Expression of Secretory Mucins in the Human Upper Gastrointestinal Tract; The Role of MUC5AC in the Adhesion of Helicobacter Pylori (2024)

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Cancer research

Intestinal metaplasia of human stomach displays distinct patterns of mucin (MUC1, MUC2, MUC5AC, and MUC6) expression

1999 •

Leonor David

Intestinal metaplasia is a well-established premalignant condition of the stomach that is characterized by mucin carbohydrate modifications defined by histochemical methods. The purpose of the present study was to see whether the expression of mucin core proteins was modified in the different types of intestinal metaplasia and to evaluate the putative usefulness of mucins as "molecular markers" in this setting. We used a panel of monoclonal antibodies with well-defined specificities to MUC1, MUC2, MUC5AC, and MUC6 to characterize the expression pattern of mucins. In contrast to normal gastric mucosa, the complete form or type I intestinal metaplasia (n = 20) displayed little or no expression of MUC1, MUC5AC, or MUC6 in the metaplastic cells and strong expression of the intestinal mucin MUC2 in the goblet cells of all cases. The incomplete forms of intestinal metaplasia, type II (n = 25) and type III (n = 16), expressed MUC1 and MUC5AC in every case, both in goblet and in c...

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Virchows Archiv

Mucins as key molecules for the classification of intestinal metaplasia of the stomach

2002 •

Celso Reis

Mucins and mucin-associated carbohydrates have a distinct expression pattern that can be modified under pathological conditions. Normal gastric mucosa expresses MUC1 and MUC5AC in foveolar epithelium and MUC6 in the glands. Lewis type-1 chain antigens (Lea and Leb) are expressed in foveolar epithelium, whereas Lewis type-2 chain antigens (Lex and Ley) are expressed in the glands. In this study we used monoclonal antibodies to evaluate the pattern of mucins and Lewis type-1 carbohydrates in intestinal metaplasia (IM) and compared it with IM types determined using histochemistry. In type-I or complete IM we found expression of MUC2 intestinal mucin and decreased/absent expression of MUC1, MUC5AC and MUC6. In type-II/III or incomplete IM there was co-expression of MUC2 and the mucins expressed in the stomach. No major differences were detected among the three IM types regarding expression of Lewis antigens. Furthermore we observed that sialylated compounds other than sialyl-Lea are responsible for histochemical detection of sialomucins and that sulpho-Lea/c is expressed in the presence or absence of sulphomucins detected using histochemistry. We conclude that mucin immunohistochemistry may replace classic histochemistry for the classification of IM into complete and incomplete types. The present study challenges the distinction of type-II from type-III IM since we did not observe major differences in the expression profile of mucins and Lewis type-1 carbohydrates. Finally, it seems necessary to evaluate the predictive value of IM according to the presence of specific sulphated carbohydrates (e.g. sulpho-Lea/c) rather than histochemically detected sulphomucins.

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Molecular cancer

Expression profile of mucins (MUC2, MUC5AC and MUC6) in Helicobacter pylori infected pre-neoplastic and neoplastic human gastric epithelium

2006 •

niranjali devaraj

Helicobacter pylori (H. pylori) causes gastritis and intestinal metaplasia (IM) that may evolve to gastric carcinoma. The objective of this study was to compare the profile of mucins in the progressive stages of H. pylori infected pre-neoplastic and neoplastic human gastric epithelium. We used a panel of monoclonal antibodies with well-defined specificities of MUC2, MUC5AC and MUC6 to characterize the expression pattern of mucins by immunohistochemistry. RUT and ELISA were down for H. pylori confirmation. Human gastric biopsy sections were stained using immunohistochemistry with MUC2, MUC5AC and MUC6 antibodies. MUC5AC was expressed in the superficial epithelium and the upper part of the gastric pits. MUC6 expression was detected in the lower part of the gastric glands. MUC2 was expressed in intestinal metaplasia, mostly in goblet cells. The mucin expression profile in the progressive stages of H. pylori infected human gastric epithelium allows the identification of intestinal metap...

