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PubMed1997

Visualization of conjunctival goblet cell actin cytoskeleton and mucin content in tissue whole mounts.

The purpose of the work was to visualize goblet cells, their cytoskeletons, and their content in tissue whole mounts of conjunctiva using confocal microscopy. Conjunctival tissue from rat, mouse, rabbit, and human were excised, fixed in 4% paraformaldehyde, and incubated either with rhodamine-labeled phalloidin to label filamentous actin or in combination with fluoresceinated lectins to label carbohydrates on goblet cell mucins. Tissues were evaluated by confocal microscopy. Phalloidin labeling of excised tissue facilitated visualization of goblet cells within the stratified epithelium of the conjunctiva. Phalloidin labeled the perimeter of the goblet cells, so that either in optical section or three-dimensional constructs of optical sections, the goblet cells appeared as plump empty clusters of cells in rat and mouse and as individual plump empty cells in rabbit and human tissues. Double labeling of excised tissue with lectins demonstrated that the plump cells visualized by labeling with phalloidin bound the label and were indeed goblet cells. At very high resolution one could see individual mucin packets within the goblet cells. Variation in intensity of lectin labeling of these mucin packets both between cells and within cells was evident. Streams of labeled mucin emanating from apical surfaces of goblet cells could be visualized using the fluoresceinated lectins. The labeling of excised conjunctiva with fluorochrome-conjugated phalloidin allows visualization by confocal microscopy of goblet cells within the stratified epithelium. Double labeling with fluorochrome-conjugated lectins allows visualization of their content. These methods may be useful in studies of goblet cell differentiation, mucin content and secretion.

Actins↗

PubMed2003

LPS up-regulates mucin and cytokine mRNA expression and stimulates mucin and cytokine secretion in goblet cells.

Bacterial inflammation in mucosa is accompanied by morphological and proliferative changes in goblet cells and mucin hypersecretion. Main stimulators of bacterial inflammation are bacterial lipopolysaccharides (LPS). In vitro investigation of the LPS effect on the molecular processes in goblet cells, using the human mucin-secreting goblet cell line HT29-MTX, showed the following results. LPS up-regulated mucin and cytokine mRNA expression and secretion in goblet cells in a concentration and time-dependent manner, with a maximum output at an LPS concentration of 100 ng/ml. LPS (100 ng/ml) increased mRNA expression of MUC5AC (2.4x), MUC5B (2.1x), and IL-8 (2.3x) and stimulated secretion of mucins (MUC5AC up to 39%, MUC5B up to 31%) and the inflammatory cytokine IL-8 (up to 10x). A significant correlation was found between the LPS-induced IL-8 secretion and secretion of mucins. These results suggest: (1) goblet cells, responding to the direct stimulation of bacterial LPS by two inflammatory-related processes such as production and secretion of the gel-forming mucins and the inflammatory cytokine IL-8, can be considered as an important part of mucosal immunity and (2) LPS- induced goblet cell mucin secretion can occur partly via IL-8-dependent pathway.

Cell Line↗

PubMed1980

Mechanism of rapid mucus secretion in goblet cells stimulated by acetylcholine.

The parasympathetic control of goblet cell secretion and the membrane events accompanying accelerated mucus release were studied in large intestinal mucosal biopsies maintained in an organ culture system. The secretory response of individual goblet cells to 10(-6) M acetylcholine chloride with 3 x 10(-3) M eserine sulfate (a cholinesterase inhibitor) was assessed by light microscopy and autoradiography, by scanning and transmission electron microscopy, and by freeze-fracture. Goblet cells on the mucosal surface are unaffected by acetylcholine. In crypt goblet cells acetylcholine-eserine induces rapid fusion of apical mucous granule membranes with the luminal plasma membrane (detectable by 2 min), followed by sequential, tandem fission of the pentalaminar, fused areas of adjacent mucous granule membranes. These events first involve the most central apical mucous granules, are then propagated to include peripheral granules, and finally spread toward the most basal granules. By 60 min, most crypt cells are nearly depleted. The apical membrane, although greatly amplified by these events, remains intact, and intracellular mucous granules do not coalesce with each other. During rapid secretion membrane-limited tags of cytoplasm are observed attached to the cavitated apical cell surface. These long, thin extensions of redundant apical membrane are rapidly lost, apparently by being shed into the crypt lumen.

