scholarly journals Correlation between mast cell density and histological parameters in Helicobacter pylori-associated gastritis

2011 ◽  
Vol 5 (1) ◽  
pp. 163-167 ◽  
Author(s):  
Mana Taweevisit ◽  
Naruemon Klaikaew
Keyword(s):  
Helicobacter Pylori ◽  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
B Cell Lymphoma ◽  
Inflammatory Cells ◽  
Chronic Inflammatory Cell ◽  
Mast Cell Density ◽  
Sydney System ◽  
H Pylori

Abstract Background: Helicobacter pylori (H. pylori) are a major cause of chronic gastritis and peptic ulcer. This organism plays a role in gastric carcinoma and B-cell lymphoma. However, the exact pathogenesis of gastric inflammation is still unclear. Mast cells, the important inflammatory cells for allergic process, may participate in the pathogenesis of gastritis related to H. pylori infection. Objective: Analyze the relationship between mast cell density, H. pylori intensity, histological alterations, and their severity of biopsy proven gastritis. Methods: One hundred eleven biopsied specimens were collected from Thai patients who were diagnosed H. pylori-associated gastritis of the antrum at King Chulalongkorn Memorial Hospital between 2002 and 2005. All biopsied specimens were examined according to the Updated Sydney System. Mast cell density was evaluated by 0.1% toluidine-stained sections. Results: The higher mast cell density was correlated with increased neutrophilic infiltration (r = 0.220, p = 0.020), chronic inflammatory cell infiltration (r = 0.381, p <0.001), and lymphoid aggregation (r = 0.271, p = 0.004). No relationship was found between mast cell density and intensity of H. pylori, glandular atrophy, or intestinal metaplasia. Conclusion: Mast cells might take part in the pathogenesis of H. pylori gastritis.

Relationship between headache and mucosal mast cells in pediatric Helicobacter pylori-negative functional dyspepsia

Cephalalgia ◽  
2013 ◽  
Vol 33 (5) ◽  
pp. 323-329 ◽  
Author(s):  
Jung Sook Yeom ◽  
Myung Bum Choi ◽  
Ji-Hyun Seo ◽  
Ji Sook Park ◽  
Jae-Young Lim ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Mast Cell ◽  
Cell Density ◽  
Functional Dyspepsia ◽  
Pediatric Patients ◽  
Inflammatory Cells ◽  
Gastroduodenal Mucosa ◽  
Mast Cell Density ◽  
Dyspeptic Symptoms ◽  
H Pylori

Background Although many patients with functional dyspepsia experience headache concurrently with dyspeptic symptoms, studies suggesting mechanisms underlying this phenomenon are limited. Herein, we explore the relationship between gastrointestinal inflammatory cells and presence of headache associated with dyspeptic symptoms in children with Helicobacter pylori-negative functional dyspepsia. Methods Fifty-six patients with H. pylori-negative functional dyspepsia underwent upper endoscopy with biopsy to investigate recurrent epigastric pain or discomfort. Patients were divided into two groups according to self-reported presence of headache associated with dyspeptic symptoms. Inflammatory cells including mast cells, and enteroendocrine cells in the gastroduodenal mucosa were evaluated. Associations between headache presence and cellular changes in the gastroduodenal mucosa were examined. Results Headache was not associated with the grade of lymphocytes, neutrophil infiltration, or enteroendocrine cell density in the gastroduedenal mucosa. However, headache was significantly associated with high mast cell density in the body (27.81 ± 8.71 vs. 20.30 ± 8.16, p < 0.01) and duodenum (23.16 ± 10.40 vs. 14.84 ± 5.88, p < 0.01). Conclusions Presence of headache associated with dyspeptic symptoms is strongly related to mucosal mast cell density in pediatric patients with H. pylori-negative functional dyspepsia. Thus, our results may help clinicians understand and treat headache during dyspeptic symptoms in such pediatric patients.

scholarly journals Association of mast cells with helicobacter pylori infection in the antral mucosa

1970 ◽  
Vol 1 (1) ◽  
pp. 34-36
Author(s):  
SR KC ◽  
GL Amatya
Keyword(s):  
Helicobacter Pylori ◽  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Helicobacter Pylori Infection ◽  
Inflammatory Cell Infiltrate ◽  
Histopathological Diagnosis ◽  
Antral Mucosa ◽  
Mast Cell Density

