A role for mast cells and mast cell tryptase in driving neutrophil recruitment in LPS-induced lung inflammation via protease-activated receptor 2 in mice

2020 ◽  
Vol 69 (10) ◽  
pp. 1059-1070 ◽  
Author(s):  
Aline Dias de Almeida ◽  
Irismara Sousa Silva ◽  
Weslley Fernandes-Braga ◽  
Antônio Carlos Melo LimaFilho ◽  
R odrigo Machado Florentino ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Lung Inflammation ◽  
Neutrophil Recruitment ◽  
Mast Cell Tryptase ◽  
Protease Activated Receptor 2

scholarly journals Correction to: A role for mast cells and mast cell tryptase in driving neutrophil recruitment in LPS-induced lung inflammation via protease-activated receptor 2 in mice

2020 ◽  
Vol 69 (10) ◽  
pp. 1071-1071
Author(s):  
Aline Dias de Almeida ◽  
Irismara Sousa Silva ◽  
Weslley Fernandes-Braga ◽  
Antônio Carlos Melo LimaFilho ◽  
Rodrigo Machado Florentino ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Lung Inflammation ◽  
Neutrophil Recruitment ◽  
Mast Cell Tryptase ◽  
Protease Activated Receptor 2

scholarly journals Mast cells and mast cell tryptase enhance migration of human lung fibroblasts through protease-activated receptor 2

2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Mariam Bagher ◽  
Anna-Karin Larsson-Callerfelt ◽  
Oskar Rosmark ◽  
Oskar Hallgren ◽  
Leif Bjermer ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Mast Cell Tryptase ◽  
Human Lung Fibroblasts ◽  
Protease Activated Receptor 2

Mastocytic Enterocolitis: Increased Mucosal Mast Cells in Chronic Intractable Diarrhea

2006 ◽  
Vol 130 (3) ◽  
pp. 362-367 ◽  
Author(s):  
Shriram Jakate ◽  
Mark Demeo ◽  
Rohan John ◽  
Mary Tobin ◽  
Ali Keshavarzian
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
High Power ◽  
Chronic Diarrhea ◽  
Duodenal Biopsy ◽  
Mast Cell Tryptase ◽  
High Power Field ◽  
Intractable Diarrhea ◽  
Biopsy Specimens ◽  
Hematoxylin Eosin

Abstract Context.—In some adult patients with chronic intractable diarrhea, the diagnosis remains elusive even after detailed evaluations, and colonic or duodenal biopsy specimens may appear unremarkable on routine hematoxylin-eosin staining. Objectives.—To assess the concentration of mast cells in colonic or duodenal biopsy specimens by immunohistochemical analysis for mast cell tryptase from patients with chronic intractable diarrhea and to evaluate their response to drugs affecting mast cell function. Design.—Mast cells per high-power field were assessed in biopsy specimens from 47 patients with chronic intractable diarrhea, from 50 control subjects, and from 63 patients with other specific diseases that cause chronic diarrhea (inflammatory bowel disease, celiac disease, collagenous colitis, and lymphocytic colitis). Patients with chronic intractable diarrhea who had more than 20 mast cells per high-power field were administered drugs affecting mast cell mediator function and release. Results.—The mean ± SD concentration of mast cells in the 50 control subjects was 13.3 ± 3.5 cells per high-power field; hence, patients with more than 20 mast cells per high-power field were considered to have increased mast cells. Thirty-three (70%) of 47 patients with chronic intractable diarrhea had increased mast cells, and symptoms were controlled by drug therapy in 22 (67%) of the 33 patients. No patient had systemic or cutaneous mastocytosis. No increase in mast cells was seen in patients with other common causes of chronic diarrhea. Conclusions.—In chronic intractable diarrhea, colonic or duodenal biopsy specimens may appear unremarkable on routine hematoxylin-eosin staining, but increased mast cells may be demonstrated by immunohistochemistry for mast cell tryptase, with the novel term mastocytic enterocolitis describing this condition. Similar increases in mast cells are not apparent in control populations or in patients with other specific diseases that cause chronic diarrhea. The cause of the increased mast cells remains to be elucidated.