Acetylcholine↗

PubMed2005

MUC5AC expression up-regulation goblet cell hyperplasia in the airway of patients with chronic obstructive pulmonary disease.

OBJECTIVE: To determine the number of goblet cells, the change of MUC5AC expression in chronic obstructive pulmonary disease (COPD) patients and the relationship of smoking with goblet cell, MUC5AC, and lung function. METHODS: Eighteen patients undergoing lung resections for a solitary peripheral carcinoma were classified by lung function as having COPD. Twenty patients with normal lung function served as the control group. Normal lobe bronchioles far away from the lesion site were taken for paraffin section. Goblet cells were identified by AB/PAS staining and the expression of MUC5AC in the paraffin's section was tested by immunohistochemistry. RESULTS: Goblet cell hyperplasia was observed in the COPD group. The positive rate of goblet cell in COPD group (0.20% +/- 0.10%) was significantly higher than that in the normal lung function group (0.13% +/- 0.06%, P < 0.05). The positive rate of MUC5AC expression in the COPD group (0.27% +/- 0.09%) was higher than that in the normal lung function group (0.20% +/- 0.10%, P < 0.05). The positive rate of goblet cell in smokers (27.93% +/- 9.00%) of the COPD group and normal lung function group was higher than that in non-smokers (17.70% +/- 9.37%, P < 0.05), while MUC5AC expression had no significant difference between smokers and non-smokers (17.88% +/- 6.44% and 10.88% +/- 7.10%, respectively). CONCLUSION: For COPD patients with declined lung function, there were goblet cell hyperplasia and increased expression of MUC5AC. MUC5AC expression up-regulation may due to goblet cell hyperplasia. Smoking may be an important factor for goblet cell hyperplasia.

Aged↗

PubMed1983

Conjunctival goblet cell frequency after alkali injury is not accurately reflected by aqueous tear mucin content.

Goblet cell counts have been used to evaluate the suitability of conjunctiva as a source of ocular surface epithelial cells. However, since tear mucin content can be determined without tissue excision, it seemed that the concentration of those compounds might be a useful indicator of conjunctival vitality. To test the extent to which aqueous tear composition reflects conjunctival goblet cell frequency, goblet cell frequency and aqueous tear mucin content were measured after alkali injury in rabbits. Mild alkali injury (0.1 N NaOH for 30 sec) caused a transient but substantial decrease in goblet cells (to 25% of normal at day 7) with a return to normal by six weeks. Tear mucin content was decreased to a lesser degree, from a normal value of 6.4 +/- 0.47 nmol oligosaccharide per microliter (n = 10) to a minimal value of 4.7 +/- 0.64 (n = 7) (73% of normal) at day 7, returning to normal 4 weeks after injury. Thus, the direction of the change was the same, but the magnitudes were quite different. These results suggest that conjunctival goblet cell frequency is not accurately reflected by aqueous tear mucin content, and therefore, that tear mucin content cannot be used directly as an indicator of conjunctival health.

Animals↗

PubMed1996

Effect of oxitropium bromide on histamine-induced airway goblet cell secretion.

