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PubMed2001

Goblet cell density in acute otitis media caused by Moraxella catarrhalis.

HYPOTHESIS AND BACKGROUND: Secretory otitis media is associated with a highly increased goblet cell density, confirming the secretory pathogenesis of this disease. Previous studies have shown that the middle ear goblet cell density, and thus the secretory capacity, are massively increased during experimental acute otitis media and at least 6 months thereafter, conceivably predisposing to the subsequent development of secretory otitis media. These studies used middle ear inoculation of either Streptococcus pneumoniae, nontypeable Haemophilus influenzae, or H. influenzae type b. The present study aimed at determining the goblet cell density during and after acute otitis media caused by Moraxella catarrhalis to clarify whether this bacterium induces an equivalently enhanced secretory capacity. METHODS: Twenty-five 25 rat middle ears were inoculated with M. catarrhalis. Five rats were killed on days 4, 8, 16, 60, and 180 after inoculation, followed by staining, dissection, and whole-mount embedding of the middle ear mucosae. The goblet cell density was determined by counting in 24 fields, covering the entire middle ear. RESULTS: In comparison with 25 normal middle ears, the goblet cell density was significantly increased in almost all counting localities, from day 4 and < or = 2 months after inoculation. The goblet cell density peaked on day 16, subsided thereafter, and in some areas reached a normal level 6 months after the acute incident. Mucosal areas containing goblet cells were consistently enlarged, thus leaving the middle ear with an increased secretory capacity during and 6 months after inoculation. CONCLUSION: The goblet cell density of the middle ear mucosa is increased during acute otitis media caused by M. catarrhalis and up to several months thereafter. This may predispose to the subsequent development of secretory otitis media. However, in comparison with acute otitis media caused by other bacteria, M. catarrhalis induced only modest changes in goblet cell density.

Acute Disease↗
PubMed1988

Morphogenesis of rat conjunctival goblet cells.

Conjunctival flat-mount preparations stained with alcian blue and PAS were used to study the development and mucin differentiation of conjunctival goblet cells in Sprague-Dawley rats from newborn to 17 months of age. In the neonatal conjunctiva, only single goblet cells containing primarily acidic mucin (alcian-blue positive) were noted. With the increase of age, the rat conjunctival goblet cells were in clusters with heterogeneous mucin contents, which differ from the nonclustered, single goblet cells of human and rabbit conjunctiva. Topographical analysis revealed that the density and size of goblet cell clusters were highest in the forniceal zone, with gradual decrease towards the bulbar and orbital zones. and were absent in the limbal and tarsal conjunctiva in all ages. The goblet cells in the forniceal zone contained predominantly acidic mucin in all ages, except that selective loss of acidic mucin with vacuolation of the clusters was noted in the 17-month-old rats. Despite the fact that the size of the goblet cell clusters increased with age, the overall density of the clusters remained rather constant throughout the ages studied. These results indicate that each goblet cell cluster may derive from a single progenitor (stem) cell and represents a glandular primordium, and that goblet cell development and mucin differentiation are modulated by the aging process.

Animals↗
PubMed1991

Effect of topical corticosteroids on goblet-cell density in an alkali-burn model.

Conjunctival alkali burns result in a loss of goblet cells in the acute postinjury period. A deficiency of goblet cells and their primary product, mucin, is associated with both short- and long-term ocular sequelas. We evaluated the effect of topical corticosteroids on goblet-cell density in a prospective, randomized, controlled trial using 24 eyes of 12 adult albino rabbits in which a standard conjunctival burn was made. The treatment group was found to have 97.38 goblet cells per unit area of conjunctiva; the control group had 65.81 goblet cells per unit area of conjunctiva. This was a statistically significant difference (P less than .02). These results suggest that topical steroids are beneficial in suppressing goblet-cell loss after a conjunctival alkali burn.

Administration, Topical↗
PubMed2006

Calcium signaling in human airway goblet cells following purinergic activation.

