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 (733 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 glandular epithelial cell or a unicellular gland. Goblet cells secrete mucus. They are scattered in the epithelial linings of many organs, especially the small intestine and the respiratory tract.
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: Cell, Goblet; Cells, Goblet; Goblet Cell.
Where it fits in the MeSH classification
- Broader topics
- Intestinal Mucosa; Laryngeal Mucosa; Nasal Mucosa; Respiratory Mucosa; Conjunctiva; Epithelial Cells
Related concepts
- Mucus
- Small Intestine
- Respiratory System
Research landscape
PubMed indexes 2,995 records tagged with the MeSH heading “Goblet Cells” (counts retrieved 2026-10-31). 760 of them (25.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,313 records.
Reviews account for 210 records (7.0%) and meta-analyses for 2. Randomized controlled trials number 41 (1.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 48 |
| 2000-2009 | 874 |
| 2010-2019 | 1,313 |
| 2020 onward | 760 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 210 | 7.0% |
| Meta-analyses | 2 | 0.1% |
| Randomized controlled trials | 41 | 1.4% |
Method: PubMed query "Goblet Cells"[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.
SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues [1]
Abstract reading summary — source excerpts
- Opening excerpt
- There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19.
- Closing excerpt
- Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.
- 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)
There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32413319 · DOI · PMC7252096
Novel dynamics of human mucociliary differentiation revealed by single-cell RNA sequencing of nasal epithelial cultures [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The upper airway epithelium, which is mainly composed of multiciliated, goblet, club and basal cells, ensures proper mucociliary function and can regenerate in response to assaults.
- Closing excerpt
- Confirmation of our results on fresh human and pig airway samples, and on mouse tracheal cells, extend and confirm our conclusions regarding the molecular and cellular choreography at work during mucociliary epithelial differentiation.
- 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 (184 words)
The upper airway epithelium, which is mainly composed of multiciliated, goblet, club and basal cells, ensures proper mucociliary function and can regenerate in response to assaults. In chronic airway diseases, defective repair leads to tissue remodeling. Delineating key drivers of differentiation dynamics can help understand how normal or pathological regeneration occurs. Using single-cell transcriptomics and lineage inference, we have unraveled trajectories from basal to luminal cells, providing novel markers for specific populations. We report that: (1) a precursor subgroup of multiciliated cells, which we have entitled deuterosomal cells, is defined by specific markers, such as DEUP1, FOXN4, YPEL1, HES6 and CDC20B; (2) goblet cells can be precursors of multiciliated cells, thus explaining the presence of hybrid cells that co-express markers of goblet and multiciliated cells; and (3) a repertoire of molecules involved in the regeneration process, such as keratins or components of the Notch, Wnt or BMP/TGFβ pathways, can be identified. Confirmation of our results on fresh human and pig airway samples, and on mouse tracheal cells, extend and confirm our conclusions regarding the molecular and cellular choreography at work during mucociliary epithelial differentiation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31558434 · DOI · PMC6826037
Bovine milk-derived exosomes enhance goblet cell activity and prevent the development of experimental necrotizing enterocolitis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Necrotizing enterocolitis (NEC) is characterized by intestinal injury and impaired mucin synthesis.
- Closing excerpt
- This research highlights the potential novel application of milk-derived exosomes in preventing the development of NEC in high-risk infants when breast milk is not available.
- 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 (245 words)
Necrotizing enterocolitis (NEC) is characterized by intestinal injury and impaired mucin synthesis. We recently showed that breast milk exosomes from rodents promote intestinal cell viability, epithelial proliferation, and stem cell activity, but whether they also affect mucus production is unknown. Therefore, the aim of this study was to investigate the effects of bovine milk-derived exosomes on goblet cell expression in experimental NEC and delineate potential underlying mechanisms of action. Exosomes were isolated from bovine milk by ultracentrifugation and confirmed by Nanoparticle Tracking Analysis and through the detection of exosome membrane markers. To study the effect on mucin production, human colonic LS174T cells were cultured and exposed to exosomes. Compared to control, exosomes promoted goblet cell expression, as demonstrated by increased mucin production and relative expression levels of goblet cell expression markers trefoil factor 3 (TFF3) and mucin 2 (MUC2). In addition, exosome treatment enhanced the expression of glucose-regulated protein 94 (GRP94), the most abundant intraluminal endoplasmic reticulum (ER) chaperone protein that aids in protein synthesis. Furthermore, experimental NEC was induced in mouse pups by hyperosmolar formula feeding, lipopolysaccharide administration and hypoxia exposure on postnatal days 5-9. Milk exosomes were given with each gavage feed. NEC was associated with ileal morphological injury and reduction in MUC2+ goblet cells and GRP94+ cells per villus. Exosome administration to NEC pups prevented these changes. This research highlights the potential novel application of milk-derived exosomes in preventing the development of NEC in high-risk infants when breast milk is not available.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30699187 · DOI · PMC6353182
Akkermansia muciniphila outer membrane protein Amuc_0904 modulates intestinal homeostasis by promoting goblet cell differentiation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Akkermansia muciniphila is recognized as a promising probiotic that improves the symptoms of a variety of diseases.