To determine whether histamine affects airway goblet cell secretion and, if so, whether cholinergic mechanism is involved, we studied guinea pig airways by a semiquantitative morphometric method. The goblet cell secretion was assessed in histologic sections of the tracheal mucosa stained with Alcian blue and periodic acid-Schiff (PAS) by determining the mucus score, which is inversely related to the magnitude of mucus discharge. Inhaled or intravenously administrated histamine dose dependently decreased the mucus score, an effect that was similarly observed in cartilaginous and muscular portions. Inhalation of the anticholinergic agent oxitropium bromide at doses of 1.5 micrograms and higher greatly attenuated the decrease in mucus score produced by intravenous histamine but not by inhaled histamine. Likewise, cutting of bilateral vagus nerves or atropine abolished intravenous histamine-induced goblet cell secretion. The response of the mucus score to inhaled histamine was abolished by cimetidine, whereas the response to intravenous histamine was reduced by mepyramine but not by cimetidine or thioperamide. These results suggest that inhaled histamine increases airway goblet secretion, probably by stimulating histamine H2-receptors on goblet cells, and that intravenous histamine produces a similar effect through a stimulation of histamine H1-receptor-mediated release of acetylcholine from cholinergic nerve terminals, presumably involving vagal reflex.

Administration, Inhalation↗

PubMed2003

Genetic alterations in goblet cell carcinoids of the vermiform appendix and comparison with gastrointestinal carcinoid tumors.

Goblet cell carcinoid is a relatively rare neuroendocrine tumor of the vermiform appendix with poorly understood molecular pathogenesis. We studied the clinicopathologic features and genetic alterations, including allelic loss of chromosomes 11q, 16q, and 18q; sequencing of the K-ras, beta-catenin, and DPC4 (SMAD4) genes; and p53 overexpression and loss of DPC4 by immunohistochemistry; in 16 goblet cell carcinoids. We compared the allelic loss in goblet cell carcinoids to those in 18 gastrointestinal carcinoid tumors. For goblet cell carcinoids, appendiceal perforation was the most common (70%, 7/10) clinical presentation. The mean tumor size was 2.0 +/- 1.5 cm (range, 0.4 to 4.5 cm). The tumor invaded to appendiceal serosa in 50% (8/16) of patients, and two patients had metastasis in lymph nodes or adjoining viscera. With mean follow-up of 24 +/- 14 months (median, 23 mo), 1 of 10 patients had died of disease, and 2 others had tumor recurrence. All four patients with metastases, recurrences, and/or death from disease had serosal involvement at presentation (P =.02). Loss of heterozygosity of chromosome 11q was present in 25% of goblet cell carcinoids, 14% of ileal carcinoid tumors, and 9% of nonileal carcinoid tumors; of chromosome 16q in 38%, 29%, and 0 (P =.02); and of chromosome 18q in 56%, 86%, and 9% (P =.002), respectively. No mutations of K-ras, beta-catenin, or DPC4 genes; p53 overexpression; or loss of staining for DPC4 was present in any tumors. These findings suggest that allelic loss of chromosomes 11q, 16q, and 18q in goblet cell carcinoids and ileal carcinoids may have an important role in the pathogenesis of these tumors.

Adult↗

PubMed2006

Role of mast and goblet cells in the pathogenesis of nasal polyps.

