Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (643 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A non-specific host defense mechanism that removes mucus and other material from the lungs by ciliary and secretory activity of the tracheobronchial submucosal glands. It is measured in vivo as mucus transfer, ciliary beat frequency, and clearance of radioactive tracers.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Clearance, Mucociliary; Clearances, Mucociliary; Mucociliary Clearances; Mucociliary Transport; Mucociliary Transports; Transport, Mucociliary; Transports, Mucociliary.
Where it fits in the MeSH classification
- Broader topics
- Diagnostic Techniques, Respiratory System; Respiratory Physiological Phenomena
Related concepts
Research landscape
PubMed indexes 2,872 records tagged with the MeSH heading “Mucociliary Clearance” (counts retrieved 2026-10-31). 354 of them (12.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,070 records.
Reviews account for 608 records (21.2%) and meta-analyses for 28. Randomized controlled trials number 208 (7.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,070 |
| 2000-2009 | 652 |
| 2010-2019 | 796 |
| 2020 onward | 354 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 608 | 21.2% |
| Meta-analyses | 28 | 1.0% |
| Randomized controlled trials | 208 | 7.2% |
Method: PubMed query "Mucociliary Clearance"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance | 2021 | Research article Design not recorded in structured metadata | 251 | cc by PMID 34272374 · DOI · PMC8285531 |
| Muc5b overexpression causes mucociliary dysfunction and enhances lung fibrosis in mice | 2018 | Research article Design not recorded in structured metadata | 216 | cc by PMID 30560893 · DOI · PMC6299094 |
| The immunometabolite itaconate stimulates OXGR1 to promote mucociliary clearance during the pulmonary innate immune response | 2023 | Research article Design not recorded in structured metadata | 70 | cc by PMID 36919698 · DOI · PMC10014103 |
| Physiology and pathophysiology of mucus and mucolytic use in critically ill patients | 2025 | Review article Design not recorded in structured metadata | 19 | cc by PMID 39920835 · DOI · PMC11806889 |
SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Understanding how SARS-CoV-2 spreads within the respiratory tract is important to define the parameters controlling the severity of COVID-19.
- Closing excerpt
- This study identifies cilia damage as a pathogenic mechanism that could facilitate SARS-CoV-2 spread to the deeper lung parenchyma.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (177 words)
Understanding how SARS-CoV-2 spreads within the respiratory tract is important to define the parameters controlling the severity of COVID-19. Here we examine the functional and structural consequences of SARS-CoV-2 infection in a reconstructed human bronchial epithelium model. SARS-CoV-2 replication causes a transient decrease in epithelial barrier function and disruption of tight junctions, though viral particle crossing remains limited. Rather, SARS-CoV-2 replication leads to a rapid loss of the ciliary layer, characterized at the ultrastructural level by axoneme loss and misorientation of remaining basal bodies. Downregulation of the master regulator of ciliogenesis Foxj1 occurs prior to extensive cilia loss, implicating this transcription factor in the dedifferentiation of ciliated cells. Motile cilia function is compromised by SARS-CoV-2 infection, as measured in a mucociliary clearance assay. Epithelial defense mechanisms, including basal cell mobilization and interferon-lambda induction, ramp up only after the initiation of cilia damage. Analysis of SARS-CoV-2 infection in Syrian hamsters further demonstrates the loss of motile cilia in vivo. This study identifies cilia damage as a pathogenic mechanism that could facilitate SARS-CoV-2 spread to the deeper lung parenchyma.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34272374 · DOI · PMC8285531
Muc5b overexpression causes mucociliary dysfunction and enhances lung fibrosis in mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The gain-of-function MUC5B promoter variant rs35705950 is the dominant risk factor for developing idiopathic pulmonary fibrosis (IPF).
- Closing excerpt
- Our findings suggest that mucociliary dysfunction might play a causative role in bleomycin-induced pulmonary fibrosis in mice overexpressing Muc5b, and that MUC5B in distal airspaces is a potential therapeutic target in humans with IPF.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
The gain-of-function MUC5B promoter variant rs35705950 is the dominant risk factor for developing idiopathic pulmonary fibrosis (IPF). Here we show in humans that MUC5B, a mucin thought to be restricted to conducting airways, is co-expressed with surfactant protein C (SFTPC) in type 2 alveolar epithelia and in epithelial cells lining honeycomb cysts, indicating that cell types involved in lung fibrosis in distal airspace express MUC5B. In mice, we demonstrate that Muc5b concentration in bronchoalveolar epithelia is related to impaired mucociliary clearance (MCC) and to the extent and persistence of bleomycin-induced lung fibrosis. We also establish the ability of the mucolytic agent P-2119 to restore MCC and to suppress bleomycin-induced lung fibrosis in the setting of Muc5b overexpression. Our findings suggest that mucociliary dysfunction might play a causative role in bleomycin-induced pulmonary fibrosis in mice overexpressing Muc5b, and that MUC5B in distal airspaces is a potential therapeutic target in humans with IPF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30560893 · DOI · PMC6299094
The immunometabolite itaconate stimulates OXGR1 to promote mucociliary clearance during the pulmonary innate immune response [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Pathogens and inflammatory conditions rapidly induce the expression of immune-responsive gene 1 (IRG1) in cells of myeloid lineage.
