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At least 19 recordsLinked to original sources

PubMed1981

Transition between columnar absorptive cells and goblet cells in the rat jejunal epithelium.

Electron microscopic observation of the jejunal epithelium of rats demonstrated morphological evidence of a transition between columnar absorptive cells and growing goblet cells. The columnar cells in both the villi and crypts have features suggestive of absorptive functions. They are provided with apical invaginations continuous to the intermicrovillous space. Absorbed lipid is observed in small vesicles in the terminal web layer, and chylomicrons derived here from are contained in large vacuoles near the Golgi apparatus. Ferritin particles artificially infused into the gut lumen were absorbed into the vacuoles in the subapical zone of columnar cells of suckling rats. Growing goblet cells situated in the crypt epithelium contain surface invaginations and lysosomes which are the same in structure as those found in absorptive cells nearby. Fat droplets evidently absorbed by the growing goblet cell were observed among immature mucus droplets. Artificially infused ferritin particles were found in vacuoles and lysosomes near the Golgi apparatus of some goblet cells of suckling rats. Some goblet cells on the intestinal villi of suckling rats looked immature and their microvilli and cytoplasmic matrix were clear like those of columnar absorptive cells. The transition between these goblet cells with clear cytoplasm and the mature goblet cells with dark cytoplasm was observed. These morphological evidences indicate that some of columnar cells already differentiated to absorptive cells are capable of transforming into mucus-producing (goblet) cells. It is suggested that not only undifferentiated columnar cells in the crypt base but also considerably differentiated columnar cells with absorptive function can differentiate into goblet cells.

Animals↗

PubMed1991

Functional biology of intestinal goblet cells.

Goblet cells reside throughout the length of the small and large intestine and are responsible for the production and maintenance of the protective mucus blanket by synthesizing and secreting high-molecular-weight glycoproteins known as mucins. To elucidate the role of goblet cells in the biology of the intestinal tract, an overview of the physiological implications of the mucus gel is presented, including a concise review of the products secreted by the cell. Because of the unique nature of this highly polarized exocrine cell, the maturational reorganization of the cytoarchitecture and the cellular mechanisms by which goblet cells secrete their products are discussed. This includes elucidation of the baseline secretory pathway, which is dependent on the cytoskeleton for granule movement, and the accelerated secretory pathway, which is independent of the cytoskeleton but requires an extracellular signal to occur. Finally, the involvement of goblet cell mucins in the pathophysiology of intestinal neoplasia and ulcerative colitis are presented.

Animals↗

PubMed1983

Immunity to intestinal parasites: role of mast cells and goblet cells.

Nippostrongylus brasiliensis infection of rats and mice is a model for studying immunity at mucosal surfaces. Adult worms are spontaneously expelled from the intestine at the end of the second week of infection. Expulsion from the jejunum requires the presence of immune T lymphocytes and IgG antibodies. Mucosal mast cells (MMCs) are a prominent part of the jejunal inflammatory response. They are derived from a hematopoietic stem cell, possibly the same precursor as basophils. Their differentiation is not absolutely T dependent but their accumulation at the site of infection is. The possible involvement of IgE antibodies and intestinal MMCs through a "leak lesion" is still uncertain. Increased mucus secretion from epithelial goblet cells is also a prominent feature of the inflammatory reaction at the site of infection. Goblet cell numbers increase two to four times at the onset of worm expulsion; this increase is regulated by T lymphocytes and possibly immune serum. The mechanism of mucus secretion in these infections is not clear; it may be a response to mast cell mediators. Together with antiworm antibodies, intestinal mucus may trap worms and prevent them from surviving in the intervillous spaces of the jejunum. Thus, expulsion of this intestinal parasite may occur through a nonspecific process that is induced by specific immune mechanisms.

Animals↗

PubMed1996

[Distribution of conjunctival goblet cells and observation of goblet cells after conjunctival autotransplantation in rabbits].