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Immunohistochemical Study of the Expression of MUC6 Mucin and Coexpression of Other Secreted Mucins (MUC5AC and MUC2) in Human Gastric Carcinomas

Filipa Carvalho

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Journal of Histotechnology

Hematoxylin and eosin staining of mucins of the gastrointestinal tract

2017 •

Tony Henwood

An infrequent observation of assessing hematoxylin and eosin sections is the blue staining of mucins (for example those in goblet cells). This is believed to be due to a low concentration of alum and high pH of the hematoxylin staining solution. This study examines the incidence of blue mucin in various sites of the gastrointestinal tract using a low alum, high pH hematoxylin solution. The results are compared with a conventional hematoxylin solution, iron alum celestine blue method and an alcian blue (pH 2.5)-periodic acid-Schiff (AB-PAS) stain to characterize the type of mucin demonstrated. This study is the first to offer evidence that blue-stained mucin with low alum, high pH hematoxylin corresponds with carboxylated mucins as shown by the AB-PAS stain in the gastrointestinal tract. Iron alum celestine blue was also found to stain the mucin of a proportion of rectal biopsies and appendix as well as the carboxylated mucin of one duodenal biopsy.

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PubMed

Biochemical and immunohistochemical characterisation of mucins in 8 cases of colonic disease--a pilot study

2007 •

Anwar Mall

Objectives: To characterise mucins in cancer of the colon and compare these with controls using stringent biochemical measures to avoid endogenous proteolysis. Design: Crude mucus scrapings were collected from 12 specimens obtained by colectomy. Specimens from 3 traumatic colectomies and 1 sigmoid volvulus were used as controls, and compared with 6 specimens from colons resected for adenocarcinoma and 2 irradiated colons. Subjects: The median age of the 4 female patients was 76 years (range 49 - 82 years), and of the 8 male patients 46.5 years (range 16 - 74 years). Results and conclusions: The crude mucus scrapings in the 9 specimens ranged in weight from 353 mg to 7 697 mg (median 4 928 mg). The median of purified mucin in the 9 specimens was 0.72 microg/mg wet weight of scraped material. Eight samples gave non-extractable pellet material, and were treated with DTT to reduce disulphide bonds for further analysis. One of these 8 pellets was resistant to reduction and had to be digested with papain before analysis. Only 5 of these pellets had mucin. Gel filtration and SDS-PAGE (sodium dodecyl sulphate polyacrylamide gel electrophoresis) analysis revealed different populations of mucin based on size and extent of degradation. Western blotting and immunohistochemical analysis confirmed the presence of MUC2 in all samples, MUC5AC in 2 and MUC5B in 5 diseased specimens. Immunohistochemical analysis showed that there was no MUC1 in the normal specimens, MUC1 apoprotein (MUC1 core) in 2 cancer specimens and MUC1 in 1 cancer specimen. Histochemical analysis showed that normal tissue expressed neutral and acidic mucins and diseased specimens predominantly expressed acidic mucins. The electrophoretic behaviour of MUC2 in sigmoid volvulus was different from that in cancer of the colon.

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Infection and Immunity

Helicobacter pylori Infection Impairs the Mucin Production Rate and Turnover in the Murine Gastric Mucosa

2013 •

Sara Lindén

ABSTRACTTo protect the surface of the stomach, the epithelial cells secrete a mucus layer, which is mainly comprised of the MUC5AC mucin. Further protection is provided by a thick glycocalyx on the apical surface of the epithelial cell, with the cell surface mucin MUC1 as a major component. Here, we investigate the production rate and turnover of newly synthesized mucin in mice and analyze the effects of early colonization and chronic infection withH. pylori. Metabolic incorporation of an azido GalNAc analog (GalNAz) was used as a nonradioactive method to perform pulse experiments in the whole animal. First, the subcellular movement of newly synthesized mucin and mucin turnover was determined in uninfected mice. Based on the time line for mucin transport and dissemination, 2, 6, and 12 h after GalNAz injection was selected to collect the stomachs from mice infected withH. pyloristrain SS1 during early colonization (7 days) and chronic infection (90 days). The results demonstrated th...

