scholarly journals Do Variations in Mast Cell Hyperplasia Account for Differences in Radiation-Induced Lung Injury among Different Mouse Strains, Rats and Nonhuman Primates?

2013 ◽  
Vol 180 (2) ◽  
pp. 216-221 ◽  
Author(s):  
Julian D. Down ◽  
Meetha Medhora ◽  
Isabel L. Jackson ◽  
J. Mark Cline ◽  
Zeljko Vujaskovic
Keyword(s):  
Mast Cell ◽  
Lung Injury ◽  
Nonhuman Primates ◽  
Mouse Strains ◽  
Cell Hyperplasia ◽  
Radiation Induced ◽  
Mast Cell Hyperplasia

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.

scholarly journals Effects of Multiple Dexamethasone Treatments on Aggravation of Allergic Conjunctivitis Associated with Mast Cell Hyperplasia

2008 ◽  
Vol 31 (3) ◽  
pp. 464-468 ◽  
Author(s):  
Takuya Nagata ◽  
Takeshi Nabe ◽  
Masanori Fujii ◽  
Nobuaki Mizutani ◽  
Shigekatsu Kohno
Keyword(s):  
Mast Cell ◽  
Allergic Conjunctivitis ◽  
Cell Hyperplasia ◽  
Mast Cell Hyperplasia

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.

Mast Cell Hyperplasia in Experimental Hypersensitivity Pneumonitis

1991 ◽  
Vol 96 (2) ◽  
pp. 168-174 ◽  
Author(s):  
Patrick J. Haley ◽  
Mark Schuyler ◽  
Katherine Gott ◽  
Thomas B. Casale
Keyword(s):  
Mast Cell ◽  
Hypersensitivity Pneumonitis ◽  
Cell Hyperplasia ◽  
Mast Cell Hyperplasia

scholarly journals PGD2 deficiency exacerbates food antigen-induced mast cell hyperplasia

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Tatsuro Nakamura ◽  
Shingo Maeda ◽  
Kazuhide Horiguchi ◽  
Toko Maehara ◽  
Kosuke Aritake ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Hyperplasia ◽  
Food Antigen ◽  
Mast Cell Hyperplasia

Association of the Q576R polymorphism in the interleukin-4 receptor α chain with indolent mastocytosis limited to the skin

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 880-882 ◽  
Author(s):  
Trisha Daley ◽  
Dean D. Metcalfe ◽  
Cem Akin
Keyword(s):  
Mast Cell ◽  
Systemic Mastocytosis ◽  
Interleukin 4 ◽  
Gain Of Function ◽  
Cell Hyperplasia ◽  
Α Subunit ◽  
Disease Markers ◽  
Α Chain ◽  
Interleukin 4 Receptor ◽  
Mast Cell Hyperplasia

Abstract Gain-of-function mutations in c-kit, which appear to contribute to mast cell hyperplasia, have been detected in both limited and aggressive forms of mastocytosis, suggesting that other mutations or polymorphisms may contribute to the clinical phenotype. Because addition of interleukin-4 (IL-4) to mast cell cultures is reported to induce apoptosis, the hypothesis was considered that individuals carrying the gain-of-function polymorphism Q576R in the cytoplasmic domain of the α-subunit of the IL-4 receptor (IL-4R) might be relatively resistant to the gain-of-function mutation in c-kit. To assess this possibility, 36 patients with either cutaneous or systemic mastocytosis were studied for association with the Q576R polymorphism. The Q576R polymorphism was found more frequently in those with disease limited to skin and who exhibited lower levels of surrogate disease markers. These data suggest that the Q576R IL-4R α- chain polymorphism may mitigate disease expression and confer a better prognosis in patients with mastocytosis.

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