Despite the general importance of Ca(2+) signaling in signal transduction, and of goblet cell mucin hypersecretion in inflammatory pulmonary diseases, measurement of airway goblet cell intracellular Ca(2+) (Ca(i)(2+)) has not been reported. In this article, we describe the results of experiments measuring Ca(i)(2+) in primary cultures of human bronchial goblet cells after stimulation with the purinergic agonist adenosine 5'-O-(3-thiotriphosphate) (ATPgammaS) and phorbol 12-myristate 13-acetate (PMA). Ca(2+) signaling in human goblet cells after purinergic stimulation follows the classic paradigm of a Ca(i)(2+) transient from a basal activity of 110 nM to a peak response of 260.1 +/- 41.2 nM within 2 min, followed by a long superbasal plateau (155.3 +/- 0.2 nM) between 10 and 15 min. The rise in Ca(i)(2+) appears to result from a mobilization of intracellular stores, because the transient was nearly abolished by inhibition of PLC with the phosphatidylinositol-specific PLC inhibitor U-73122, and it was not affected significantly by removal of extracellular Ca(2+). Loading goblet cells with BAPTA inhibited the ATPgammaS-induced Ca(2+) transient by 86.0 +/- 13.1%, relative to control. Finally, in contrast to the massive effects of high doses of PMA (300 nM) on mucin secretion from goblet cells, phorbol ester stimulated a small (27.1 +/- 7% of the ATPgammaS control peak), brief rise in Ca(i)(2+). This diminutive signal likely denotes a local Ca(2+) gradient, which may be associated with the mucin granule exocytotic process.

Adenosine Triphosphate↗
PubMed1996

Vasoactive intestinal peptide-stimulated glycoconjugate secretion from conjunctival goblet cells.

We have developed an in vitro and in vivo method to determine if VIP-stimulates conjunctival goblet cell secretion in the rat as nerves which contain vasoactive intestinal peptide (VIP) and are most likely parasympathetic are localized around these cells. For the in vitro method, pieces of rat conjunctiva were incubated for 1 hr with no additions or increasing concentrations of VIP (10(-10)-10(-6)M). Goblet cell secretion was measured by determining the amount of Helix pomatia agglutinin (HPA)-detectable glycoconjugates secreted into the medium. HPA-detectable glycoconjugates were assayed using an enzyme-linked lectin assay. For the in vivo method, drops of buffer containing no additions or varying concentrations of VIP (10(-10)-10(-6) M) were placed on the ocular surface of anesthetized rats for 60 min. The rats were killed, the ocular surface chemically fixed, and a button of conjunctiva removed. Mucin-containing goblet cells were stained by Alcian blue-periodic acid Schiff's reagent and the number of cells per 0.16 mm2 was quantified. A decrease in the number of mucin-containing goblet cells indicated an increase in mucous secretion. By immunofluorescent histochemistry, we found that the lectin HPA was localized predominantly in the secretory granules of rat conjunctival goblet cells with little binding present in the remainder of the conjunctiva. Nerves containing VIP surrounded goblet cells labelled with HPA. In pieces of conjuctiva, in vitro VIP (10(-8)-10(-6) M) stimulated HPA-detectable glycoconjugate secretion in a concentration dependent manner. When applied topically to the ocular surface, in vivo VIP AT 10(-8) M stimulated mucous secretion from conjunctival goblet cells. We conclude that VIP is present in nerves around conjunctival goblet cells and stimulates glycoconjugate secretion from these cells.

Animals↗
PubMed1981

Goblet cells of the human conjunctiva.

We correlated histologic findings concerning conjunctival goblet cells with findings concerning the mucous membrane surfaces of the conjunctiva. Ten biopsy specimens were obtained from the upper tarsal conjunctiva and ten from the perilimbal bulbar conjunctiva. Changes in goblet cells just before and during secretion included changes in surface cell diameter, evagination of the apical surface of the cell membrane, decrease in the number of microvilli, and alteration in the arrangement and morphologic characteristics of microvilli. Changes seen by light and transmission electron microscopy correlated with those observed by scanning electron microscopy. Goblet cells were often associated with crypt openings; some crypts served as conduits for the secretion of mucus from underlying goblet cells. This study supports the hypothesis that crypts in the conjunctiva seen by scanning electron microscopy are often associated with goblet cells and their mucus secretion.

Adult↗
PubMed1990

Cytoskeleton of intestinal goblet cells: role of actin filaments in baseline secretion.