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Journal of Clinical Medicine

Helicobacter pylori Infection and the Patterns of Gastric Mucin Expression in Children

Dan Gheban

Background: The updated model for the mechanism of gastric carcinogenesis demonstrates that Helicobacter pylori (H. pylori) is a risk factor in every step of the process. The expression of certain gastric mucins is altered by H. pylori infection in adult patients. The aim of our research was to assess the impact of H. pylori infection on the expression of secretory mucins in the pediatric antral mucosa. Methods: Slides were stained with monoclonal antibodies for MUC5AC, MUC6 and MUC2, digitalized and scored using both a semiquantitative and a quantitative approach. Results: The expression of MUC5AC was significantly lower in infected children. Also, MUC2 expression was more pronounced in infected children. MUC6 expression did not differentiate between infected and noninfected children. Additionally, the presence of chronic inflammation significantly altered the expression of MUC6 and MUC2. The expression of MUC6 was significantly higher in patients with gastric atrophy. Conclusion: ...

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IP innovative publication pvt. ltd

Mucin histochemical profile in a variety of human colonic non-neoplastic and neoplastic lesions

2019 •

IP Innovative Publication Pvt. Ltd.

Introduction: Mucin deregulation occurs in gastrointestinal lesions progressing to cancer. Evidences advocate utility of mucin profile to predict malignant transformation in preneoplastic colonic lesions, however data are controversial. Objectives: This clinicopathological descriptive study identifies the histochemical profiles of acidic and neutral mucins in human colonic tissues including inflammatory, non-neoplastic and neoplastic lesions. Mucin alteration in different histological grades of adenocarcinoma is also evaluated. Materials and Methods: After collection of relevant data, tissue samples from a cohort of 88 patients recruited from King Abdul Aziz Specialized Hospital, Taif, Saudi Arabia were examined. Dual Alcian Blue (AB; pH 2.5)/ Diastase (D) Periodic Acid Schiff (PAS) technique was used to differentiate acidic and neutral mucins respectively. Statistical analysis including descriptive statistics, Pearson’s chi-square test and linear regression was performed using SPSS. Results: Acidic and neutral mucins were positive in 67.1 and 46.6% of lesions, respectively. All ulcerative colitis tissues were positive for acidic mucin and 75% for neutral mucin. All non-neoplastic polyps were positive for both mucins. Adenomatous polyps demonstrated reduced mucin but more neutral (59.3%) than acidic one (44.4%). About 86% of adenocarcinomas revealed acidic mucin and 22.2% showed neutral mucin with trends for acidic mucin to decrease with grade and for neutral mucin to increase with grade. Conclusion: Altered both acidic and neutral mucin profiles occur in colonic lesions of different pathologies. As colonic adenocarcinoma progresses from grade 1 to grade 3, acid mucin declines with a corresponding increase in neutral mucin. Mucin profile may be of value in evaluating the preneoplastic colorectal lesions.

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International Journal of Colorectal Disease

Characterization of the mucins produced by normal human colonocytes in primary culture

1996 •

Fabio Magliocca, Giovanni Latella, Renato Fonti

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Expression of Secretory Mucins in the Human Upper Gastrointestinal Tract; The Role of MUC5AC in the Adhesion of Helicobacter Pylori (2024)

FAQs

What does H. pylori poop look like? ›

In most cases, the blood appears very dark — almost black. Your stools might have a tarry appearance or consistency.

Why might H. pylori require powerful flagella and adhesion surface proteins to survive in the stomach? ›

Flagella-mediated motility is then required for H. pylori to move toward host gastric epithelium cells, followed by specific interactions between bacterial adhesins with host cell receptors, which thus leads to successful colonization and persistent infection.

How does H. pylori affect gastric mucosa? ›

H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid. This cell injury may lead to cell death, believed to result from induction of apoptosis.