In this study, the role of mast and goblet cells and eosinophils in the pathogenesis of nasal polyposis was investigated. The study group consisted of 28 adult patients (15 males, 13 females) with nasal polyposis who underwent functional endoscopic sinus surgery (FESS). All patients in the study group were examined with a questionnaire, an otolaryngologic examination, an endoscopic examination with 0 degrees and 30 degrees endoscopes, Waters' graphy, and axial and coronal computed tomography of the paranasal sinuses. The control group consisted of 10 adult patients without nasal polyp (7 males and 3 females) who underwent septoplasty. They gave written approval to enter the study. The polyp specimens from the study group were excised from four regions: the maxillary sinus, ethmoid sinus, sphenoid sinus, and nasal cavity. They were examined at x400 magnification by light microscopy, and only the slides with polypoid tissue were included in the study. Slides including a chronic inflammatory process without polypoid tissue were excluded from the study. The control group was composed of the slides of specimens from the inferior turbinate. Forty slides (10 in each group) in the study group and 10 slides in the control group were included in the study. The surgical specimens from the study and control groups were examined with a histochemical staining technique. In every surgical specimen, the type of epithelium and the numbers of goblet and mast cells and eosinophils were calculated in x400 high-magnification field in 10 areas on light microscopy, as well as the mean number of these cells, and for mast cells separately, cell count in the epithelium and the stromal layer of polyp tissue and total mast cell count, including both epithelial and stromal mast cells, were identified. Goblet cells, mast cells, and inflammation with eosinophils were observed in all sinonasal mucosa. The common epithelial type in the polyp tissue was pseudostratified ciliated cylindric epithelium, which contains goblet cells. Goblet cell numbers in the maxillary, ethmoid, and sphenoid sinuses and nasal cavity were found to be significantly higher than in the control group (p < .05). For total mast cell and eosinophil count, no statistically significant difference was found between all five groups. In each group, there was no statistically significant difference between goblet and mast cells. Increased goblet cells in sinonasal polyps indicated that systemic factors also affect nasal polyposis as much as local factors, such as airflow and mucosal contact. Surgical treatment of sinonasal polyps by FESS causes more sufficient air ventilation in the nasal cavity and paranasal sinuses. Therefore, the goblet cell density will decrease because of the exposure of the mucosal surfaces to the air. In particular, FESS and then the appropriate medical treatment may decrease the recurrence rates and increase the patient's comfort. The significantly increased goblet cell count in the sinonasal mucosa demonstrated the importance of these cells in the pathogenesis of nasal polyposis. Also, mast cells and eosinophils may have a role in the inflammatory processes, leading to nasal polyposis formation.

Adolescent↗

PubMed1976

The influence of 400 r x-irradiation on the number and the localization of mature and immature goblet cells and Paneth cells in intestinal crypt and villus.

The influence of 400 R X-irradiation on the localization and the number of mature and immature goblet cells and Paneth cells in rat duodenal epithelium has been studied. At short times after irradiation, when the total proliferative activity in the crypts of Lieberkuhn is reduced, the proportion of mature and immature goblet cells of the total number of crypt cells was increased; also an absolute increase in the number of goblet cells in the crypts was found. The immature goblet cells were localized in the lower half of the crypt as in control animals, whereas the number of the mature cells increased over the whole crypt length. When the proliferative activity of the crypt cells increases again from 12 to 48 hr after irradiation the number of both types of goblet cells decreases. Between 48 and 72 hr, when the whole crypt is involved in proliferation, a second increase of both types of goblet cells was found. However, the localization of the immature goblet cells is no longer restricted to the lower half of the crypt but they also appear at the higher cell positions. On the villus no immature goblet cells were found and the changes in the numbers of mature goblet cells do reflect the changes induced by irradiation in the goblet cell population in the crypt. The absolute number and localization of Paneth cells did not change under the experimental conditions. The findings are discussed in relation to cell proliferation and differentiation processes in intestinal crypts.

Animals↗

PubMed2001

Stat6 dependent goblet cell hyperplasia during intestinal nematode infection.

To identify the role of signal transducer and activator of transcription factor 6 (Stat6) in the development of intestinal goblet cell hyperplasia during nematode infection, we compared the number of goblet cells in Stat6 deficient (Stat6 -/-) mice with that generated in wild-type (Stat6 +/+) mice in Trichinella spiralis infection. The number of goblet cells significantly increased with infection in wild-type mice. However, Stat6 -/- failed to generate infection-induced goblet cell hyperplasia and a significantly lower number of goblet cells was observed in Stat6 -/- mice on days 14 and 21 postinfection compared to Stat6 +/+ mice. In addition to suppressed goblet cell numbers, Stat6 -/- mice exhibited severe impairment in their ability to produce IL-4 and IL-13 and to expel the parasites from the gut. Our study clearly shows an essential role of Stat6 in intestinal goblet cell hyperplasia which accompanies this infection. We postulate that Th2 cytokines regulate the development of goblet cell hyperplasia in gut during nematode infection via Stat6 activation and that the increased number of goblet cells plays an important role in host protective immunity against the infection.