Although microtubules appear necessary to maintain mucin granule transport in intestinal goblet cells, the role of microfilaments in mucus secretion is unknown. To determine the functional significance of microfilaments in goblet cell secretion, fluorescent cytochemistry of microfilaments and autoradiographic studies on granule movement were performed on rabbit intestinal goblet cells, with and without the actin depolymerizing agents, cytochalasin D (cyto D), and dihydro-cytochalasin B (dihydro B). In normal goblet cells, cytochemical localization of F-actin with NBD-phallacidin demonstrated their restriction to the apical surface of the goblet cell. Visualization of the goblet cell apical surface by electron microscopy revealed the presence of a thin layer of cytoplasm overlying the granule mass. Treatment with cyto D and dihydro B eliminated NBD-phallacidin staining of the apical cell surface. Quantitative analysis of baseline granule translocation demonstrated that treatment with cyto D and dihydro B resulted in dramatic acceleration of granule movement through goblet cells. This cellular response results from an increase in baseline secretion and facilitation of secretion of newly synthesized mucins, not stimulation of an accelerated secretory event. These data imply that actin filaments fulfill a barrier function in baseline secretion by hindering granule access to the plasma membrane; once the granule contacts the plasma membrane, exocytosis occurs. Secretion is balanced by the translocation of subjacent granules. In contrast, an accelerated secretory event is not triggered by plasma membrane access alone; this event requires a regulatory signal. We hypothesize that, unlike accelerated secretion, baseline secretion is constitutive, with exocytosis limited solely by the physical constraint of secretory granule access to the apical plasma membrane.

Actins↗
PubMed1998

Goblet cell carcinoid of the appendix endoscopically diagnosed and examined with p53 immunostaining.

We report a case of a 62-year-old woman with goblet cell carcinoid of the appendix. She was admitted to our hospital in September 1994 after the discovery of liver tumors. After admission, a tumor in the right kidney and multiple tumors in the liver were found. She was diagnosed with renal cell cancer and metastasis to the liver and underwent excision of the kidney and enucleation of the largest liver tumor. Histological examination revealed that the liver tumor was a metastatic carcinoid tumor. As carcinoid tumors have frequently been found in the appendix, endoscopic examination was performed and a lesion was found in the appendix by colonoscopy. As predicted, the biopsy specimen was a carcinoid tumor, and she underwent an appendectomy. Histologically, the tumor was a goblet cell carcinoid. Goblet cell carcinoid is a rather rare neoplasm that has the histologic features of both carcinoids and adenocarcinoma. Forty-two cases of goblet cell carcinoid of the appendix have been reported thus far in Japan. However, few were diagnosed via endoscopic examination before surgical operation. We also carried out an immunohistochemical study with anti p53 antibody on the goblet cell carcinoid tumor of the appendix. Most tumor cells were strongly positive, while in three benign carcinoid tumors investigated simultaneously they were negative. These findings suggest that goblet cell carcinoid has an aggressive phenotype compared with benign carcinoid tumors.

Appendiceal Neoplasms↗
PubMed2005

Ferroportin is expressed on the mucous granule membrane of a subpopulation of goblet cells in the duodenum of the rat.

Ferroportin is a basolateral transporter involved in the release of iron from cells. In addition to expression on the basolateral membrane of enterocytes, ferroportin is also seen on the microvillus membrane. This led us to consider that ferroportin might be expressed by other cells of the intestine where it contributes to iron metabolism. Ferroportin gene and protein expression in rat duodenum was studied by in situ hybridisation and immunohistochemistry, respectively in rats with different efficiencies of iron absorption. Ferroportin mRNA localised to enterocytes of the villus only. Ferroportin was demonstrated in enterocytes and in 30% of goblet cells. In goblet cells it localised to the mucous granule membrane. In iron-loaded intestine some goblet cells contained iron suggesting that ferroportin may transport iron into the mucous granule where it would be lost during discharge of mucous. The finding of ferroportin in iron deficient goblet cells also suggests an additional role to iron excretion.

Animals↗
PubMed2001

Goblet cell carcinoids of the appendix: immunophenotype and ultrastructural study.