- Closing excerpt
- muciniphila-mediated intestinal homeostasis recovery and provides a bioactive molecule with the potential to treat intestinal disorders.
- 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 (146 words)
Akkermansia muciniphila is recognized as a promising probiotic that improves the symptoms of a variety of diseases. However, the role and mechanism of A. muciniphila in regulating intestinal homeostasis remain to be explored. Here, we discovered that A. muciniphila was dramatically increased during colitis recovery, and its colonization greatly increased goblet cells to protect the intestinal barrier in mice. Amuc_0904, a previously uncharacterized A. muciniphila outer membrane protein, was identified to induce goblet cell differentiation. Mechanistically, Amuc_0904 directly interacted with MET and decreased its phosphorylation in epithelia, leading to decreased Wnt/β-catenin signaling and enhanced oxidative phosphorylation and mitochondrial function. Furthermore, Amuc_0904 and engineered probiotic Escherichia coli Nissle 1917 expressing Amuc_0904 were demonstrated to protect mice from colitis and colitis-associated colorectal cancer. The study reveals a previously unknown mechanism of A. muciniphila-mediated intestinal homeostasis recovery and provides a bioactive molecule with the potential to treat intestinal disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41424360 · DOI · PMC12810044
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 Intestinal goblet cells and mucins in health and disease: recent insights and progress [5]
- Research article The mucus and mucins of the goblet cells and enterocytes provide the first defense line of the gastrointestinal tract and interact with the immune system [6]
- Research article Microbial modulation of innate defense: goblet cells and the intestinal mucus layer [7]
- Research article New developments in goblet cell mucus secretion and function [8]
- Research article The role of goblet cells and mucus in intestinal homeostasis [9]
- Research article Role of hyperosmolarity in the pathogenesis and management of dry eye disease: proceedings of the OCEAN group meeting [10]
References
- Ziegler CGK, Allon SJ, Nyquist SK, Mbano IM, Miao VN, Tzouanas CN, et al.. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues. . 2020. PMID 32413319 · DOI · PMC7252096
- Ruiz García S, Deprez M, Lebrigand K, Cavard A, Paquet A, Arguel MJ, et al.. Novel dynamics of human mucociliary differentiation revealed by single-cell RNA sequencing of nasal epithelial cultures. . 2019. PMID 31558434 · DOI · PMC6826037
- Li B, Hock A, Wu RY, Minich A, Botts SR, Lee C, et al.. Bovine milk-derived exosomes enhance goblet cell activity and prevent the development of experimental necrotizing enterocolitis. . 2019. PMID 30699187 · DOI · PMC6353182
- Yang L, Yang J, Kong X, Tang Q, Song R, Zhou K, et al.. Akkermansia muciniphila outer membrane protein Amuc_0904 modulates intestinal homeostasis by promoting goblet cell differentiation. . 2026. PMID 41424360 · DOI · PMC12810044
- Kim YS, Ho SB. Intestinal goblet cells and mucins in health and disease: recent insights and progress. Curr Gastroenterol Rep. 2010. PMID 20703838 · DOI · PMC2933006
- Pelaseyed T, Bergström JH, Gustafsson JK, Ermund A, Birchenough GM, Schütte A, et al.. The mucus and mucins of the goblet cells and enterocytes provide the first defense line of the gastrointestinal tract and interact with the immune system. Immunol Rev. 2014. PMID 24942678 · DOI · PMC4281373
- Deplancke B, Gaskins HR. Microbial modulation of innate defense: goblet cells and the intestinal mucus layer. Am J Clin Nutr. 2001. PMID 11393191 · DOI
- Birchenough GM, Johansson ME, Gustafsson JK, Bergström JH, Hansson GC. New developments in goblet cell mucus secretion and function. Mucosal Immunol. 2015. PMID 25872481 · DOI · PMC4631840
- Gustafsson JK, Johansson MEV. The role of goblet cells and mucus in intestinal homeostasis. Nat Rev Gastroenterol Hepatol. 2022. PMID 36097076 · DOI
- Baudouin C, Aragona P, Messmer EM, Tomlinson A, Calonge M, Boboridis KG, et al.. Role of hyperosmolarity in the pathogenesis and management of dry eye disease: proceedings of the OCEAN group meeting. Ocul Surf. 2013. PMID 24112228 · DOI
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.