Animals↗

PubMed2001

Microbial modulation of innate defense: goblet cells and the intestinal mucus layer.

The gastrointestinal epithelium is covered by a protective mucus gel composed predominantly of mucin glycoproteins that are synthesized and secreted by goblet cells. Changes in goblet cell functions and in the chemical composition of intestinal mucus are detected in response to a broad range of luminal insults, including alterations of the normal microbiota. However, the regulatory networks that mediate goblet cell responses to intestinal insults are poorly defined. The present review summarizes the results of developmental, gnotobiotic, and in vitro studies that showed alterations in mucin gene expression, mucus composition, or mucus secretion in response to intestinal microbes or host-derived inflammatory mediators. The dynamic nature of the mucus layer is shown. Available data indicate that intestinal microbes may affect goblet cell dynamics and the mucus layer directly via the local release of bioactive factors or indirectly via activation of host immune cells. A precise definition of the regulatory networks that interface with goblet cells may have broad biomedical applications because mucus alterations appear to characterize most diseases of mucosal tissues.

Animals↗

PubMed2000

The pathogenesis of duodenal gastric metaplasia: the role of local goblet cell transformation.

BACKGROUND AND AIMS: Gastric metaplasia is frequently seen in biopsies of the duodenal cap, particularly when inflamed or ulcerated. In its initial manifestation small patches of gastric foveolar cells appear near the tip of a villus. These cells contain periodic acid-Schiff (PAS) positive neutral mucins in contrast with the alcian blue (AB) positive acidic mucins within duodenal goblet cells. Previous investigations have suggested that these PAS positive cells originate either in Brunner's gland ducts or at the base of duodenal crypts and migrate in distinct streams to the upper villus. To investigate the origin of gastric metaplasia in superficial patches, we used the PAS/AB stain to distinguish between neutral and acidic mucins and in addition specific antibodies to immunolocalise foveolar cell mucin MUC5AC, the foveolar cell secretory product, gastric trefoil factor (TFF1), the mature goblet cell mucin MUC2, and MUC2 core antigen. RESULTS: Cells in focal patches of gastric metaplasia contained secretory granules of both gastric and goblet cell phenotypes. MUC5AC and TFF1 were present as expected in gastric foveolar cells but in addition, MUC2 core antigen, normally present only in the Golgi of intestinal goblet cells, was expressed in secretory granules. Goblet cells in the vicinity of metaplastic patches also expressed both gastric and intestinal antigens. MUC5AC/MUC2 containing goblet cells were most common near the villus tip but were also seen at the base of crypts. Where crypts and Brunner's gland ducts merged they were always seen on the crypt side of the junction. Goblet cells were the only cells to express gastric antigens in these areas. In advanced metaplastic lesions, dual phenotype goblet cells were less evident and fewer cells expressed intestinal mucin antigens. CONCLUSIONS: We suggest that goblet cells that express both intestinal and gastric antigens may represent local precursors of gastric metaplasia undergoing a transition to foveolar-like cells of mixed phenotype at the site of early metaplastic patches. As metaplasia becomes more widespread, a more pure gastric phenotype emerges. This progression is likely to be controlled by local inflammatory signals.

Adolescent↗

PubMed1988

Human intestinal goblet cells in monolayer culture: characterization of a mucus-secreting subclone derived from the HT29 colon adenocarcinoma cell line.

