lung exhibit altered phenotypes and impaired functionality that contribute to persistent inflammation and ineffective pathogen clearance. Airway epithelial cells display abnormal inflammatory signaling, while monocytes and macrophages show compromised antigen presentation and microbial response. Neutrophils, although abundant, often fail to eradicate pathogens effectively and instead exacerbate tissue damage through excessive protease and reactive oxygen species release. miRNA dysregulation within these cells modulates key immune pathways, shaping the balance between host defense and chronic inflammation, and thereby playing a central role in CFLD progression.

MicroRNA-Mediated Control of Inflammatory Signaling Pathways

miRNAs regulate multiple layers of inflammatory signaling by targeting transcripts encoding cytokines, chemokines, and intracellular signaling molecules. In CF, altered expression of specific miRNAs disrupts pathways such as NF-κB, MAPK, and interferon signaling, leading to sustained hyperinflammation. Some miRNAs appear to act as compensatory mechanisms attempting to dampen excessive immune activation, while others amplify inflammatory cascades. These findings suggest that miRNAs function as critical molecular switches controlling immune homeostasis in the CF lung microenvironment.

Impaired Pathogen Response and Antigen Presentation

Effective pathogen recognition and antigen presentation are essential for coordinating innate and adaptive immune responses. In CF, miRNA dysregulation interferes with pattern recognition receptor signaling, phagocytosis, and antigen processing in airway epithelial cells and macrophages. These defects contribute to persistent bacterial colonization and recurrent infections. By targeting genes involved in microbial sensing and antigen presentation machinery, miRNAs play a decisive role in shaping host–pathogen interactions and may explain the reduced efficiency of immune clearance observed in CFLD.

Role of miRNAs in Wound Healing and Tissue Remodeling

Chronic inflammation in CF lungs leads to repeated epithelial injury and defective repair processes. miRNAs have been implicated in regulating epithelial regeneration, cell proliferation, and wound healing responses. Altered miRNA expression in CF airway epithelial cells and macrophages influences extracellular matrix remodeling and fibrosis, potentially contributing to irreversible lung damage. Understanding how miRNAs control these repair mechanisms may reveal new opportunities to restore epithelial integrity and slow disease progression.

miRNome Profiling for Therapeutic and Biomarker Development

While individual miRNA studies have provided valuable mechanistic insights, large-scale genomic and transcriptomic analyses are essential to capture the full complexity of miRNA networks in CFLD. Comprehensive miRNome profiling in large patient cohorts may identify miRNA signatures associated with disease severity, progression, and therapeutic response. Circulating miRNAs also hold promise as non-invasive diagnostic and prognostic biomarkers, supporting precision medicine approaches in CF. Future clinical studies integrating miRNA biology with patient outcomes will be critical for translating these findings into effective therapies.

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Hashtags

#CysticFibrosis, #CFResearch, #MicroRNA, #InnateImmunity, #LungDisease, #CFLD, #AirwayEpithelium, #ChronicInflammation, #HostDefense, #PathogenResponse, #Macrophages, #Neutrophils, #ImmuneDysregulation, #miRNome, #PrecisionMedicine, #Biomarkers, #Transcriptomics, #GenomicResearch, #RespiratoryInfections, #PulmonaryImmunology