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 109 records · Page 6Linked to original sources
PubMed1990

Hymenolepis diminuta: intestinal goblet cell response to infection in male C57 mice.

Intestinal goblet cell numbers in two regions of the small intestine (20-30% and 60-70% distance form the pylorus) of male, 6- to 8-week-old C57 mice have been monitored following a 5-cysticercoid infection of the rat tapeworm, Hymenolepis diminuta. Test and sham-infected control mice were autopsied 0, 4, 8, 10, 14, and 28 days postprimary infection (p-1 degree-i) and 2, 4, 5, 7, and 14 days postsecondary infection (p-2 degree-i), administered 28 days p-1 degree-i. Results show a statistically significant increase in the number of mucus-containing goblet cells in both regions of the intestine during primary and secondary infections. Peak goblet cell numbers occurred on Day 8 p-1 degree-i and Day 5 p-2 degree-i in the 20-30% region and on Day 10 p-1 degree-i and Day 5 p-2 degree-i in the 60-70% region. In both regions, cell numbers declined to control levels by Day 14 p-1 degree-i, but remained significantly above control values 14 days p-2 degree-i. The increase in cell numbers correlated with an increase in goblet cell theca size and observable amounts of luminal mucus. The same infection regime in mice treated with cortisone elicited no goblet cell response. Male Wistar rats given a 10-cysticercoid infection and autopsied on Day 0, Day 10, and 15 months p-i showed a statistically significant increase in mucus-containing goblet cells only in the 60-70% region of intestine 10 days p-i; however, the worm burden was not eliminated. The functional significance of these results is discussed in relation to host immunity and murine cestode rejection.

Animals↗
PubMed1984

Combined production of mucus, amines and peptides by goblet-cell carcinoids of the appendix and ileum.

Goblet-cell carcinoids are particular mucus-producing tumors combining features of typical carcinoids and adenocarcinomas. The immunoreactivity of five goblet-cell carcinoids of the appendix and one tumor of the ileum for 5-hydroxytryptamine (5-HT, serotonin), glucagon, somatostatin, substance P (SP), neuron-specific enolase (NSE), lysozyme, secretory component (SC) and carcino-embryonic antigen (CEA) was compared with that of the mucosa of the appendix (n = 24) and ileum (n = 12), and of typical carcinoids (appendix: n = 10; ileum: n = 3). The goblet-cell carcinoids were consistently lysozyme-, SC- and CEA-reactive and contained weakly NSE reactive endocrine cells, while typical carcinoids were lysozyme-, SC- and CEA-negative, but strongly NSE- reactive. Two goblet-cell carcinoids were glucagon-reactive, one displayed SP-reactivity, one malignant tumor was reactive to the alpha-chain of glycoprotein hormones; six of ten typical appendix carcinoids were SP reactive, as were the three typical ileum carcinoids. Using the immunogold technique combined with the alcian-blue reaction, the presence of 5-hydroxytryptamine (5-HT) and mucus was demonstrated within the same cell. These findings suggest histogenetic differences between goblet-cell carcinoids and typical carcinoids; the former are possibly derived from undifferentiated stem cells, whereas the latter probably arise from endocrine cells in the mucosal stroma.

Aged↗
PubMed1980

Anaphylactic release of intestinal goblet cell mucus.

The effect of intestinal anaphylaxis on goblet cell mucus release was tested in rats immunized with small doses of egg albumin and alum and challenged intraduodenally with antigen. The alteration in vascular and mucosal permeability which accompanies intestinal anaphylaxis was reflected by increased retention of 125I-labelled rat serum albumin in gut wall segments and increased amounts of protein-bound radioactivity in the intestinal secretion from the segments. Intestinal goblet cell mucus was labelled in vivo with 35S. Infusion of antigen, into the duodenum of actively immunized rats led to the appearance of 35S-labelled high molecular weight glycoprotein, presumably of goblet cell origin, in the intestinal secretions. Goblet cell mucus release was dependent on the dose of antigen infused, was antigen-specific and was inhibited by pretreatment of rats with cyproheptidine. Enhanced release of goblet cell mucus was observed in normal rats prepared by intravenous injection of rat antiserum rich in IgE anti-egg albumin antibodies and challenged by intraduodenal infusion of antigen. Prior heating of the antiserum inhibited passive transfer of the reaction; this finding is consistent with the heat lability of IgE antibodies. The latter class of antibodies are presumed to be responsible for intestinal anaphylaxis and its associated mucus release in the model system examined.