HT29-18N2 (N2) cells, a subclone of the HT29 human colon carcinoma cell line, are shown in this report to be a model system for the study of human goblet cell differentiation and mucin secretion. Grown in the absence of glucose, these cells formed homogeneous epithelial monolayers of columnar cells with typical goblet cell morphology. Differentiation occurred on uncoated glass; laminin, fibronectin, or collagen type I or IV did not enhance differentiation. HT29-18N2 cells grown on uncoated or matrix-coated permeable filters formed differentiated monolayers, but mucin granules within some of these cells polarized along intraepithelial lumens. Polyclonal antibodies raised against purified human colonic mucin, and also a monoclonal antibody against a protease-sensitive epitope of human colonic mucin, stained secretory granules of all differentiated goblet cells within N2 cell monolayers but did not stain predifferentiated goblet cells lacking large secretory granules. Monoclonal antibodies against specific carbohydrate sequences of human mucins also failed to stain N2 cells before differentiation, but recognized varying fractions of differentiated N2 goblet cells. Autoradiographic visualization of radiolabeled glycoproteins demonstrated transport and secretion of N2 cell mucin granules. Cholinergic stimulation of differentiated N2 cell monolayers resulted in depletion of intracellular mucin granules.

Adenocarcinoma↗

PubMed1990

"Mucin types" in normal and neoplastic colonic goblet cells: a mucin histochemical study.

Goblet cells in normal colon mucosa from 100 individuals histochemically showed two major "mucin types" in sialic acid composition. One type revealed mixed reactivities for N-acetyl-neuraminic acid (NANA, abbreviated C0), 7-O- acylated NANA (C7) and 9-O-acylated NANA (C9), and represented 25% of the individuals examined. The other type of mucin, seen in 69% of the cases, exhibited reactivity for 8-O-acylated NANA or pluri-O-acylated NANA (C8). C0 and C8 were observed simultaneously in 5% of the individuals. In addition, 8% displayed a mosaic pattern in which isolated "blue" crypts containing sialic acids of the C0 + C7 + C9 type were detected in the "red" colonic mucosa, which was predominantly C8. Little correlation was found between the mucin types and their site in the colon, or with the age, sex, ABO blood groups and degree of sulphation. O-acylated NANA was also observed, though reduced in amount, in all 22 colonic adenocarcinomas in which evaluable numbers of neoplastic goblet cells were found. The mucin types in colon cancer were fundamentally indistinguishable from those seen in the surrounding noncancerous colonic mucosa.

Adenocarcinoma↗

PubMed2000

Expression of MUC5AC mRNA in the goblet cells of human nasal mucosa.

OBJECTIVES/HYPOTHESIS: Mucus hypersecretion is a common feature in chronic sinusitis with polyps. Because mucus hypersecretion is commonly accompanied by goblet cell hyperplasia, it is important to identify which mucin gene mRNAs are expressed in the goblet cells of the surface epithelium in the human airway. This study aims to investigate the pattern of expression of MUC5AC messenger RNA (mRNA) in the goblet cells of human nasal mucosa. METHODS: Six nasal polyps, five inferior turbinate mucosa specimens, and three normal-appearing mucosa specimens of the posterior ethmoid sinus were obtained. Each of the specimens was cut into 10-microm-thick serial frozen sections, and in situ hybridization of MUC5AC mRNA was performed with an oligonucleotide probe. Alcian blue (pH 2.5)-periodic acid-Schiff (AB-PAS) staining was performed on the serial sections. RESULTS: In human nasal polyps, MUC5AC mRNA was expressed in the cytoplasm of most of the goblet cells. However, in the inferior turbinate, MUC5AC mRNA was expressed in only some of the goblet cells. On the contrary, in the normal-appearing mucosa of the posterior ethmoid sinus, MUC5AC mRNA was barely expressed in the goblet cells. Furthermore, MUC5AC mRNA was mainly expressed in some of the PAS-positive goblet cells. CONCLUSIONS: Only a portion of the goblet cells in the human nasal mucosa expressed MUC5AC mRNA. This result suggests that surface goblet cells might have other mucin genes, in addition to MUC2 and MUC5AC.

Goblet Cells↗

PubMed1996

Histochemical, lectin-histochemical and morphometrical characteristics of intestinal goblet cells of germfree and conventional mice.