Background: Helicobacter pylori infection is associated with mixed inflammatory cell infiltrate consisting of neutrophils, eosinophils, lymphocytes and plasma cells. Helicobacter pylori lead to mast cell degranulation and release of active chemical compounds in in-vitro conditions. The objective of this study was to find out the association of mast cell density and Helicobacter pylori in the antral mucosa of the stomach. Materials and Methods: A total of 150 endoscopic biopsies were included in the study. In addition to routine Hematoxylin and Eosin stained slides, Giemsa stain was done in each case for the evaluation of Helicobacter pylori and mast cell density in the gastric mucosa. Results: Out of 150 gastric biopsies with histopathological diagnosis of chronic gastritis, 36 cases (24%) were positive for Helicobacter pylori. In the antral mucosa, mast cell density was significantly higher in the Helicobacter pylori-positive group than in the Helicobacter pylori-negative group (P<0.01). Conclusion: Mast cells may play a role in the development of Helicobacter pylori gastritis. Keywords: Gastritis; Mast Cell; Helicobacter pylori DOI: 10.3126/jpn.v1i1.4448 Journal of Pathology of Nepal (2011) Vol.1, 34-36

Lung mast cell density and distribution in chronically hypoxic animals

1977 ◽  
Vol 42 (2) ◽  
pp. 174-178 ◽  
Author(s):  
A. Tucker ◽  
I. F. McMurtry ◽  
A. F. Alexander ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Cell Proliferation ◽  
Pulmonary Hypertension ◽  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Mammalian Species ◽  
Cell Hyperplasia ◽  
Mast Cell Density ◽  
Lung Mast Cell ◽  
Mast Cell Hyperplasia

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19–48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30–500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats

2008 ◽  
Vol 294 (3) ◽  
pp. H1251-H1257 ◽  
Author(s):  
David B. Murray ◽  
Jason D. Gardner ◽  
Gregory L. Brower ◽  
Joseph S. Janicki
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Volume Fraction ◽  
Volume Overload ◽  
Receptor Antagonism ◽  
Collagen Volume Fraction ◽  
Endothelin 1 ◽  
Mast Cell Density ◽  
Chronic Volume Overload

The objective of this study was to investigate the effect a nonselective endothelin-1 (ET-1) receptor antagonist (bosentan) had on the acute myocardial remodeling process including left ventricular (LV) mast cells and matrix metalloproteinase (MMP) activity secondary to volume overload. Additionally, we investigated the overall functional outcome of preventative endothelin receptor antagonism during 14 days of chronic volume overload. LV tissue from sham-operated (Sham), untreated-fistula (Fist), and bosentan (100 mg·kg−1·day−1)-treated animals (Fist + Bos) was analyzed for mast cell density, MMP activity, and myocardial collagen volume fraction at 1 and 5 days after the creation of an aortocaval fistula. When compared with untreated fistulas, bosentan treatment prevented the marked increase in LV mast cell density at 1 day postfistula (3.1 ± 0.3 vs. 1.3 ± 0.3 LV mast cells/mm2, Fist vs. Fist + Bos, P ≤ 0.01). Additionally, the substantial increase in MMP-2 activation in the untreated fistula at 1 day was prevented following bosentan treatment (1.6 ± 0.3 vs. 0.9 ± 0.1 arbitrary activity units, Fist vs. Fist + Bos, P ≤ 0.01). The marked decrease in collagen volume fraction seen in the Fist group (1.4 ± 0.1 vs. 0.8 ± 0.1% myocardial tissue, Sham vs. Fist, P ≤ 0.01) was significantly attenuated following bosentan treatment at both the 1- and 5-day time points. Lastly, a 2-wk preventative treatment with bosentan resulted in significant attenuation of the increase in LV end-systolic and -diastolic volumes compared with those in untreated fistula hearts. In summary, nonselective ET-1 antagonism prevents the acute increases in cardiac mast cell density and MMP activation induced secondary to chronic volume overload. By preventing these events, ET-1 antagonism was efficacious in attenuating ventricular dilatation and limiting the development of structural and functional deficits in the first 2 wk of chronic volume overload. Accordingly, these results are the first to demonstrate that cardiac mast cells are responsive to the endogenous endothelin system in vivo. Another novel finding from this study is that chronic nonspecific endothelin antagonism may inadvertently potentiate ET-1-mediated signaling.