Anaphylaxis↗
PubMed1988

Histochemical changes in the composition of mucins in goblet cells during methotrexate-induced mucosal atrophy in rats.

Changes in the composition of mucins in jejunal goblet cells were investigated histochemically after a single intraperitoneal injection of methotrexate in rats (40 mg methotrexate/kg body weight). At 48 h after injection of methotrexate, when mitotic activity in the crypts approximates to zero, an almost complete disappearance of mucin-containing goblet cells can be observed. At 96h, when proliferative activity in crypts is excessive, neutral mucin- and sialomucin-containing goblet cells dominate in the crypts, whereas in controls the crypts display sulphomucin-containing goblet cells. At 144h neutral mucin- and sulphomucin-containing goblet cells dominate in the crypts. Both at 48 and 96h after injection of methotrexate a significant decrease in the number of villous goblet cells takes place, whereas with respect to the quality of the mucins in the goblet cells no difference can be found in comparison with control rats. At 144h the villi have recovered from the preceding temporary decrease of goblet cells. The histochemical composition of the population of goblet cells is still aberrant and shows goblet cells containing neutral mucins and sulphomucins principally, whereas in controls sialomucin-containing goblet cells dominate on the villi. The established changes in the composition of mucins in goblet cells cannot be attributed to methotrexate-induced malnutrition, as pair-fed control rats clearly demonstrate. Our results clearly demonstrate that conspicuous quantitative as well as qualitative changes in the synthesis of mucins in goblet cells occur during the hyporegenerative and hyperregenerative phase of methotrexate-induced mucosal atrophy.

Animals↗
PubMedDate not supplied

Goblet cell metaplasia in the pulmonary alveolar epithelium in a rat.

Spontaneous goblet cell metaplasia in the pulmonary alveolar epithelium in a 110-wk-old male Jcl:Wistar rat is described. The rat had a dark red spherical mass in the center of the left lobe of the lung. The mass consisted of distended alveoli and bronchioles filled with mucus and nonciliated epithelial cells with numerous goblet cells lining the alveoli on the periphery of the mass. The goblet cells produced Alcian blue- and high iron diamine-positive sulfated glycoprotein differing from the sialylated glycoprotein seen in the normal rat airway surface epithelium. To the best of this investigator's knowledge, this is the first report dealing with detailed morphological and histochemical features of goblet cell metaplasia in the pulmonary alveolar epithelium resulting in mass formation due to mucous production.

Animals↗
PubMed1988

Dexamethasone reduces rat tracheal goblet cell hyperplasia produced by human neutrophil products.

An experimental model leading to goblet cell hyperplasia was developed in order to examine the possible preventive effects of glucocorticosteroids. Human peripheral blood neutrophils were isolated and either freeze-thaw lysed or activated with serum opsonized zymosan. Supernatants from these neutrophil preparations were then instilled transorally into the tracheas of male Sprague-Dawley rats. After 7-35 days, the rats were sacrificed; the lower tracheas were excised, fixed in formalin, and stained with periodic acid-Schiff and alcian blue; and the goblet cells and total epithelial cells were counted. Supernatants from both lysed neutrophils and zymosan-activated neutrophils stimulated a 50% and 42% (respectively) increase in goblet cells after 3 weeks as compared to controls. Purified human neutrophil or porcine pancreatic elastase also caused goblet cell hyperplasia, while sham challenge, challenge with buffer, or challenge with lysates of human mononuclear cells failed to affect goblet cell number. The increase in goblet-cell number was maximal by three weeks and persisted through 35 days. Treatment of animals with glucocorticosteroids administered by the addition of dexamethasone to the drinking water (2 mg/l for 1 week followed by 0.2 mg/l for 2 weeks) ablated the goblet cell hyperplasia produced by neutrophil lysates or elastase alone. We conclude that goblet cell hyperplasia may be induced with insufflated neutrophil products and that this action can be inhibited by treatment with corticosteroids.

