Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Goblet Cells”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2001

Ileal mucosal mast cell, eosinophil, and goblet cell populations during Hymenolepis diminuta infection of the rat.

The population dynamics in the enteric connective tissues of eosinophils, mucosal mast cells (MMC), and in the mucosal epithelium of goblet cells were examined morphometrically in fixed ileal tissue of outbred Sprague Dawley rats during the first 32 days of infection with the tapeworm Hymenolepis diminuta. MMC and eosinophils were present in the lamina propria and submucosa; however, only eosinophils were also present in the muscularis externa. Eosinophilic infiltrate was first observed in the lamina propria at 15 days postinfection (dpi) and the numbers of eosinophils remained elevated through 32 dpi. Initial mucosal mastocytosis was detected on 6 dpi and MMC numbers continued to rise over the study period without reaching a plateau. Goblet cell hyperplasia occurred only at 32 dpi. In contrast to some intestinal nematode infections where these same 3 cell types are associated with the host's expulsion responses, H. diminuta is not lost by a rapid host response in the outbred Sprague Dawley rat strain used in these experiments. We suggest that either the induction of hyperplasia of these host effector cells in ileum tissue during H. diminuta infection is not capable of triggering parasite rejection mechanisms, or the function of the induced hyperplasia is necessary for some as yet unassociated physiological or tissue architecture change in the host's intestine.

Animals↗
PubMed1988

Histochemistry of mucosubstances in Brunner's-gland cells and duodenal goblet cells of two New World monkey species (Saimiri sciureus and Saguinus fuscicollis).

Duodenal goblet cells and Brunner's-gland cells obtained from two species of New World monkeys (Saimiri sciureus and Saguinus fuscicollis) were studied using conventional histochemical methods and by applying a panel of 17 labelled lectins. The secretions of both goblet and Brunner's-gland cells were found to contain neutral mucosubstances, while those of goblet cells also exhibit acid and sulphated carbohydrate components. Lectin binding studies allowed a more detailed analysis of the mucus glycoproteins. Marked differences between the two examined species were not detected. N-Acetyl-galactosamine, galactose, fucose and N-Acetyl-glucosamine were found to be the predominant sugar residues in Brunner's-glands glycoproteins, with mannose and glucose being only minor components.

Animals↗
PubMed1997

Protein kinase C and Ca2+ activation of mucin secretion in airway goblet cells.

Airway goblet cells secrete mucin in response to ATP and uridine 5'-triphosphate (UTP), but the underlying signal transduction pathways are poorly understood. Cultures of SPOC1 cells (L. H. Abdullah, S. W. Davis, L. Burch, M. Yamauchi, S. H. Randell, P. Nettesheim, and C. W. Davis. Biochem. J. 316: 943-951, 1996) secreted mucin on exposure to phorbol 12-myristate 13-acetate (PMA) [apparent affinity (K0.5) approximately 100 nM] and ionomycin (K0.5 approximately 5 microM) almost fivefold over baseline. Thapsigargin also elicited secretion (K0.5 approximately 20 nM). Ionomycin and PMA together elicited approximately twice the secretion of either agent alone. Overnight exposure to half-maximal PMA abolished the response to maximal doses of UTP and PMA, whereas ionomycin was fully effective. Protein kinase C (PKC) activity in the membrane fraction was increased by maximal doses of PMA and UTP, whereas ionomycin had no effect. PKC inhibitors were relatively ineffective against PMA- and UTP-induced mucin secretion. Human and canine goblet cells in epithelial explants, by video microscopy, underwent exocytosis with ionomycin (1 microM) and PMA (0.1 or 1 microM). SPOC1 cell mucin secretion was not stimulated by forskolin, 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate, or 8-bromoguanosine 3',5'-cyclic monophosphate. Cystic fibrosis transmembrane conductance regulator was not detected in SPOC1 cells by Western blotting, and its mRNA was detected by reverse transcriptase polymerase chain reaction (PCR) only as a very weak band and after 55 PCR cycles. Multidrug resistance (MDR1), however, was readily detected by Western blotting, and its mRNA was detected as a major band after 35 PCR cycles. Thus airway goblet cell mucin secretion, distal to receptor activation, may be regulated independently by Ca(2+)- and PKC-dependent pathways. Cystic fibrosis transmembrane conductance regulator and cyclic nucleotides, however, may not play a major role in this secretion.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Effect of sensory neuropeptides on mucus secretion from cultured goblet cells.