The role of tumour infiltrating mast cells (TIM) in gastric carcinoma remains an enigma : Clinicopathological correlation of mast cell density

2019 ◽  
Vol 5 (4) ◽  
pp. 210-216
Author(s):  
Dr. C.D. Anand ◽  
◽  
Dr. Shivashekar G. ◽  
Dr. Muthu Sudalaimuthu ◽  
Dr. Amitkumar Kalaivani ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Gastric Carcinoma ◽  
Cell Density ◽  
Clinicopathological Correlation ◽  
Mast Cell Density

scholarly journals Mast cell density in gastric biopsies of pediatric age group and its relation to inflammation and presence of Helicobacter pylori

2007 ◽  
Vol 2 (1) ◽  
pp. 14 ◽  
Author(s):  
Fatemeh E Mahjoub ◽  
Behnam Hassanbeglou ◽  
Zahra Pourpak ◽  
Fatemeh Farahmand ◽  
Nasim Kashef ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Mast Cell ◽  
Cell Density ◽  
Age Group ◽  
Pediatric Age ◽  
Pediatric Age Group ◽  
Mast Cell Density ◽  
Gastric Biopsies

scholarly journals Immunohistochemical Expression of Mast Cells Using c-Kit in Various Grades of Oral Submucous Fibrosis

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Musarrat J. Khatri ◽  
Rajiv S. Desai ◽  
G. S. Mamatha ◽  
Meena Kulkarni ◽  
Jay Khatri
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Cell Density ◽  
Toluidine Blue ◽  
Oral Submucous Fibrosis ◽  
Blue Staining ◽  
Mast Cell Density ◽  
Submucous Fibrosis ◽  
Pharmacologically Active

Oral submucous fibrosis (OSF) is a high risk precancerous condition characterized by changes in the connective tissue fibers of lamina propria and deeper parts of mucosa. Mast cells are local residents of connective tissue and have been identified to participate in fibrotic process. These cells produce pharmacologically active substances necessary for the physiological function of our body in response to various stimuli as and when required and also play a significant role in the pathogenesis of oral diseases. Ten healthy volunteers and 30 clinically diagnosed OSF cases with histopathological confirmation were included in the study. Immunohistochemical (c-kit) as well as acidified toluidine blue staining techniques were used to evaluate density and expression of mast cells. The mast cell density assessed using c-kit and toluidine blue showed significant difference in various stages of OSF. In general the mean number of mast cells obtained using c-kit was found to be more than that obtained using toluidine blue in various stages of OSF. The comparison of mast cell densities using immunohistochemistry (c-kit) and toluidine blue stain confirmed that c-kit is a more reliable technique to assess mast cell density in OSF.

scholarly journals High Mast Cell Density Predicts a Favorable Prognosis in Patients with Pancreatic Neuroendocrine Neoplasms

2021 ◽  
Author(s):  
Shengwei Mo ◽  
Liju Zong ◽  
Xianlong Chen ◽  
Xiaoyan Chang ◽  
Zhaohui Lu ◽  
...  
Keyword(s):  
T Cells ◽  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
Immune Cells ◽  
Clinicopathological Parameters ◽  
Neuroendocrine Neoplasms ◽  
Pancreatic Neuroendocrine Neoplasms ◽  
Entire Cohort ◽  
Mast Cell Density

Introduction: Mast cells are involved in allergic diseases, immune regulation, and tumor microenvironment modulation, with both pro- and anti-tumorigenic functions, and could serve as a prognostic factor in various cancers. However, their potential role in pancreatic neuroendocrine neoplasms (PanNENs) is largely unknown. Here, our aim was to investigate the presence of mast cells in PanNENs and evaluate their association with clinicopathological parameters and other common tumor-infiltrating immune cells. Methods: Tissue microarrays containing PanNEN samples from 187 patients were constructed and stained immunohistochemically for CD117, CD15, CD68, CD3, CD4, and CD8. Immune cells were counted from four high-power fields (HPFs; 400×) at maximal concentrations, and the mean counts were calculated per HPF. The cut-off values were set by X-tile. Results: The median (interquartile range) counts of CD117+ mast cells, CD15+ neutrophils, CD68+ macrophages, CD3+ T cells, and CD4+ T cells were 3.5 (2.0–6.0), 3.0 (1.3–6), 3.8 (2.5–5.8), 13 (8.0–24.0), 2.0 (1.0–4.0)/HPF, respectively. CD8+ T cells were not detected. The cut-off values for these immune cells were 1.5/HPF, 6/HPF, 4.8/HPF, 32.5/HPF, and 2/HPF, respectively. Low mast cell density was correlated with higher grades, non-insulinoma, and advanced stages. Moreover, high mast cell infiltration was associated with elevated CD4+ T cell and CD15+ neutrophil counts. Multivariate analysis revealed that high mast cell density was an independent predictor of prolonged progression-free survival in the entire cohort, in pancreatic neuroendocrine tumors, and in intermediate-grade, non-insulinoma, and advanced stage subgroups. Conclusions: These findings suggest a protective role of mast cells in PanNENs.

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