Animals↗
PubMed2003

Spontaneous remission of edema and regranulation of goblet cells in rat tracheae after capsaicin-induced acute inflammation.

Previous studies have investigated the short-term effect of capsaicin on edema formation and goblet-cell secretion in the trachea. The present study sought to investigate the long-term effect of a high dose of capsaicin (90 micro g/ml/kg), administered intravenously, on changes in the formation of endothelial gaps among venular endothelial cells, mucosal tissue edema and the secretory activity of goblet cells, including the number and size of goblet cells, and the mucus score and secretory ratio of goblet-cell mucus secretion in the trachea of rats. The tracheal whole mounts with silver staining, those stained with chloroacetate esterase reagent and Alcian blue and tracheal tissue sections stained with Alcian blue and periodic acid-Schiff reagent were used for evaluation. Formation of endothelial gaps occurred a few min after administration of capsaicin, and gaps almost closed within 12 min after capsaicin injection. Five min after capsaicin, the leaky blood vessels were numerous and the subepithelial edema ratio (% of length of edema along the inner circumference of tracheal cross section) was found to be 57.8+/-3.0% ( n=6). The number of Alcian blue-positive goblet cells (1,090+/-220 per mm(2) of mucosal surface) was reduced to half the number of goblet cells in the vehicle-treated rats (2,200+/-230). The mucus score of goblet cell secretion was not changed. The secretory ratio was greatly increased. One day after capsaicin, the edema ratio remained large and the number of Alcian blue-positive goblet cells was also small. The mucus score was also not changed. The secretory ratio was still large. On day 3, the edema ratio remained large, but the number of Alcian blue-positive goblet cells was increased to the level of the controls. The mucus score and secretory ratio returned to the control level. On day 5, the edema ratio was greatly decreased, but it was still significantly larger than that of the controls. The mucus score and secretory ratio remained at the baseline level. Seven days after capsaicin, the edema ratio was similar to the controls. The number of goblet cells was even larger than controls. It is concluded that capsaicin-induced acute inflammation in the rat trachea involves formation of endothelial gaps, extensive plasma extravasation and edema formation, and depletion of goblet-cell secretory granules. Spontaneous gradual remission of edema was accompanied by regranulation of goblet cells with gradual mucogenesis for several days.

Acute Disease↗
PubMed2000

Goblet cell hyperplasia in the airway of Nippostrongylus brasiliensis-infected rats.

BACKGROUND: In rats, the intestinal parasite Nippostrongylus brasiliensis is recognized as a strong inducer of intestinal goblet cell hyperplasia. Although this parasite migrates through the airways during the course of its infection, airway goblet cell response remains unknown. OBJECTIVE: This study was designed to examine airway goblet cell response during the course of N. brasiliensis infection in rats and to characterize these goblet cells. METHODS: Airway goblet cells were stained with Alcian blue and periodic acid-Schiff. To characterize the goblet cells, mebendazole treatment, lectin histochemistry, and RNA blot analysis using probes for rat MUC2 and trefoil peptides were examined. RESULTS: Airway and small intestinal goblet cell hyperplasia were observed at days 14 and 21 after infection but not at day 7. In rats treated with mebendazole, goblet cell hyperplasia was not present in the small intestine, but was observed in the lung on day 14. These results indicate that airway goblet cell hyperplasia may be induced by local pulmonary factors. By lectin histochemistry, the stainability of airway goblet cells at day 21 was similar to that of small intestine goblet cells even though rat MUC2 and trefoil peptide mRNA were not detected in the lung. CONCLUSIONS: Airway goblet cell hyperplasia observed at days 14 and 21 after N. brasiliensis infection may be induced by local factors. Airway goblet cells have characteristics that differ from those of the small intestine.