BACKGROUND: Airway goblet cell secretion is under the control of capsaicin-sensitive sensory nerves. Administration of capsaicin or antidromic stimulation of nerves can stimulate goblet cell secretion and also induce plasma exudation and smooth muscle contraction via a release of neuropeptides from sensory nerve endings in the airway. This study was designed to explore whether the effect of capsaicin or neuropeptides on goblet cell secretion is direct or secondary to other airway responses. MATERIALS AND METHODS: We examined the effects of sensory neuropeptides including substance P (SP), neurokinin A (NKA) and neurokinin B (NKB), as well as capsaicin on cultured guinea pig tracheal goblet cells by measuring the rate of mucus discharge visually under a microscope and the release of 35SO4 radiolabeled mucin-like glycoconjugates. RESULTS: Goblet cells in culture spontaneously secreted intracellular granules at a mean rate of about 3 times/min. SP and NKA increased secretion in a dose-dependent manner. SP was more potent than NKA with maximum responses of 52% and 37% at 10(-8) M, respectively. Quantitative measurements of 35SO4 radiolabeled mucin-like glycoprotein (MLGP) secreted by goblet cells also revealed an increase (109.2%) in mucin secretion caused by SP (10(-8) M) compared with the vehicle control. Neither capsaicin nor NKB caused any significant change in the goblet cell secretory rate. The effects of SP on the secretory rate or release of radiolabeled mucin were not potentiated by an enkephalinase inhibitor, thiorphan (10(-5) M). CONCLUSION: Sensory neuropeptides SP and NKA directly stimulate goblet cell secretion, probably through the tachykinin receptor of the NK-1 subtype as suggested by a greater potency of SP. There was no direct effect of capsaicin on goblet cell secretion.

Animals↗
PubMed2002

Cholinergic agonists transactivate EGFR and stimulate MAPK to induce goblet cell secretion.

Conjunctival goblet cells are the primary source of mucins in the mucous layer, the innermost layer of the tear film. Conjunctival goblet cell mucin secretion is under neural control because exogenous addition of parasympathetic agonists stimulates goblet cell secretion. To elucidate the intracellular signal pathways used by cholinergic agonists to stimulate goblet cell mucin secretion, we determined whether p42/p44 mitogen-activated protein kinase (MAPK) is activated during cholinergic agonist-stimulated mucin secretion. Rat conjunctiva was removed, preincubated with or without antagonists, and stimulated with the cholinergic agonist carbachol (10(-4) M). Carbachol statistically significantly stimulated the phosphorylation of MAPK in a time- and concentration-dependent manner. U-0126, an inhibitor of MAPK activation, completely inhibited both the activation of MAPK and goblet cell secretion stimulated by carbachol. The M(1) muscarinic antagonist pirenzepine, the M(2) muscarinic antagonist gallamine, and the M(1)/M(3) muscarinic receptor antagonist N-(3-chloropropyl)-4-piperidinyl diphenylacetate (4-DAMP) also inhibited carbachol-stimulated MAPK activation. Increasing the intracellular Ca(2+) concentration with a Ca(2+) ionophore increased MAPK activation, and chelation of extracellular Ca(2+) inhibited carbachol-stimulated activation. Carbachol also increased tyrosine phosphorylation of Pyk2, p60Src, and the epidermal growth factor receptor (EGFR). The Src inhibitor PP1 and the EGFR inhibitor AG-1478 completely inhibited carbachol-stimulated MAPK activation. AG-1478 also inhibited goblet cell secretion. We conclude that carbachol transactivates the EGFR to activate MAPK, leading to conjunctival goblet cell secretion. In addition, carbachol also activates Pyk2 and p60Src that could play a role in the transactivation of the EGFR.

Animals↗
PubMed2002

In vitro study of IL-8 and goblet cells: possible role of IL-8 in the aetiology of otitis media with effusion.