- Closing excerpt
- Our study thus identifies ITA as a bona fide ligand for OXGR1 and the ITA/OXGR1 paracrine signaling pathway during the pulmonary innate immune response.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (157 words)
Pathogens and inflammatory conditions rapidly induce the expression of immune-responsive gene 1 (IRG1) in cells of myeloid lineage. IRG1 encodes an aconitate decarboxylase (ACOD1) that produces the immunomodulatory metabolite itaconate (ITA). In addition to rapid intracellular accumulation, ITA is also secreted from the cell, but whether secreted ITA functions as a signaling molecule is unclear. Here, we identified ITA as an orthosteric agonist of the GPCR OXGR1, with an EC50 of approximately 0.3 mM, which was in the same range as the physiological concentration of extracellular ITA upon macrophage activation. ITA activated OXGR1 to induce Ca2+ mobilization, ERK phosphorylation, and endocytosis of the receptor. In a mouse model of pulmonary infection with bacterial Pseudomonas aeruginosa, ITA stimulated Oxgr1-dependent mucus secretion and transport in respiratory epithelium, the primary innate defense mechanism of the airway. Our study thus identifies ITA as a bona fide ligand for OXGR1 and the ITA/OXGR1 paracrine signaling pathway during the pulmonary innate immune response.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36919698 · DOI · PMC10014103
Physiology and pathophysiology of mucus and mucolytic use in critically ill patients [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Airway mucus is a highly specialised secretory fluid which functions as a physical and immunological barrier to pathogens whilst lubricating the airways and humifying atmospheric air.
- Closing excerpt
- This review summarises the physiology and pathophysiology of mucus and the existing evidence for the use of mucolytics in critically ill patients and speculates on journey to individualised mucolytic therapy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Airway mucus is a highly specialised secretory fluid which functions as a physical and immunological barrier to pathogens whilst lubricating the airways and humifying atmospheric air. Dysfunction is common during critical illness and is characterised by changes in production rate, chemical composition, physical properties, and inflammatory phenotype. Mucociliary clearance, which is determined in part by mucus characteristics and in part by ciliary function, is also dysfunctional in critical illness via disease related and iatrogenic mechanisms. The consequences of mucus dysfunction are potentially devastating, contributing to prolonged ventilator dependency, increased risk of secondary pneumonia, and worsened lung injury. Mucolytic therapies are designed to decrease viscosity, improve expectoration/suctioning, and thereby promote mucus removal. Mucolytics, including hypertonic saline, dornase alfa/rhDNase, nebulised heparin, carbocisteine/N-Acetyl cysteine, are commonly used in critically ill patients. This review summarises the physiology and pathophysiology of mucus and the existing evidence for the use of mucolytics in critically ill patients and speculates on journey to individualised mucolytic therapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39920835 · DOI · PMC11806889
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Airway mucus function and dysfunction [5]
- Research article Mucus clearance as a primary innate defense mechanism for mammalian airways [6]
- Research article Cilia and Mucociliary Clearance [7]
- Research article Cystic fibrosis [8]
- Research article Mucociliary clearance in the airways [9]
- Research article Airway Epithelial Differentiation and Mucociliary Clearance [10]
References
- Robinot R, Hubert M, de Melo GD, Lazarini F, Bruel T, Smith N, et al.. SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance. . 2021. PMID 34272374 · DOI · PMC8285531
- Hancock LA, Hennessy CE, Solomon GM, Dobrinskikh E, Estrella A, Hara N, et al.. Muc5b overexpression causes mucociliary dysfunction and enhances lung fibrosis in mice. . 2018. PMID 30560893 · DOI · PMC6299094
- Zeng YR, Song JB, Wang D, Huang ZX, Zhang C, Sun YP, et al.. The immunometabolite itaconate stimulates OXGR1 to promote mucociliary clearance during the pulmonary innate immune response. . 2023. PMID 36919698 · DOI · PMC10014103
- Roe T, Talbot T, Terrington I, Johal J, Kemp I, Saeed K, et al.. Physiology and pathophysiology of mucus and mucolytic use in critically ill patients. . 2025. PMID 39920835 · DOI · PMC11806889
- Fahy JV, Dickey BF. Airway mucus function and dysfunction. N Engl J Med. 2010. PMID 21121836 · DOI · PMC4048736
- Knowles MR, Boucher RC. Mucus clearance as a primary innate defense mechanism for mammalian airways. J Clin Invest. 2002. PMID 11877463 · DOI · PMC150901
- Bustamante-Marin XM, Ostrowski LE. Cilia and Mucociliary Clearance. Cold Spring Harb Perspect Biol. 2017. PMID 27864314 · DOI · PMC5378048
- Shteinberg M, Haq IJ, Polineni D, Davies JC. Cystic fibrosis. Lancet. 2021. PMID 34090606 · DOI
- Wanner A, Salathé M, O'Riordan TG. Mucociliary clearance in the airways. Am J Respir Crit Care Med. 1996. PMID 8970383 · DOI
- Whitsett JA. Airway Epithelial Differentiation and Mucociliary Clearance. Ann Am Thorac Soc. 2018. PMID 30431340 · DOI · PMC6322033
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.