Animals↗
PubMed1994

Secretion from gland and goblet cells in infected sinuses.

The number of goblet cells in the normal mucosa in the paranasal sinuses is comparable to that in the nasal mucosa. There are relatively few mucosal glands in the sinuses. In recent years, the maxillary sinus of the rabbit has been used for experimental studies. After induced infections, the number of goblet cells increases. In pneumococcal sinusitis, the number reaches a peak after 3 weeks and then declines. In sinusitis induced by St. aureus and the anaerobic bacteria B. fragilis, the number is more progressive over time and persistent during 12 weeks. The number of glands shows no hyperplasia, but occasionally atypical glands can be found. In patients with chronic sinusitis, the number of goblet cells is usually not affected but the number of glands increases, and the glands usually have a pathological shape. A decreased ciliary beating frequency correlates well with an increase in number of goblet cells. However, 75% of patients with chronic sinusitis have a normal frequency. When performing studies in patients with sinusitis one should be aware of the dynamic course of the disease and the difficulty in evaluating single mucosal biopsies.

Animals↗
PubMed1986

Human colonic goblet cells. Demonstration of distinct subpopulations defined by mucin-specific monoclonal antibodies.

We studied glycoprotein content of human colonic goblet cells, using a library of monoclonal antibodies (MAbs) directed against purified human colonic mucin (HCM). Using indirect immunofluorescence (IIF), we found that 17 of 23 anti-HCM MAbs stained some or all goblet cells of normal human colonic mucosa. We observed a variety of cellular staining patterns, including (a) diffuse (homogeneous) staining of intracellular mucin, (b) speckled (inhomogeneous) staining of mucin droplets, (c) peripheral staining of intracellular droplets, (d) cytoplasmic staining of goblet cells, and (e) apical (luminal) surface staining. Staining patterns were not associated with particular HCM species. In addition to variable patterns of IIF within individual cells, anti-HCM MAbs varied in the proportion of goblet cells stained. Some MAbs stained all goblet cells, while others stained a limited number of goblet cells. Although each goblet cell contained more than one type mucin, HCM species III, and IV and V appeared to exist in mutually exclusive goblet cell populations and it was possible to define at least seven subpopulations of goblet cells in colonic mucosa by their content of various combinations of HCM species. Anti-HCM MAbs stained goblet cells from other sites within the gastrointestinal tract to a varying extent. Anti-HCM MAbs also showed extensive cross-reactivity with rodent, rabbit, and monkey colonic mucosa. However, several anti-HCM MAbs stained only human colonic mucosa. These data show that human colonic mucosa contains discrete subpopulations of goblet cells that produce distinctive combinations of specific mucin glycoprotein species.

Animals↗
PubMed1993

[A study of goblet cells in the rat nasal septum by quantitative histological techniques].

The number and area of goblet cells in the normal rat septum were examined quantitatively using a whole-mount method and image analysis. With this approach, the number of goblet cells can easily be counted and quantitative analysis of secretory granules under different conditions can be determined histologically. When the whole mucosa of the nasal septum was divided from anterior to posterior into 8 equal sections, the third and fourth sections contained many large goblet cells. This finding may reflect the physiological role of the nasal mucosa, which warms and humidifies nasal air streams. The distribution of goblet cells in the nasal septum seems to be complementary with that of glandular orifices, which may serve the purpose maintaining the mucous blanket in the nasal cavity. ACh perfusion demonstrated an area of alcian-blue-positive secretory granules in goblet cells which decreased immediately afterwards, but recovered in 10 minutes. These results strongly suggest that ACh initially increases secretion in goblet cells and then enhances the production of secretory granules in these cells approximately 10 minutes later. IPR perfusion, on the other hand, showed an area of alcian-blue-positive secretory granules in goblet cells which decreased 30 minutes after treatment. Furthermore, there was variety in the area of each goblet cell. These results strongly suggest the possibility that IPR may slowly elevate secretion from goblet cells. It seems most likely that goblet cells have the same secretory reaction characteristics to autonomic nerve agents as glandular secretory cells.