One of the main characteristics of otitis media with effusion (OME) is the differentiation of basal cells into goblet cells with subsequent proliferation in a modified respiratory epithelium leading to the formation of mucin-rich effusion in the middle ear cleft. In order to determine the effect of pro-inflammatory cytokines identified in OME, e.g. IL-1beta, tumour necrosis factor (TNF)-alpha, IL-6 and IL-8, on goblet cells, and to clarify the role of IL-8 in particular, we used the human goblet cell line HT29-MTX, which secretes two OME-related mucins: MUC5AC and MUC5B. IL-1beta and TNF-alpha stimulated the secretion of IL-8 in HT29-MTX goblet cells. Dose- (2-200 ng/ml) and time- (0-5 days) response studies of IL-8-induced mucin secretion were carried out. IL-8 upregulated the secretion of MUC5AC and MUC5B mucins in a concentration-dependent manner, with a maximum response at an IL-8 concentration of 20 ng/ml. IL-8 (20 ng/ml)-mediated mucin secretion persisted for up to 5 days, with a peak response 72 h after the addition of cytokine. These results suggest that: (i) goblet cells are target cells for the pro-inflammatory cytokines IL-1beta, TNF-alpha and IL-8 and can contribute to the pathogenesis of OME by increasing both the concentration of IL-8 and the secretion of mucin; and (ii) IL-8 stimulates prolonged mucin secretion from goblet cells and may be involved in the maintenance of the disease in the chronic stage.

Cell Differentiation↗
PubMed2005

Establishment and characterization of a human colonic mucinous carcinoma cell line with predominant goblet-cell differentiation from liver metastasis.

Many human colorectal adenocarcinoma cell lines have been developed. However, differentiated type colorectal cancer cell lines, particularly, the goblet-cell differentiated type, are scarce. In the present study a novel colorectal adenocarcinoma cell line (designated as COLM-6) with predominant goblet-cell differentiation was established from the rectal mucinous adenocarcinoma of a Japanese woman. COLM-6 cells grow in a typical epithelial monolayer in culture. They expressed epidermal growth factor (EGF) receptor and HER2 on their surface and accordingly, their growth was significantly stimulated by EGF, transforming growth factor (TGF)-alpha and heregulin. COLM-6 cells form tumor with typical mucinous adenocarcinomatous appearance in nude mice. Immunohistochemical analysis of these subcutaneous tumors demonstrated that COLM-6 cells strongly express MUC2 as a goblet-cell marker and Cdx2 in the nucleus. Some weakly express villin and carbonic anhydrase 1 as a columnar absorptive-cell marker as well. They were also positive for adenomatous polyposis coli (APC) cytoplasmically and expressed beta-catenin in their cytoplasm and cell membrane without nuclear accumulation. These results indicate that COLM-6 cell line has unique characteristics and may provide a useful tool to study the mechanism of growth and differentiation of colonic epithelium as well as the biological behavior of colorectal mucinous adenocarcinoma.

Adenocarcinoma, Mucinous↗
PubMed1980

Ciliated and goblet cells in craniopharyngioma. Light and electron microscopic studies at surgery and autopsy.

A case of a suprasellar epithelial cyst in a 48-year-old man is reported. The cyst was lined with two different types of stratified epithelium: one was two to three or more layers of squamous cells with overlying ciliated columnar cells and goblet cells at the surface and the other was tyical stratified squamous epithelial cells. The tumor was neither a pure Rathke's cleft cyst nor a typical craniopharyngioma but was considered essentially to be a craniopharyngioma with ciliated columnar cells and goblet cells. Thus it might be considered a mixed form of these two tumors. This case indicates the close relationship between craniopharyngiomas and Rathke's cleft cysts.

Autopsy↗
PubMed1976

Human intestinal goblet cell mucin.

Goblet cell mucin (GCM) has been purified for the first time from mucosal scrapings of human small intestine. Proteolytic enzymes and organic solvents were avoided during the isolation procedure. The mucin was purified by Sepharose 4B and 2B column chromatography of high-speed supernatant fractions. The most purified fraction was compared with rat intestinal GCM. The two were similar with respect to chemical composition, antigenic features, and polyacrylamide disc gel electrophoresis. The major chemical differences included a higher hexosamine-fucose and hexosamine-sialic acid ratio in human mucin. The two mucins showed strong concentration dependence in sedimentation velocity studies. Human mucin at a concentration of 0.2 to 1.5 mg protein per millilitre gave multiple associated peaks with variable So values (10.8-36.6). Rat mucin, in contrast, gave a constant (although polydisperse) pattern with So = 15.15. To explore these differences both mucins were stained with periodic acid - Schiff reagent and subjected to band ultracentrifugation at concentrations of 0.6-1.9 mug protein per millilitre. At this low concentration, rat mucin did not change in its sedimentation characteristics. In contrast, human GCM produced a single peak with So = 37.9. Thus dilution abolished polydispersity in the human but not the rat mucin, suggesting that intermolecular bonding forces in the human mucin are weaker.

Amino Acids↗
PubMed1982

Structure and permeability of goblet cell tight junctions in rat small intestine.