Conjunctival goblet cells are essential for maintaining a normal ocular surface and important for recovering a diseased ocular surface. However, how goblet cells in conjunctival epithelium evolve after transplantation are uncertain. We experimented with albino rabbits to study the distribution of goblet cells in normal conjunctiva. We performed autograftings of conjunctiva which contained many goblet cells on the sclera of albino rabbits, and made histological observations on how goblet cells evolved after transplantation. The results were as follows. 1. Goblet cells in the normal rabbits were most abundant at the lid margin of both upper and lower tarsal conjunctiva. 2. We made autograftings of conjunctiva on the sclera of albino rabbits. The goblet cells on the transplanted conjunction disappeared for a short time on the 3rd day after transplantation. On the 7th day and onwards they reappeared, and by the 14th day a large number of goblet cells were observed. 3. Between the 7th and 14th day after autografting, epithelial differentiation of the grafted conjunctiva occurred.

Animals↗

PubMed1994

Goblet cell mucins as the selective barrier for the intestinal helminths: T-cell-independent alteration of goblet cell mucins by immunologically 'damaged' Nippostrongylus brasiliensis worms and its significance on the challenge infection with homologous and heterologous parasites.

The aim of this study was to examine the role of T cells on the alteration of terminal sugars of goblet cell mucins in the small intestinal mucosa of parasitized rats and to clarify the biological significance of the altered mucins in the mucosal defence against intestinal helminths. For this purpose, Nippostrongylus brasiliensis adult worms obtained from donor rats at 7 ('normal' worms) or 13 days ('damaged' worms) post-infection were implanted intraduodenally into euthymic and hypothymic (rnu/rnu) rats. Expulsion of implanted normal worms and associated goblet cell changes were extremely delayed in hypothymic recipients compared with euthymic recipients. In contrast, intraduodenally implanted damaged worms were expelled by day 5 regardless of the strains. Around the time of expulsion of implanted damaged worms, euthymic recipients showed both goblet cell hyperplasia and alteration of mucins, whereas hypothymic rats showed only the latter. Dexamethasone treatment completely abolished goblet cell changes of both strains of recipients. To clarify the importance of the constitutional changes of goblet cell mucins in mucosal defence, euthymic rats were primed by implantation of damaged worms to induce goblet cell changes, and then 3 or 5 days later they were challenged by implantation with normal worms. The results show that when goblet cell changes were induced by priming with damaged worms, recipient rats could completely prevent the establishment of normal worms. When hypothymic rats were primed and challenged in the same manner, a similar but slightly less preventive effect was observed. Such a protective effect of altered mucins seems to be selective because priming of euthymic rats with damaged N. brasiliensis did not affect the establishment of Strongyloides venezuelensis. These results suggest that: (1) once N. brasiliensis adult worms are 'damaged' by the host's T-cell-dependent immune mechanisms, they can induce alteration of sugar residues of goblet cell mucins via host-mediated, T-cell-independent processes; (2) the expression of such altered mucins is highly effective not only in causing expulsion of established damaged worms but also in preventing establishment of normal worms; and (3) the preventive effect of altered mucins is selective against parasite species.

Animals↗

PubMed1996

P2u purinoceptor regulation of mucin secretion in SPOC1 cells, a goblet cell line from the airways.

The SPOC1 cell, a novel goblet cell line derived from rat trachea, was tested for its ability to exhibit regulated mucin secretion in response to purinergic (P2) agonists. High-molecular mass glycoconjugates (HMMGs) purified by CsCl-density-gradient centrifugation had a buoyant density of 1.45 g/ml. The purified HMMG material exhibited a single major band with an apparent molecular mass of greater than 1000 kDa in SDS/ polyacrylamide gels stained with silver or blotted and stained with soya-bean agglutinin. [3H]HMMG was resistant to proteoglycan-degrading enzymes, but was susceptible to neuraminidase. The HMMG was approx. 91% carbohydrate by weight, and the glycosides were O-linked. The HMMG amino acid composition was enriched in Ser and Thr (sum 27%). Thus SPOC1-cell HMMG possess the characteristics of mucin. Mucin secretion by SPOC1 cells, grown on permeable supports and perfused luminally, was stimulated by ATP, UTP and adenosine 5'-[gamma-thio]triphosphate (100 microM) 4-5-fold over a baseline of 4 ng/min. The three dose-effect relations were nearly identical (K0.5 approximately 4 microM). SPOC1 cells grown on plastic and rat tracheal epithelial primary cells responded similarly to ATP and/or UTP. SPOC1 cells failed to respond to other purinergic agonists, either luminally or serosally, and consequently seem to possess an apical membrane P2u purinoceptor. SPOC1-cell total RNA was probed for P2u purinoceptor mRNA. Using conserved primers for both reverse transcriptase and PCR, a single band of the predicted size was observed, which had a nucleotide base sequence identical with the rat P2u purinoceptor mRNA. Thus SPOC1 cells secrete mucin under the control of a P2u purinoceptor; they should prove useful in dissecting the associated cellular regulatory pathways.