Animals↗
PubMed2003

A mechanism of antigen-induced goblet cell degranulation in the nasal epithelium of sensitized rats.

BACKGROUND: We have produced hypertrophic and metaplastic changes of goblet cells in nasal epithelium of ovalbumin (OVA)-sensitized rats by intranasal challenge with OVA. A variety of allergic mediators and inflammatory cells are capable of stimulating goblet cell degranulation (epithelial mucus secretion); however, little is known about the mechanism by which antigen induces mucus hypersecretion. OBJECTIVE: Our aim was to explain the mechanism of goblet cell degranulation in allergic inflammation. METHODS: Antigen-induced goblet cell degranulation was evaluated by the transient decrease of epithelial mucosubstance 1 to 6 hours after intranasal challenge with OVA in nasal epithelium of OVA-sensitized rats. The effects of the H(1)-antagonist (d -chlorpheniramine malate), H(2)-antagonist (cimetidine), atropine, indomethacin, cysteinyl leukotriene (cysLT) antagonist (ONO1078), and antirat PMN antiserum on OVA-induced goblet cell degranulation were examined. RESULTS: Goblet cell secretion 1 hour after OVA challenge was significantly inhibited by H(1)-antagonist, atropine, and cysLT antagonist, whereas the secretion 6 hours after the challenge was significantly inhibited by cysLT antagonist and antirat PMN antiserum. Circulating PMN cells and mucosal infiltrating eosinophils were completely abolished by antirat PMN antiserum. CONCLUSIONS: These results indicate the different mechanisms of goblet cell secretion between early-phase (1 hour after OVA challenge) and late-phase (6 hours after the challenge) reactions. Histamine stimulates early-phase secretion through the H(1)-receptor of cholinergic nerve terminals, and infiltrating inflammatory cells (eosinophils and/or neutrophils) play a role in late-phase secretion. CysLTs (leukotrienes C(4), D(4), and E(4)) are important for both early-phase and late-phase secretion.

Animals↗
PubMed1990

Interaction of cholera toxin with cloned human goblet cells in monolayer culture.

Exposure of the intestinal mucosa to Vibrio cholerae enterotoxin (CT) results in mucus secretion from intestinal goblet cells. On the other hand, there is evidence that elevation of intracellular adenosine 3',5'-cyclic monophosphate levels is not sufficient to induce rapid mucin secretion. To determine whether CT has direct effects on human goblet cells and whether CT alone can elicit rapid exocytosis of apical mucin granules, purified CT was applied to monolayer cultures of well-differentiated HT-29-18 N2 cells, a goblet cell subclone derived from the human colon carcinoma line HT-29. CT bound with high affinity (dissociation constant = 10.5 +/- 1.9 nM) to receptors on these cells (approximately 60,000/apical membrane). Binding of radiolabeled CT was inhibited by excess CT or B subunit but not by A subunit. Preincubation of goblet cells with CT blocked the subsequent CT-specific ribosylation of a 45-kDa protein in membrane fractions of the cells and increased the activity of adenylate cyclase by 2- and 10-fold after 1 and 20 h, respectively. Light micrographs revealed that goblet cells incubated with CT, like control cells, contained abundant apical mucin granules. In contrast, goblet cells incubated with Ca2+ inophore A23187 and phorbol ester were rapidly depleted of mucin granules. Thus CT has direct physiological effects on HT-29 goblet cells, but these do not lead to rapid mucin secretion. These results raise the possibility that CT may accelerate mucin secretion in intact mucosa by an indirect mechanism perhaps mediated by mucosal nerves or other cell types.

Cell Line↗
PubMed2001

Allergen challenge causes inflammation but not goblet cell degranulation in asthmatic subjects.