What does it mean when your H. pylori test is positive? ›

A positive test result means that you have an H. pylori infection. Your provider will usually prescribe one or more antibiotics to treat the infection. You will usually take other medicines to relieve your symptoms and help heal your stomach.

Does H. pylori ever go away? ›

Once H. pylori colonises the gastric mucosa, it can persist for a lifetime, and it is intriguing why our immune system is able to tolerate its existence. Some conditions favour the persistence of H. pylori in the stomach, but other conditions oppose the colonisation of this bacterium.

How bad can H. pylori make you feel? ›

It can damage the tissue in your stomach and the first part of your small intestine (the duodenum). This can cause redness and soreness (inflammation). In some cases it can also cause painful sores called peptic ulcers in your upper digestive tract.

What kills H. pylori naturally? ›

Licorice root is a common natural remedy for stomach ulcers. It may also help fight H. pylori. A 2020 review found that licorice root increased the eradication rate of the bacteria and has an antibacterial effect. It also seems to help prevent H. pylori from sticking to cell walls and helped promote ulcer healing.

What happens if H. pylori goes untreated? ›

Long-term infection with Helicobacter pylori could potentially lead to asymptomatic chronic gastritis, chronic dyspepsia, duodenal ulcer disease, gastric ulcer disease, or gastric malignancy, including both adenocarcinoma and B-cell lymphoma.

What are the signs of H pylori infection? ›

H. pylori is a bacteria that can cause peptic ulcer disease and gastritis. It mostly occurs in children. Only 20% of those infected have symptoms. Symptoms include dull or burning stomach pain, unplanned weight loss and bloody vomit.

How did I get H. pylori? ›

H. pylori bacteria are usually passed from person to person through direct contact with saliva, vomit or stool. H. pylori may also be spread through contaminated food or water. The exact way H. pylori bacteria causes gastritis or a peptic ulcer in some people is still unknown.

Can you live a normal life with H. pylori? ›

Most people infected with H. pylori have no problems. However, some people develop problems such as chronic gastritis, stomach ulcers and, rarely, stomach tumors.

Should I get tested for H. pylori if my partner has it? ›

H pylori is highly prevalent in the healthy partners of patients with H pylori infection. To decrease long-term re-infection rates, family members of H pylori-positive patients should be tested and, if positive, treated for H pylori infection.

Should I be worried about Helicobacter pylori? ›

For most people the infection won't cause them any problems. But in some, H. pylori can cause long-lasting irritation, swelling and pain in the stomach (known as 'severe chronic atrophic gastritis' or SCAG) and stomach ulcers. This can lead to cancer.

What to do after testing positive for H. pylori? ›

H. pylori infections are usually treated with at least two different antibiotics at once. This helps prevent the bacteria from developing a resistance to one particular antibiotic. Treatment may also include medications to help your stomach heal, including: Proton pump inhibitors (PPIs).

How do you treat a positive H. pylori test? ›

H. pylori is typically treated with a combination of antibiotics plus a proton pump inhibitor (PPI). Patients should be asked about previous antibiotic exposure to help guide the treatment regimen. There is no regimen with a 100% cure rate for H.

What color is H. pylori poop? ›

What does H. pylori poop look like? Most people infected with H. pylori will have normal-looking poop. But if yours looks dark, black, tarry, or has any blood in it, call your doctor right away.

Can you see H. pylori in your stool? ›

How Is the Test Done? At the lab, a technician puts a small amount of stool in tiny vials, then adds chemicals and a color developer. A blue color indicates the presence of H. pylori antigens.

Does H. pylori affect bowel movements? ›

Although H pylori infection may play a protective role against bacterial diarrhea in children, it is known to affect the gastric and intestinal microbiota[2123] and may cause chronic diarrhea due to any cause other than infection.

Is H. pylori visible in stool? ›

Helicobacter pylori infection can be diagnosed by invasive methods using the gastric biopsied specimens or noninvasively by examining serum, urine, breath, or stool.

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