Goblet Cells In Mice Research Articles

TSP50 Attenuates DSS-Induced Colitis by Regulating TGF-β Signaling Mediated Maintenance of Intestinal Mucosal Barrier Integrity.

The integrity of the intestinal mucosal barrier is crucial for protecting the intestinal epithelium against invasion by commensal bacteria and pathogens, thereby combating colitis. The investigation revealed that the absence of TSP50 compromised the integrity of the intestinal mucosal barrier in murine subjects. This disruption facilitated direct contact between intestinal bacteria and the intestinal epithelium, thereby increasing susceptibility to colitis. Mechanistic analysis indicated that TSP50 deficiency in intestinal stem cells (ISCs) triggered aberrant activation of the TGF-β signaling pathway and impeded the differentiation of goblet cells in mice, leading to impairment of mucosal permeability. By inhibiting the TGF-β pathway, the functionality of the intestinal mucosal barrier is successfully restored and mitigated colitis in TSP50-deficient mice. In conclusion, TSP50 played a crucial role in maintaining the intestinal mucosal barrier function and exhibited the preventive effect against the development of colitis by regulating the TGF-β signaling pathway.

Lactobacillus paracasei from koumiss ameliorates diarrhea in mice via tight junctions modulation

ObjectivesProbiotics are gaining interest as alternative options for antibiotic or antiinflammatory drugs. Probiotics can affect the health of the host through metabolites and competitive inhibition adhesion of pathogenic microorganisms. Koumiss is an important part of the diet of Asian nomads, and is rich in a broad array of probiotics that can benefit the body. Mongolians have developed koumiss therapy to assist in the treatment of various diseases. In the present study, we investigate the beneficial effect of Lactobacillus paracasei, a strain isolated from koumiss, on a mouse model of diarrhea induced by Escherichia coli O8 (E. coli O8). MethodsProbiotics were isolated from Mongolian koumiss. The resistance of probiotics against acid, bile salts, gastric juice, and intestinal juice was evaluated. The mouse model of diarrhea was established by the intragastric administration of E. coli O8 after NaHCO3 treatment. L. paracasei was intragastrically administered before or after E. coli O8 exposure in mice. The plasma levels of diamine oxidase and zounlin were quantified using an enzyme-linked immunosorbent assay, and the integrity of the intestinal barrier and goblet cells of mice with diarrhea were observed using hematoxylin and eosin and Alcian blue periodic acid-Schiff staining. The expression of tight junction (TJ) proteins was detected by immunohistochemistry and Western blot. ResultsA total of five lactic acid bacteria and two yeast strains were isolated from koumiss, and L. paracasei was screened for animal experiments. Experimental results showed that L. paracasei could reduce the increase in diamine oxidase and zonulin caused by E. coli (P < 0.05); increase goblet cells and the expression of TJ proteins ZO-1, occludin, and claudin-1 (P < 0.05); increase the expression of mucin 2, oligomeric mucus/gel-forming (P < 0.05) protein; and reduce the level of inhibitor kappa B-alpha and myosin light-chain kinase. ConclusionsL. paracasei reduced the intestinal permeability, induced the expression of mucin 2, oligomeric mucus/gel-forming protein, and increased the number of goblet cells in mice by the upregulation of the expression of TJ proteins via the nuclear factor kappa B cells–myosin light-chain kinase signaling pathway.

The distribution of conjunctival goblet cells in mice

PurposeTo evaluate the density and distribution of conjunctival goblet cells in mice without clinical evidence of ocular surface diseases. MethodsImmediately after euthanasia of C57BL/6 wild-type mice, the eyes including eyelids were removed and fixed in paraformaldehyde. Entire eyeballs and eyelids were cut in series along the sagittal axis from nasal to temporal on a microtome and then stained with Periodic Acid-Schiff acid to visualize the goblet cells. At each section stained in this way, the conjunctival goblet cells of the entire upper and lower lid conjunctiva were counted by light microscopy. Additional (transmission electron microscopy) (TEM)-Analysis on ultrathin sections was performed to evaluate morphological differences. ResultsThe total number of conjunctival goblet cells differs markedly between individual animals. Categorisation into upper eyelid (UL) and lower eyelid (LL) and into regions (nasal, middle, temporal) revealed a significant increase of goblet cells from nasal to temporal in the UL and a significant decrease in the LL. ConclusionThe distribution of conjunctival goblet cells in mice differs considerably from humans and between individual animals. Therefore, precise selection of sampling and methods are needed to obtain comparable data. We recommend to use the middle region of the conjunctiva of UL/LL for goblet cell studies in mice. These findings are of particular interest for dry eye mouse models as well as pharmacological studies on mice with influence on their goblet cells.