BACKGROUND: Goblet cell carcinoids of the appendix are rare neoplasms with uncertain biological behavior. OBJECTIVE: The aims of our study were to evaluate the immunophenotype of this neoplasm with cell cycle/cell proliferation markers and to understand their histogenesis with ultrastructural analysis using conventional carcinoids as a frame of reference. METHODS: Clinical data and archival pathologic material of all goblet cell carcinoids of the appendix recorded by the Saskatchewan Cancer Registry between 1970 and 1998 were reviewed and evaluated by light microscopy, histochemistry, immunohistochemistry, and electron microscopy. RESULTS: Seven cases of goblet cell carcinoids were identified among 110 cases of conventional carcinoids of the appendix. Histopathology revealed widespread infiltration of the periappendiceal fat in all cases, with extensive perineural invasion. The cells stained strongly positive for mucicarmine, periodic acid-Schiff, periodic acid-Schiff diastase, Alcian blue, cytokeratin, and carcinoembryonic antigen. Most cases were positive for synaptophysin. Increased expression of cell proliferation markers and cell cycle markers was observed. Expression of p53 was strong in one case. Electron microscopy demonstrated the presence of mucinous vacuoles of varying sizes and occasional membrane-bound neuroendocrine granules. CONCLUSIONS: Goblet cell carcinoids of the appendix arise from a pluripotent cell with divergent neuroendocrine and mucinous differentiation. These neoplasms are widely invasive; they demonstrate a high cellular proliferation rate and dysregulation of the cell cycle with up-regulation of cyclin D1 and p21, and down-regulation of p16. Complete removal of the tumor is recommended because of the unpredictable biological behavior of this tumor, which includes delayed local recurrences and lung metastases.

Adult↗
PubMed1976

The fine structural localization of peroxidase activity in goblet cells of the conjunctival epithelium of rats.

Cytochemical investigation of peroxidase was made on the conjunctival goblet cells, using the diaminobenzidine method. Many goblet cells in the conjunctiva demonstrated this reaction. The reaction was present in secretory granules as well as in the perinuclear cisterna, the rough endoplasmic reticulum, several Golgi saccules and adjacent small smooth-surfaced vesicles, and condensing vacuoles. Each secretory granule within a goblet cell showed a different degree of reaction, hence it is concluded that some goblet cells probably produce both mucous substance and peroxidase in one cell. The mode of production of peroxidase in goblet cells is concluded to be similar to that of secretory proteins in pancreatic exocrine cells. The enzyme, together with thiocyanate and endogenous hydrogen peroxide, is thought to serve as an anti-infectious agent in tears.

Amitrole↗
PubMed1996

Hypertrophic and metaplastic changes of goblet cells in rat nasal epithelium induced by endotoxin.

To elucidate the mechanisms of epithelial mucus hypersecretion in upper respiratory airway inflammation, we produced hypertrophic and metaplastic changes of goblet cells in rat nasal respiratory epithelium by intranasal instillation of endotoxin. Significant increase of hypertrophic goblet cells was induced in the septal epithelium transversely sectioned at the level of incisive papilla at 24 h after the intranasal instillation of 0.1 mg of endotoxin. This change was completed after 3 d of endotoxin instillations and recovered by normal epithelium 7 d after the last instillation. Total cell number and the number of basal and ciliated cells counted over 2 mm of basal lamina did not change; however, the number of goblet cells increased and that of nongranulated secretory cells decreased time-dependently after endotoxin instillations. Mitotic rates examined after a 6-h colchicine metaphase blockade were very low at any time point studied, and cell division did not play a major role in this process. These results indicate that endotoxin induces hypertrophic and metaplastic changes of goblet cells in rat nasal epithelium rather than a hyperplastic change, and this metaplasia is produced by direct conversion of nongranulated secretory cells into the goblet cells. Histochemical examination of this epithelium revealed that most of the mucus produced by these goblet cells was sulfomucin. Intraperitoneal injection of antirat neutrophil antiserum or cyclophosphamide depleted circulating blood neutrophils. Endotoxin-induced changes of goblet cells were significantly inhibited in these neutrophil-depleted rats, and intranasal instillation of elastase also induced hypertrophic and metaplastic changes of goblet cells.

Animals↗
PubMed1991

Effects of Yersinia enterocolitica infection on rabbit intestinal and colonic goblet cells and mucin: morphometrics, histochemistry, and biochemistry.

