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.

Mast cells express IL-13Rα1: IL-13 promotes human lung mast cell proliferation and FcɛRI expression

Allergy ◽  
2006 ◽  
Vol 61 (9) ◽  
pp. 1047-1053 ◽  
Author(s):  
D. Kaur ◽  
F. Hollins ◽  
L. Woodman ◽  
W. Yang ◽  
P. Monk ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mast Cell ◽  
Mast Cells ◽  
Human Lung ◽  
Lung Mast Cell

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 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.

scholarly journals Lung Mast Cell Density Defines A Subpopulation Of Patients With Idiopathic Pulmonary Fibrosis

2011 ◽  
Author(s):  
Seung Ick Cha ◽  
Christine S. Chang ◽  
Jae W. Lee ◽  
Michael A. Matthay ◽  
Brett M. Elicker ◽  
...  
Keyword(s):  
Mast Cell ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Cell Density ◽  
Mast Cell Density ◽  
Lung Mast Cell

scholarly journals Development of Mast Cell and Eosinophil Hyperplasia and HLH/MAS-Like Disease in NSG-SGM3 Mice Receiving Human CD34+ Hematopoietic Stem Cells or Patient-Derived Leukemia Xenografts

2020 ◽  
pp. 030098582097014
Author(s):  
Laura J. Janke ◽  
Denise M. Imai ◽  
Heather Tillman ◽  
Rosalinda Doty ◽  
Mark J. Hoenerhoff ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mast Cell ◽  
Mast Cells ◽  
Hematopoietic Stem Cells ◽  
Human Cells ◽  
Mouse Strains ◽  
Cell Hyperplasia ◽  
Hematopoietic Stem ◽  
Human Cd34 ◽  
Mast Cell Hyperplasia

Immunocompromised mouse strains expressing human transgenes are being increasingly used in biomedical research. The genetic modifications in these mice cause various cellular responses, resulting in histologic features unique to each strain. The NSG-SGM3 mouse strain is similar to the commonly used NSG (NOD scid gamma) strain but expresses human transgenes encoding stem cell factor (also known as KIT ligand), granulocyte-macrophage colony-stimulating factor, and interleukin 3. This report describes 3 histopathologic features seen in these mice when they are unmanipulated or after transplantation with human CD34+ hematopoietic stem cells (HSCs), virally transduced hCD34+ HSCs, or a leukemia patient-derived xenograft. The first feature is mast cell hyperplasia: unmanipulated, naïve mice develop periductular pancreatic aggregates of murine mast cells, whereas mice given the aforementioned human cells develop a proliferative infiltrative interstitial pancreatic mast cell hyperplasia but with human mast cells. The second feature is the predisposition of NSG-SGM3 mice given these human cells to develop eosinophil hyperplasia. The third feature, secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome (HLH/MAS)–like disease, is the most pronounced in both its clinical and histopathologic presentations. As part of this disease, a small number of mice also have histiocytic infiltration of the brain and spinal cord with subsequent neurologic or vestibular signs. The presence of any of these features can confound accurate histopathologic interpretation; therefore, it is important to recognize them as strain characteristics and to differentiate them from what may be experimentally induced in the model being studied.

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