Effects of Trichuris Muris Infection on Mice (Mus musculus) Intestine

Helminth infection can influence immunopathology in human body. Changes in the length of intestine and release an increased goblet cell is one of the defense mechanisms against worm infections. In this study, we analyze effects of Trichuris muris infection towards goblet cells number and the l e n g t h o f villi and crypt intestine of mice This research was a true experimental with the posttest control group design. The subjects were 30 males mice types BALB/c which 2 months old with an average weight 20–30 grams. Samples were taken by simple random sampling. Mice divided into a control group, low-dose group and high-dose groups. All subject was observed for 30 days, and the intestine was taken for measured length of villi and crypt. Counting of goblet cells used preparation of intestine. Data analysis used one way Anova and continued by post hoc test. The result show that crypt and villi on large and small intestine will be longer in mice with Trichuris muris infection. The average value of the goblet cells number in the control group, low-dose and high dose increased by higher dose worm eggs and had the value (p =< 0.05). Trichuris muris infection has influenced t h e l e n g t h o f villi and crypt intestine and the number of goblet cells in mice (Mus musculus).

Beneficial effects of extracellular polysaccharide from Rhizopus nigricans on the intestinal immunity of colorectal cancer mice

An extracellular polysaccharide (EPS1-1) extracted from the fermentation broth of Rhizopus nigricans has been proved to enhance the immunity of immunosuppressed mice. The purpose of this study was to investigate the beneficial effects of EPS1-1 on the intestinal immunity of mice with colorectal cancer induced by azoxymethane (AOM) and dextran sodium sulfate (DSS). The results showed that EPS1-1 could resist hydrolysis in an artificial stomach. Oral EPS1-1 modulated gut microbiota and increased the concentration of total short-chain fatty acids (SCFAs) in the feces of colorectal cancer mice compared with the AOM/DSS only-treated mice. Furthermore, EPS1-1 increased the villus length, ratio of villus length and crypt depth in colonic tissues, and improved the number of acid mucus-secreting goblet cells in mice with colorectal cancer. These findings suggest that EPS1-1 might play an important role in the improvement of intestinal function in mice with colorectal cancer, which indicate its strong potential as efficient bio-secure immunotherapy for clinical applications or adjuvant drug.

Efficacy of Sodium Hyaluronate in Murine Diabetic Ocular Surface Diseases.

To evaluate the efficacy of sodium hyaluronate (HA) eye drops for the treatment of diabetic ocular surface diseases in mice. Male 6- to 8-week-old C57BL/6 mice underwent induction of type 1 diabetes with intraperitoneal injections of streptozotocin, with normal mice as the control. Topical 0.3% HA, 0.1% HA, 0.4% polyethylene glycol eye drops, and normal saline were administered to diabetic mice with an intact or debrided corneal epithelium. Normal saline was applied in the controls. Corneal epithelial wound healing rate, corneal sensation, nerve fiber density, conjunctival goblet cell number, and MUC-5AC content were measured and compared. Compared with the controls, topical 0.3% HA use in diabetic mice showed significant improvements in the corneal epithelial wound healing rate (48 hours: 91.5% ± 4.8% vs. 79.8% ± 6.1%; P < 0.05), corneal sensitivity (4.1 ± 0.3 cm vs. 3.5 ± 0.3 cm; P < 0.05), nerve fiber density (12.9% ± 2.3% vs. 6.6% ± 2.4%; P < 0.05), conjunctival goblet cell number (31.0 ± 8.4/100 μm vs. 19.6 ± 7.1/100 μm; P < 0.05), and MUC-5AC content (12.5 ± 1.4 ng/mg vs. 7.8 ± 1.5 ng/mg protein; P < 0.05). The beneficial effects of 0.3% HA were better than those of 0.1% HA and 0.4% polyethylene glycol. Topical 0.3% HA treatment promoted corneal epithelial regeneration, improved corneal sensation, and increased density of corneal nerve fibers and conjunctival goblet cells in mice with diabetic ocular surface diseases.