The effects of Yersinia enterocolitica on intestinal goblet cells were investigated in New Zealand white rabbits. Animals infected with Y enterocolitica were compared with weight matched and pair fed controls. Goblet cell hyperplasia developed in the distal small intestine of infected rabbits on day 1, in the mid small intestine on day 3, and in the upper small intestine on day 6. In all regions hyperplasia persisted throughout the 14 day study. The degree of hyperplasia was greater in the distal small intestine than the upper and mid regions. Goblet cells in the proximal colon of infected animals seemed to respond as those in the distal small intestine. Thus goblet cell hyperplasia developed more rapidly and to a greater extent in the ileocaecal region where mucosal injury was most severe. These changes resulted directly from Y enterocolitica infection since goblet cell numbers did not increase in pair fed controls. Histochemically, goblet cell mucins from infected rabbits were unchanged at either six or 14 days. Biochemical analysis, however, established that purified mucins from animals on day 6 after infection were less sialylated (in the small intestine) and more sulphated (in the small intestine and proximal colon). In addition, mucins from the distal small intestine and the proximal colon seemed to contain fewer but longer oligosaccharide chains.

Amino Acids↗
PubMed2002

Interleukin-13 induces goblet cell differentiation in primary cell culture from Guinea pig tracheal epithelium.

The Th2 cytokines, interleukin (IL)-4 and IL-13, bind to IL-4Ralpha, and cause goblet cell metaplasia/hyperplasia with increased mucin expression in vivo. However, there is not enough evidence that these cytokines directly induce mucin production in vitro. In this study, primary epithelial cells from guinea pig trachea were cultured at an air-liquid interface, and immediately after achieving confluence at Day 7 they were treated with human recombinant IL-4 or IL-13 for 14 d. IL-13-treated cells consisted of a large number of fully mature goblet cells with a smaller number of ciliated cells. Secretory granules of the goblet cells were positive for both periodic acid-Schiff and toluidine blue, and showed exocytosis. By contrast, IL-4 failed to induce goblet cell differentiation. The electric resistances of IL-13-treated cells were lower than those of IL-4-treated cells and nontreated cells, suggesting leaky epithelia. MUC5AC protein level in cell lysates measured by ELISA was several-fold higher in IL-13-treated cells than in nontreated cells, whereas the level in IL-4-treated cells was not changed. These data suggest that human recombinant IL-13, but not IL-4, can induce differentiation into mature goblet cells that produce MUC5AC protein in guinea pig tracheal epithelial cells in vitro.

Animals↗
PubMed2001

Alteration in goblet cell numbers and mucin gene expression in a mouse model of allergic conjunctivitis.

PURPOSE: To determine whether the number of filled conjunctival goblet cells and mucin gene expression are altered in a mouse model of allergic conjunctivitis. METHODS: A/J mice were sensitized intraperitoneally with cat dander or the peptide P3-1 from the protein Fel d1. Two weeks later, the mice were challenged for 7 consecutive days with eye drops containing the allergens. Conjunctival tissue was harvested at 0, 6, 24, or 48 hours after final antigen challenge. Control samples were naïve animals and mice sensitized with cat dander and challenged with OVA-peptide or PBS. The mean number of filled goblet cells per square millimeter in three forniceal fields for each group was determined in wholemounts of conjunctiva prepared using rhodamine-phalloidin labeling followed by confocal microscopy. RNA was isolated from conjunctiva of the contralateral eye and taken for relative quantitation of mRNA of the goblet cell mucin Muc5AC and the epithelial membrane-spanning mucin Muc4, by real-time RT-PCR. RESULTS: The number of filled goblet cells was significantly decreased with both cat dander and P3-1, after final ocular challenge (P < 0.001). The most significant decrease over naïve mice was seen at 6 hours after final challenge with both allergens. The number of filled goblet cells was still decreased but was returning toward naïve levels at 24 hours (P < 0.05), and at 48 hours no significant difference was seen compared with naïve, PBS-treated, and OVA-peptide-treated control samples. For both cat dander and P3-1, Muc5AC and Muc4 mRNA was found to be decreased at the time of final ocular challenge. The level of Muc5AC mRNA from goblet cells rebounded from the decrease to show an increase over control by 24 hours after final challenge, and by 48 hours, the mRNA level had returned to naïve control range. In contrast, significant increases in Muc5AC mRNA were evident after final control challenge with PBS or OVA-peptide, indicating a potential irritant effect of drop application. The Muc4 mRNA level was significantly reduced at all time points except 24 hours after the last challenge. By comparison with allergen-challenged eyes, no change in Muc4 message levels was noted at any time point in OVA-peptide- or PBS-treated control eyes. CONCLUSIONS: These findings demonstrate that, in the conjunctiva of mice, repetitive application of allergens induces a reduction in the number of filled goblet cells and a decrease in Muc5AC and Muc4 mRNAs. After a period of 24 to 48 hours, the goblet cell number return to naïve levels, and goblet cell mucin mRNA levels return to above or within normal range, indicating a rapid recovery in the mucus secretion system.