Histochemical, lectin-histochemical and morphometrical studies were carried out on intestinal goblet cells of 8-week-old germfree (GF) and conventional (CV) mice of the BALB/c strain. Except for the reactivity of cecal goblet cells to Dolichos biflorus agglutinin (DBA) and Ulex europeus-I agglutinin (UEA-I), there was no difference between GF and CV mice in histochemical and lectin-histochemical properties. In the cecal mucosa, DBA stained the goblet cells strongly in CV mice but not in GF mice and UEA-I stained the goblet cells strongly in the lower part of crypts in CV mice but only faintly in GF mice. These findings suggest that terminal residues of cecal goblet cell mucin were different in GF and CV mice. Morphometrically, cecal goblet cells were fewer in number and smaller in size in GF mice than in CV mice. In addition, high iron diamine-alcian blue staining made a very clear border between the cecum and colon, because cecal goblet cells were exclusively positive for sulfomucin and colonic goblet cells were predominantly positive for sialomucin.

Alcian Blue↗

PubMed1998

Platelet-activating factor induces goblet cell hyperplasia and mucin gene expression in airways.

In patients dying from asthma, extensive mucous plugging occurs in the airways, associated with goblet cell hyperplasia. In this study, we examined the hypothesis that platelet-activating factor (PAF) induces goblet cell hyperplasia and mucin gene expression. After instilling PAF into the airways of guinea pigs and rats, we stained airway goblet cells with Alcian blue/periodic acid-Schiff and determined the number of goblet cells and percentage of stained area within the epithelium. In guinea pigs, one instillation of PAF (10(-)5 M, 100 microl) increased the goblet cell-stained area time-dependently, beginning at 24 h, maximum at 72 h. PAF also caused tracheal recruitment of eosinophils by 24 h, maximum at 48 h. In rats, which have few goblet cells in airways, PAF (3 instillations, 10(-)5 M, 200 microl) caused striking goblet cell hyperplasia, greatest in peripheral airways. Tumor necrosis factor alpha (TNFalpha) alone had no significant effect on goblet cells, but together with PAF, it caused exaggerated goblet cell hyperplasia. In rat tracheas studied by in situ hybridization, PAF induced mucin MUC5 gene expression in epithelial cells that stained for mucosubstances. In summary, PAF induces goblet cell hyperplasia and TNFalpha potentiates this effect.

Animals↗

PubMed1984

Goblet cells in the normal adult human larynx--studies on morphology, distribution and density.

From 12 clinically and macroscopically normal larynges from adult persons all the mucosa was prepared and stained with PAS-alcian blue to study the morphology, distribution, and density of the goblet cells. In each larynx goblet cells were counted in 600 fields of 0.01768 mm2 mucosal surface, distributed on 18, 18 and 24 localities in the subglottis, glottis with the sinus of Morgagni, and supraglottis respectively. The goblet cells form a continuous pattern, comprising the entire subglottis, the anterior commissure, the sinus of Morgagni, the false vocal cords, vestibule of the larynx, and reaching to the cranial part of the laryngeal surface of the epiglottis. Another continuous, but goblet cell-free area extended from a couple of mm posterior to the anterior commissure, posteriorad on the cranial surface of the vocal cords, ary regions, aryepiglottic fold, the edge of the epiglottis, and 4-5 mm of the laryngeal surface of the epiglottic top, epiglottic vallecula, piriform recess, and the postcricoid region. Between the pseudostratified, ciliated columnar epithelium with goblet cells and the goblet cell-free stratified squamous epithelium there is a transitional epithelium in which the goblet cells alter from the 40 micron tall goblet cells characteristic of the respiratory tract epithelium to being quite flattened in order to disappear completely in the stratified squamous epithelium. The goblet cell density is significantly lower in the subglottis, viz. 125 cells per field, than in the glottis with the sinus of Morgagni and supraglottis, where the median density is 166 and 161 cells respectively per field. A possible correlation between the influence of the respiratory air upon the density of goblet cells and the complex anatomy of the larynx is discussed.

Adult↗