Adenosine Triphosphate↗

PubMedDate not supplied

Gut mucosal mast cells and goblet cells during acute graft-versus-host disease in rats.

Intestinal inflammation occurs in both nematode infections and graft-versus-host disease (GVHD). In nematode infections, this involves the proliferation of mucosal mast cells (MMC) and goblet cells (GC). To examine MMC and GC responses in GVHD, female Lewis rats were given allogeneic bone marrow (BM). Each animal received 1,020 rads and, one day later, 6 X 10(7) ACI BM cells plus 2 X 10(7) ACI spleen cells i.v. Control rats received 6 X 10(7) BM cells. On days 4, 8, 12, 16 and 20 post-transplant, rats were sacrificed and their intestines removed and prepared for histological examination of MMC and GC. Cells in 10 villus-crypt units (VCU) of the gut were counted for each animal. Skin and tongue were also removed and examined to determine the degree of GVHD. GVHD was first evident on day 8 in allogeneic BM recipients and progressed thereafter. No evidence of GVHD was seen in syngeneic BM recipients. Rats receiving allogeneic BM showed a 10-fold increase from day 12 to day 20 (p less than 0.01). Rats receiving syngeneic BM showed no significant change in MMC through the 20th day. In animals with GVHD, GC decreased by day 12 and remained lower than control animals during the subsequent 8 days. It was concluded that, similar to nematode infection, MMC proliferation is a feature of GVHD. In contrast, GC do not appear to proliferate in an acute GVHD.

Animals↗

PubMed1991

Chronic inflammation is associated with an increased proportion of goblet cells recovered by bronchial lavage.

To evaluate the possibility that bronchoalveolar lavage could provide sufficient respiratory epithelial cells to quantify changes in epithelial cell types associated with chronic inflammation, we examined the epithelial cells obtained in the first infused (20 ml) aliquots that were processed separately from later aliquots, a process known to enrich for bronchial contents. Epithelial cells, including ciliated cells, goblet cells, and fragments of desquamated epithelium, were easily identified after preparation by cytocentrifugation and staining with a modified Giemsa stain. Quantification of the columnar cell types revealed that those with chronic bronchitis and asymptomatic smokers have increased goblet cells as a percentage of the total columnar epithelial cells (chronic bronchitics 36 +/- 2 percent, asymptomatic smokers 22 +/- 2 percent) compared with normal subjects (9 +/- 1 percent, p less than 0.001, ANOVA). Significantly, the goblet cell percentage was strongly correlated with other measures of bronchitis and measures of airflow obstruction such as the bronchitis index, a visually derived score at bronchoscopy of airway inflammation (r = 0.72, p less than 0.001), the percent neutrophils in the first infused aliquots (r = 0.44, p less than 0.05), and the FEV1 percent (r = -0.74, p less than 0.001). Thus, bronchoalveolar lavage is capable of providing sufficient bronchial epithelial cells for analysis, and the changes seen in the spectrum of columnar epithelial cells may reflect important underlying pathologic changes.

Airway Obstruction↗

PubMed1997

Role of T helper 2 cells in intestinal goblet cell hyperplasia in mice infected with Trichinella spiralis.

BACKGROUND & AIMS: The four principal types of intestinal epithelial cells are derived from multipotent stem cells. Currently, there is no information on factors that regulate commitment of stem cells to differentiate along one lineage vs. another. The aim of our study was to investigate the role of T cells in the regulation of small intestinal goblet cell hyperplasia in mice infected with the parasite Trichinella spiralis. METHODS: NIH mice were infected with T. spiralis, and intestinal goblet cells and cytokine response were studied. Interferon gamma and interleukin 5 were used as candidate T helper (Th)1 and Th2 cytokines, respectively. Adoptive transfer experiments were also performed. RESULTS: Small intestinal goblet cell hyperplasia occurred 8 days after infection with T. spiralis. Th1-type cells were predominant in the mesenteric lymph nodes early in the course of infection, with a switch to Th2-predominant cells around the time of goblet cell hyperplasia. Transfer of Th2-enriched mesenteric lymph node cells further enhanced goblet cell hyperplasia in recipient mice. Neutralization of interleukin 5 activity did not affect T. spiralis-induced goblet cell hyperplasia. CONCLUSIONS: Small intestinal goblet cell hyperplasia in T. spiralis-infected mice is probably regulated by Th2 cells. We postulate that Th2-derived factors (other than interleukin 5) induce stem cells to differentiate preferentially along the goblet cell lineage.