Allergens↗
PubMed2003

Temporal analysis of goblet cells and mucin gene expression in murine models of allergic asthma.

In murine models of allergic asthma, mice repeatedly exposed to allergens or interleukin (IL)13 have numerous goblet cells in their airway epithelium, in contrast to healthy naïve mice. This study evaluated whether a single airway exposure of ovalbumin or IL13 would produce goblet cell metaplasia. Following ovalbumin challenge, airway goblet cells were present by 1 day, increased further by day 2 and day 3, and decreased by day 8. Following IL13 exposure, some goblet cells were detected at 6 hours and increased by 18 and 48 hours. Goblet transition cells, which are morphologically but not histologically similar to goblet cells, were observed at 6 and 18 hours following IL13 exposure and day 1 following ovalbumin challenge. Increased Muc5ac and Muc2 mRNA expression occurred following ovalbumin or IL13, but not saline, exposure. Mucin transcripts were localized to goblet cells in the surface airway epithelium. Muc5ac protein was expressed in some goblet transition and goblet cells. Overall, these data demonstrated that a single airway exposure to ovalbumin or IL13 is sufficient to generate goblet cell metaplasia and thus increase mucin gene expression in two strains of mice.

Animals↗
PubMed1997

Histamine H2 receptor-mediated airway goblet cell secretion and its modulation by histamine-degrading enzymes.

BACKGROUND: Airway goblet cell hypersecretion may contribute to the pathophysiology of asthma. However, it is unknown whether histamine affects goblet cell secretion and, if so, which subtype of histamine receptor is involved and whether endogenous histamine-degrading enzymes modulate these actions. METHODS: We morphometrically assessed goblet cell secretion in the guinea pig trachea stained with alcian blue and periodic acid Schiff stains by measuring the mucus score, which was inversely related to the degree of mucus glycoprotein discharge. RESULTS: Inhalation of histamine caused a dose-dependent decrease in mucus score, an effect that was inhibited by pretreatment with the H2-receptor antagonist cimetidine but not with the H1-receptor antagonist mepyramine or the H3-receptor antagonist thioperamide. Inhaled Dimaprit, a selective H2-receptor agonist, likewise decreased mucus score; whereas stimulation of H1- and H3-receptors with 2-methylhistamine and (R)-alpha-methylhistamine, respectively, had no effect. Pretreatment with the histamine N-methyltransferase inhibitor SKF 91488, but not the diamine oxidase inhibitor aminoguanidine, potentiated the dose-dependent effect of histamine on goblet cell secretion, causing a decrease in the concentration of inhaled histamine required to produce a half-maximal effect from 0.80 +/- 0.12 to 0.48 +/- 0.09 mg/ml (p < 0.01). The histamine methyltransferase activity in the tracheal mucosa was 29 times higher than diamine oxidase activity. CONCLUSION: These findings suggest that histamine stimulates airway goblet cell secretion through H2-receptors and that this effect may be modulated principally by endogenous histamine methyltransferase through a degradation of histamine.

Amine Oxidase (Copper-Containing)↗
PubMed1997

[Lectin histochemistry of the glycoconjugates in conjunctival goblet cells].

The distribution of O- and N-linked glycoconjugates in human conjunctival goblet cells was examined histochemically using biotinylated and fluorescence-labeled lectins simultaneously. Both peanut agglutinin and Erythrina cristagalli agglutinin, specific for O- and N-linked sugar chains, respectively, bound to the same goblet cell, which demonstrated that a conjunctival goblet cell produces and contains both types of glycoconjugates. Maackia amurensis lectin II, specific for sialic acid alpha 2, 3 galactose, bound to the goblet cells, while Sambueus nigra agglutinin, specific for sialic acid alpha 2, 6 galactose, did not. This observation suggested that the terminal galactosyl residue of the glycoconjugates is alpha 2, 3-sialylated in the human conjunctival goblet cells.

Conjunctiva↗