BACKGROUND: An allergen challenge to the airways of sensitized mice causes eosinophilic airway inflammation and degranulation of goblet cells, which lead to airway obstruction. However, whether allergen challenge causes a similar pattern of airway inflammation and goblet cell degranulation in human beings is unknown. OBJECTIVE: The purpose of this study was to determine whether allergen challenge increases airway inflammatory cells and causes goblet cell degranulation in human subjects with asthma. METHODS: In bronchial biopsy specimens taken from 8 asthmatic subjects at 1 and 24 hours after allergen challenge, we measured eosinophil and neutrophil numbers as indicators of inflammation. We also measured goblet cell mucin stores and the amounts of secreted mucin in bronchial lavage as indicators of goblet cell degranulation. RESULTS: Airway eosinophil numbers at both 1 and 24 hours after allergen challenge were twice as high as those after diluent challenge. Changes in neutrophil numbers were smaller and statistically insignificant. Goblet cell mucin stores measured in tissue stained with alcian blue/periodic acid-Schiff did not decrease significantly from baseline to 1 hour and actually tended to increase at 24 hours. This increase was significant in the subgroup of subjects with normal stored mucin levels at baseline. Mucin-like glycoprotein concentrations in bronchial lavage did not change significantly at either time point. CONCLUSION: Although allergen challenge in asthmatic subjects increases airway eosinophil numbers as early as 1 hour after challenge, this inflammatory response does not cause goblet cell degranulation. In fact, in subjects with normal baseline mucin stores, allergen challenge increases goblet cell mucin stores.

Adult↗
PubMed1999

Immunolocalization of muscarinic and VIP receptor subtypes and their role in stimulating goblet cell secretion.

PURPOSE: To determine the subtypes of cholinergic muscarinic receptors and receptors for vasoactive intestinal peptide (VIP) present in rat conjunctival goblet cells and whether cholinergic agonists and VIP stimulate goblet cell secretion. METHODS: Immunofluorescence studies were performed using antibodies against the m1, m2, and m3 muscarinic receptor subtypes and VIP receptors 1 and 2 (VIPR1 and VIPR2). The lectin Ulex europeus agglutinin I was used to measure glycoconjugate secretion, the index of secretion, from goblet cells in an enzyme-linked lectin assay. In this assay, pieces of conjunctiva were placed on filter paper and incubated for 15 to 120 minutes, with or without increasing concentrations of the cholinergic agonist carbachol or VIP. The muscarinic antagonist atropine and the muscarinic receptor-subtype-selective antagonists pirenzepine (M1), gallamine (M2), and 4-4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (4-DAMP mustard; M3) were incubated with carbachol to determine specificity of receptor activation. RESULTS: Immunoreactivity to M2 and M3 receptors was found on goblet cell membranes subjacent to the secretory granules. Immunoreactivity to M1 receptor was not on goblet cells but was on the stratitfied squamous cells. Immunoreactivity to VIPR2 was found on goblet cells with a localization similar to that of the M2 and M3 receptors. VIPR1 was not found on goblet cells or on the stratified squamous cells. Carbachol and VIP induced a time- and concentration-dependent stimulation of glycoconjugate secretion. Carbachol, at 10(-4) M, induced a threefold increase in glycoconjugate secretion, which was completely inhibited by atropine (10(-5) M). Carbachol-induced secretion was inhibited 54% +/- 8% by pirenzepine (10(-5) M), 69% +/- 14% by gallamine (10(-5) M), and 72% +/- 11% by 4-DAMP mustard (10(-5) M). A twofold increase in glycoconjugate secretion was obtained with VIP at 10(-8) M. CONCLUSIONS: Cholinergic agonists, through M2 and/or M3 muscarinic receptors, and VIP, through VIPR2, regulate conjunctival goblet cell secretion, suggesting that goblet cell secretion in vivo is under the control of parasympathetic nerves.

Animals↗
PubMed2006

[Goblet cell distribution and epithelial cell morphology in pterygium].