CCN3 Expression Marks a Sulfomucin-nonproducing Unique Subset of Colonic Goblet Cells in Mice.

Intestinal goblet cells are characterized by their unique morphology and specialized function to secrete mucins. Although it is known that they are a heterogeneous population of cells, there have been few studies that relate the expression of a particular gene with functionally distinct subpopulations of intestinal goblet cells. Here we show that CCN3, a gene encoding a member of the CCN family proteins, is induced by inhibition of Notch signaling in colonic epithelial cells and expressed in goblet cells in mice. We demonstrate that CCN3 expression is confined to a subpopulation of goblet cells in the lower crypt of the proximal and middle colon. In addition, CCN3+ cells in the colon correlate well with the cells that are positive for alcian blue (AB) staining but negative for high-iron diamine (HID) staining in histology. We also show that CCN3+ cells, which are absent in the normal distal colon, transiently and ectopically emerge in regenerating crypts during the repair phase of DSS-induced colitis model. Our study thus suggests that CCN3 labels a unique subpopulation of sulfomucin-nonproducing colonic goblet cells that function in both normal and diseased colonic epithelia.

Increasing fat content from 20 to 45 wt% in a complex diet induces lower endotoxemia in parallel with an increased number of intestinal goblet cells in mice

The impacts of high-fat diets (HFDs) on the onset of metabolic endotoxemia and low-grade inflammation are well established in rodent models. However, the dose-effect of dietary lipid intakes on these parameters is not known. We hypothesized that increasing dietary lipid amounts could be linked to parallel increases of endotoxemia, low-grade inflammation, and metabolic and intestinal alterations. Six-week-old male C57BL/6J mice were fed a low-fat diet (LFD, 2.6 wt% of lipids), a moderate HFD (mHFD, 22 wt% of lipids), or a very HFD (vHFD, 45 wt% of lipids) formulated mainly using chow ingredients and milk fat. After 12 weeks, white adipose tissues, liver, intestine, distal colon contents, and plasma were collected. Only vHFD mice significantly increased body weight and fat mass vs LFD mice. This was associated with increases of plasma concentrations of triglycerides, leptin and adiponectin, and liver lipids. No such differences were observed between LFD and mHFD mice. However, mHFD developed metabolic endotoxemia and inflammation, unlike vHFD mice. In turn, vHFD mice showed more goblet cells in all intestine segments vs both other groups and a decrease of Bacteroides-Prevotella in their microbiota vs LFD mice. Finally, mHFD mice colon exhibited a decrease in lactobacilli and in the levels of occludin phosphorylation. Altogether, using complex HFD, no associations were observed between dietary lipid amounts and the magnitude of endotoxemia, inflammation, and physiological alterations developed. These results reveal the impact of the diet composition on intestinal goblet cells and mucus coat, bringing new insights about further consequences on HFD-induced metabolic disorders.

Cloning of the gene gob-4, which is expressed in intestinal goblet cells in mice

We isolated the novel cDNA gob-4, which was shown to be expressed in intestinal goblet cells. The deduced amino acid sequence is similar to the gene coding for the Xenopus laevis cement gland-specific XAG-2. These sequence and expression data suggest this gene may be involved in the secretory function.

Cloning and Identification of the Gene Gob-5, Which Is Expressed in Intestinal Goblet Cells in Mice

By using the large-scalein situhybridization system (Analytical Biochemistry(1997) 254, 23–30), we isolated the cDNA gob-5, which is expressed in the intestinal goblet cells in mice. The transcript was also found to be abundantly expressed in small intestine, colon, stomach, and uterus and slightly expressed in trachea tissue. The gob-5 cDNA was shown to be 3 kb in size. After screening digestive tract tissues using ourin situhybridization method we demonstrate that gob-5 is expressed in mucous cells. The deduced amino acid sequence is similar to the gene which encodes the epithelial chloride channel in the bovine trachea.