Animals↗

PubMed1996

Different expression of IL-2 receptor alpha-chain on a lamina propria T cell population and goblet cells in rats orally tolerized or sensitized to ovalbumin (OA) after colonization with an OA-producing Escherichia coli.

The aim of this study was to compare the local gut immune response in sensitized and orally tolerized experimental animals. The development of IgE/IgG antibodies and the DTH to OA was studied in rats made orally tolerant to OA and compared with sensitized control rats after colonization with an Escherichia coli genetically engineered to produce OA. At 3 weeks of age, pups were weaned onto a standard diet without OA or an OA-containing diet for 4 weeks and then switched to a standard diet without OA. Both groups of rats were parenterally immunized with a mixture of OA and human serum albumin (HSA) in Freund's complete adjuvant when they were 8 weeks old. After DTH measurement 2 weeks later, all rats were colonized with an E. coli producing OA for 5 days. The local immune response in the small intestine was assessed, using immunohistochemistry, as the expression of MHC class II molecules and IL-2 receptor (IL-2R) alpha-chain. The OA-tolerant rats showed the classical signs of oral tolerance, with a reduced IgE and IgG antibody and DTH response to OA before colonization. The difference between the two groups in the anti-OA antibody response became even more pronounced after colonization with the E. coli that produce OA. Rats orally tolerant to OA maintained a normal villus architecture after colonization, with a normal expression of MHC class II molecules similar to non-treated adult rats, but with a significantly higher (P = 0.004) expression of IL-2R alpha-chain on T cells in the lamina propria of the villus core compared with sensitized control rats. The tolerant rats showed a very weak staining with the anti-IL-2R alpha-chain-specific antibody on a few goblet cells in only one out of seven rats. In the sensitized control rats, a marked local immune response was seen with an intense staining with a monoclonal anti-IL-2R alpha-chain-specific antibody on goblet cells in five out of seven rats (P = 0.019) and also an increased expression of MHC class II molecules in the epithelial cells and cells in the lamina propria of all rats. Rats orally tolerant to OA maintained a normal villus architecture after colonization, but with a significantly higher (P = 0.004) expression of IL-2R alpha-chain on T cells in the lamina propria of the villus core compared with sensitized control rats. The novel finding that goblet cells express IL-2R alpha-chain and the striking difference in expression of the receptor and the numbers of goblet cells between tolerant and sensitized rats may suggest a direct T cell regulation of the goblet cells. A possibility that oral tolerance might be maintained by the activated T cells expressing IL-2R alpha-chain in the lamina propria of the villus core is also discussed.

Administration, Oral↗

PubMed1987

Density and distribution of canine conjunctival goblet cells.

Conjunctival goblet cells (GCs) were quantitated to establish baseline values for density and distribution of these cells in healthy canine eyes. From each of 18 sites, tissue was collected, sectioned at 2 micron, and stained with periodic acid Schiff stain. Within each sampling site, 500 epithelial cells (GCs, squamous, polygonal, and basal epithelial cells) were counted and the ratio of GCs to total epithelial cells was computed as an index of goblet cell density or goblet cell index (GCI). A heterogenous distribution of canine conjunctival goblets cells was demonstrated. Lower nasal fornix (LNf) and adjacent sites, lower middle fornix (LMf) and lower nasal tarsal (LNt), had the highest mean densities of goblet cells. In contrast, GCs were essentially absent from the upper and lower bulbar areas. Remaining sites had intermediate GCIs. Sex differences in GCIs were noted for LNf and LNt sites. Mean tear film breakup times (BUTs) were determined, and, for normal beagle dogs, were 19.38 (+/- 4.80 secs) OS and 19.96 (+/- 5.01 secs) OD. The similarities between canine and human conjunctival goblet cell distributions support the use of the dog for studying the conjunctival mucous system.