Two major cell types, goblet and absorptive cells, dominate the epithelial lining of small intestinal villi. We used freeze-fracture replicas of rat ileal mucosa to examine the possibility that tight junction structure, known to relate to transepithelial resistance, might vary with cell type. Tight junctions between absorptive cells were uniform in structure while those associated with villus goblet cells displayed structural variability. In 23% of villus goblet cell tight junctions the strand count was less than 4 and in 30% the depth was less than 200 nm. In contrast, only 4% of absorptive cell tight junctions had less than 4 strands and only 9% had depth measurements less than 200 nm. Other structural features commonly associated with villus goblet cell tight junctions but less commonly with absorptive cell tight junctions were: deficient strand cross-linking, free-ending abluminal strands, and highly fragmented strands. Both in vivo ileal segments and everted loops were exposed to ionic lanthanum. Dense lanthanum precipitates in tight junctions and paracellular spaces were restricted to a subpopulation of villus goblet cells and were not found between villus absorptive cells. After exposure of prefixed ileal loops to lanthanum for 1 hour, faint precipitates of lanthanum were found in 14% of tight junctions and paracellular spaces between absorptive cells compared to 42% of tight junctions and paracellular spaces adjacent to villus goblet cells. When tested in Ussing chambers, the methods used for lanthanum exposure did not lower transepithelial resistance. Everted loops exposed to ionic barium and examined by light microscopy showed dense barium precipitates in the junctional zone and region of the paracellular space of villus goblet cells but not in these regions between absorptive cells. However, the macromolecular tracers, microperoxidase, cytochrome c and horseradish peroxidase, were excluded from both villus goblet cell and absorptive cell paracellular spaces in in vivo segments. These findings suggest that a subpopulation of villus goblet cells may serve as focal sites of high ionic permeability and contribute to the relatively low resistance to ionic flow which characterizes the small intestinal epithelium.

Animals↗
PubMed2003

T helper type-2 cells induce ileal villus atrophy, goblet cell metaplasia, and wasting disease in T cell-deficient mice.

BACKGROUND & AIMS: T helper (Th) 1 and Th2 cell subsets significantly influence the pathological features of inflammation in the gastrointestinal tract in a distinct manner. It is now established that the transfer of CD4(+)CD45RB(Hi) (RB(Hi)) T cells to either severe combined immunodeficient (SCID) or recombinase activation gene 2-deficient (RAG(-/-)) mice results in a severe granulomatous hypertrophic colitis mediated by Th1 cells. We have modified this approach to address the role of Th2 cells. METHODS: RB(Hi) T cells from wild-type (Wt) mice or mice genetically predisposed to Th2 responses (interferon-gamma-defective [IFN-gamma(-/-)]) with or without B cells were transferred to T cell receptor (TCR)-beta and delta-chain-defective (TCR(-/-)) or SCID mice. RESULTS: Transfer of Wt RB(Hi) T cells induced wasting disease with severe colitis in the TCR(-/-) mice. In contrast, IFN-gamma(-/-) RB(Hi) T cells induced severe weight loss and hypoalbuminemia without significant inflammation in the colon. The small intestine of these mice exhibited villus atrophy, a decrease in brush-border enzymes, reduced enterocyte proliferation, and an increased number of goblet cells. The presence of B cells was necessary for these changes, because SCID recipients required cotransfer of B cells, together with IFN-gamma(-/-) RB(Hi) T cells for ileal lesions to develop. Treatment of TCR(-/-) recipients of IFN-gamma(-/-) RB(Hi) T cells with anti-IL-4 mAb abrogated both the wasting disease and the villus atrophy. CONCLUSIONS: Dysregulated Th2 cells cause atrophic changes and goblet cell transformation in the small intestinal epithelium and wasting disease mediated by excess interleukin-4 and B cells.

Animals↗
PubMed1987

Immune regulation of goblet cell development.

In rats, goblet cells were found in the bronchiole epithelium surrounding enlarged lymphoid noduli. The goblet cell number increased with age. Old rats had goblet cells in the columnar epithelium. Immunization with aerosolized antigen increased goblet cell hyperplasia in bronchioli with a luminal diameter of 0.5-1.0 mm. In mice, goblet cell differentiation in the respiratory epithelium was caused by local delayed-type hypersensitivity reactions. Manipulations of the delayed hypersensitivity reactions with immune suppression and depletion of helper T cells eliminated the increase in goblet cell number.

Animals↗