BACKGROUND: Studies conducted to date on the distribution density of goblet cells and epithelial cell morphology in pterygium have yielded contradictory findings. OBJECTIVE: To evaluate the density of goblet cells in pterygium and possible correlation between clinical and demographic features and goblet cell distribution. METHODS: The methodology involved retrospective case series. The study sample included 45 consecutive patients undergoing bare sclera operation. Biopsy specimens were examined under light microscopy. The goblet cells were counted in four fields under X480 magnification and determined by the density range. Demographic features were evaluated for every patient. The relationships between elastosis, inflammation, congestion of blood vessels and the density range in goblet cell count were determined. RESULTS: Distribution density of goblet cells was found to be homogenous among cases. In 16 cases (35%) the count showed more than 120 cells in a field, while in 13 cases (30%) the authors calculated under 15 cells in a field. In 27 cases (60%) there was a high rate of elastosis. In only 3 cases (6.6%) the authors found mild dysplasia of the epithelium. There was a low rate of congestion of blood vessels in only 5 cases (11%). In all cases inflammation was found. There was no significant correlation found with all demographic parameters evaluated. CONCLUSION: There is a high rate of difference in the distribution and density of goblet cells in pterygia, without any correlation with demographic and clinical features listed. There is a variable elastosis rate, significant congestion of blood vessels and a low rate of dysplasia. All cases presented with chronic inflammatory reaction.

Adult↗
PubMed2001

Airway goblet cells and respiratory epithelial injury in an animal model of obliterative airways disease (OAD).

UNLABELLED: Goblet cells are important in the maintenance of the epithelial cell population in the airway, defense against injury and storage and release of mucins, which can protect the surface epithelial layer. In our rat tracheal model of acute rejection, there is injury and loss of respiratory epithelium in allografts. This loss of epithelium is associated with obliteration of the airway lumen. In small bowel allografts, studies have shown that the loss of goblet cells is an important histologic feature of rejection. The aims of this study were: (i) to examine for the first time the close time-course of goblet cell proliferation in acute rejection; and (ii) to compare the isograft vs. allograft morphometric changes associated with epithelial damage. METHODS: Heterotopically transplanted rat tracheas (n = 45) were harvested at days 3,5,7, 10 and 12. Hematoxylin & eosin (H & E), Alcian blue and PAS staining was completed. Computerized image analysis was used to assess epithelial coverage. The mean number of PAS-positive goblet cells counted at 40x/field was determined, and 10 fields were counted per tracheal section. RESULTS There was a significant decrease in the number of goblet cells in the allografts between days 5 and 12 (p < 0.006). In the isografts, there was a gradual increase from day 3 to 10 (p < 0.05), then a sharp fall from day 10 to 12 (p < 0.03). In isografts from day 7 to 10, the goblet cell number increased, while the percentage respiratory epithelium remained the same. The percentage respiratory epithelial coverage and the number of goblet cells showed a direct correlation in the allografts (r2 = 0.57). CONCLUSIONS: Our study shows, for the first time, that goblet cell proliferation occurs in the epithelial repair phase in isografts, whereas in allografts the goblet cells are lost and do not recover.

Animals↗
PubMed1999

IL-4 induces mucin gene expression and goblet cell metaplasia in vitro and in vivo.

Goblet cell metaplasia and mucus hypersecretion are important features in the pathogenesis of asthma. The cytokine IL-4 has been shown to play a role in animal models of asthma, where it induces Th2 lymphocyte differentiation and B lymphocyte IgE class switch. IL-4 has also been implicated in the differentiation of goblet cells via effects on lymphocytes and eosinophils. In this study we hypothesized that IL-4 induces airway epithelial cell mucin gene expression and mucous glycoconjugate production by direct action on these cells. In vitro, cultured airway epithelial cells (NCI-H292) expressed IL-4R constitutively, and IL-4 (10 ng/ml) induced MUC2 gene expression and mucous glycoconjugate production. In vivo, mouse airway epithelial cells expressed IL-4R constitutively, and IL-4 (250 ng) increased MUC5 gene expression and Alcian blue/periodic acid-Schiff-positive staining at 24 h; IL-4 did not increase inflammatory cell numbers in airway tissue or in bronchoalveolar lavage. TNF-alpha and IL-1beta levels in bronchoalveolar lavage were not increased in response to IL-4 instillation. These results indicate that airway epithelial cells express IL-4R constitutively and that IL-4 directly induces the differentiation of epithelium into mucous glycoconjugate-containing goblet cells.

Animals↗