Animals↗

PubMed1993

Conjunctival epithelial cell hypermitosis and goblet cell hyperplasia in atopic keratoconjunctivitis.

Atopic diseases that include eczema (atopic dermatitis), asthma, and seasonal and perennial rhinoconjunctivitis are common manifestations of abnormal immediate hypersensitivity. Ocular involvement, such as atopic keratoconjunctivitis, characteristically includes conjunctival and corneal inflammation, and in a severe form, conjunctival scarring, symblepharon, corneal epitheliopathy, and visual loss. To examine the conjunctival cellular abnormalities in atopic keratoconjunctivitis, we studied the in vivo differentiation and tissue-culture growth characteristics of conjunctiva from normal subjects and patients with severe atopic keratoconjunctivitis. We examined conjunctival biopsy specimens to determine epithelial mitotic rate and goblet cell frequency, and we studied conjunctival explants to determine the latent period for fibroblast outgrowth and fibroblast doubling time. The mitotic rate for atopic keratoconjunctivitis, 6.7% +/- 2.1% (11 patients), was statistically significantly greater than for normal subjects, 2.0% +/- 0.63% (seven subjects) (P = .05). Also the goblet cell frequency for atopic keratoconjunctivitis, 14.6% +/- 3.4% (11 patients), was statistically significantly greater than for normal subjects, 4.8% +/- 0.92% (seven subjects) (P = .02). The latent period for fibroblast outgrowth and the fibroblast doubling time for atopic keratoconjunctivitis were not statistically significantly different from normal control subjects. Therefore, atopic keratoconjunctivitis was associated with conjunctival epithelial hypermitosis, goblet cell hyperplasia, and normal fibroblast tissue-culture growth. These characteristics may be useful in the diagnosis of atopic keratoconjunctivitis. We previously studied another disease characterized by chronic conjunctival inflammation and scarring, cicatricial pemphigoid, which also demonstrated conjunctival epithelial hypermitosis, but in contrast there was near absence of goblet cells, and the fibroblasts were hyperproliferative. These differences may be used to distinguish atopic keratoconjunctivitis from cicatricial pemphigoid.

Aged↗

PubMed1997

Gastric mucous neck cell and intestinal goblet cell phenotypes in gastric adenocarcinoma.

AIM: To investigate the phenotype of cells comprising diffuse and intestinal-type gastric cancers using monoclonal antibodies to two antigens. One antigen (designated D10) is characteristic of gastric mucous neck cells, cardiac glands, pyloric glands, and Brunner's glands. The second antigen (designated 17NM) is specific to the mucous vacuole of intestinal goblet cells. METHODS: Thirty two gastrectomy specimens with adenocarcinoma were studied. Serial paraffin sections were stained immunohistochemically for D10 and 17NM and histochemically for acid and neutral mucins. The cancers were classified histologically as of either diffuse or intestinal type according to Lauren. RESULTS: Of 15 diffuse-type gastric carcinomas, 11 showed the majority of cancer cells staining for D10 while four were typical signet ring cell cancers staining predominantly for 17NM; five tumours displayed both phenotypes with the two phenotypes segregated in different areas of the tumours. In contrast, of 16 intestinal-type cancers, six expressed 17NM, three D10, five neither antigen, and two expressed both antigens. One indeterminate-type cancer expressed both antigens. The staining of individual cells for D10 and 17NM was mutually exclusive in both diffuse and intestinal types. In contrast to the diffuse cancers, intestinal-type cancers typically expressed either antigen only in occasional small groups of cells and individual cells. CONCLUSIONS: In disease, the gastric stem cell can assume the capacity of the duodenal stem cell for divergent differentiation into either intestinal goblet cells (for example, as in intestinal metaplasia) or Brunner's gland cells (for example, as in pyloric gland/Brunner's gland metaplasia). With neoplastic transformation, this potential for divergent differentiation is maintained and gives rise to diffuse-type cancers that display either the D10 phenotype, the 17NM phenotype, or the clonal expression of both phenotypes. In the more cell cohesive (intestinal-type) tumours, differentiation for antigen expression is poorly developed and more frequently directed towards the intestinal goblet cell phenotype.

Adenocarcinoma↗

PubMed1973