Distinct expression of mast cell tryptase and protease activated receptor-2 in synovia of rheumatoid arthritis and osteoarthritis

2007 ◽  
Vol 26 (8) ◽  
pp. 1284-1292 ◽  
Author(s):  
Shunji Nakano ◽  
Takuya Mishiro ◽  
Shigeyuki Takahara ◽  
Hiromichi Yokoi ◽  
Daisuke Hamada ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mast Cell ◽  
Mast Cell Tryptase ◽  
Protease Activated Receptor 2

scholarly journals Role of mast cells and protease-activated receptor-2 in cyclooxygenase-2 expression in urothelial cells

2009 ◽  
Vol 297 (4) ◽  
pp. R1127-R1135 ◽  
Author(s):  
Zun-Yi Wang ◽  
Peiqing Wang ◽  
Dale E. Bjorling
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Primary Cultures ◽  
Cyclooxygenase 2 ◽  
Protein Abundance ◽  
Urothelial Cells ◽  
Cellular Mechanisms ◽  
Bladder Inflammation ◽  
Cox 2 ◽  
Protease Activated Receptor 2

Mast cells have been shown to play a role in development and persistence of various inflammatory bladder disorders. Mast cell-derived tryptase specifically activates protease-activated receptor-2 (PAR-2), and PAR-2 is known to be involved in inflammation. We investigated whether mast cells participate in increase of cyclooxygenase-2 (COX-2) protein abundance in urothelium/suburothelium of bladders of mice subsequent to cyclophosphamide (CYP)-induced bladder inflammation. We also used primary cultures of human urothelial cells to investigate cellular mechanisms underlying activation of PAR-2 resulting in increased COX-2 expression. We found that treatment of mice with CYP (150 mg/kg ip) increased COX-2 protein abundance in bladder urothelium/suburothelium 3, 6, and 24 h after CYP ( P < 0.01), and increased COX-2 protein abundance was prevented by treatment of mice with the mast cell stabilizer sodium cromolyn (10 mg/kg ip) for 4 consecutive days before CYP treatment. Incubation of freshly isolated mouse urothelium/suburothelium with a selective PAR-2 agonist, 2-furoyl-LIGRLO-amide (3 μM), also increased COX-2 protein abundance ( P < 0.05). We further demonstrated that 2-furoyl-LIGRLO-amide (3 μM) increased COX-2 mRNA expression and protein abundance in primary cultures of human urothelial cells ( P < 0.01), and the effects of PAR-2 activation were mediated primarily by the ERK1/2 MAP kinase pathway. These data indicate that there are functional interactions among mast cells, PAR-2 activation, and increased expression of COX-2 in bladder inflammation.

scholarly journals Cloning of the cDNA encoding mast cell tryptase of Mongolian gerbil, Meriones unguiculatus, and its preferential expression in the intestinal mucosa

1995 ◽  
Vol 309 (3) ◽  
pp. 921-926 ◽  
Author(s):  
Y Murakumo ◽  
H Ide ◽  
H Itoh ◽  
M Tomita ◽  
T Kobayashi ◽  
...  
Keyword(s):  
Amino Acids ◽  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Intestinal Mucosa ◽  
Mongolian Gerbil ◽  
Meriones Unguiculatus ◽  
Amino Acid Sequences ◽  
Mast Cell Tryptase ◽  
Mucosal Mast Cells

By using the combination of reverse-transcription PCR and rapid amplification of cDNA ends methods, a cDNA encoding mast cell tryptase was successfully cloned from the small intestine of Mongolian gerbil, Meriones unguiculatus, infected with Nippostrongylus brasiliensis. The cDNA was 1219 bp long including 810 bp of an open reading frame. Based on the deduced amino acid sequences of known mast cell tryptases of other species, the gerbil mast cell tryptase (gMCT) was highly similar to mouse mast cell protease (mMCP)-7, and seems to be translated as a prepro-enzyme with 25 amino acids of signal and activation peptides and 245 amino acids of mature enzyme. The gMCT mRNA was preferentially transcribed in the intestinal mucosa and to a far lesser extent in the connective tissue such as skin and tongue. Moreover, kinetic study after infection revealed that the amount of gMCT mRNA in the small intestine correlated well with the degree of intestinal mastocytosis. Throughout the course of infection, enzyme-histochemically detectable tryptase activity was limited to mucosal mast cells. Since mucosal mast cells of other rodents, including mice and rats, do not express tryptases, this is the first report of rodent mast cell tryptase expressed in the intestinal mucosa.

scholarly journals Immunohistochemical analysis of the arterial supply and mast cells of the trigeminal ganglion

2021 ◽  
pp. 16-16
Author(s):  
Aleksandar Mircic ◽  
Aleksandar Malikovic ◽  
Bojan Stimec ◽  
Aleksandra Milosavljevic ◽  
Dejan Cetkovic ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Trigeminal Ganglion ◽  
Regional Differences ◽  
Immunohistochemical Analysis ◽  
Mast Cell Tryptase ◽  
Significant Statistical Difference ◽  
Migraine Pain ◽  
Mast Cell Density ◽  
Ganglionic Cell

The aim of this study was to quantify the distribution of microvessels and mast cells in all three parts of the trigeminal ganglion (TG). Statistical analyses were applied to investigate possible micromorphological regional differences in their density. Five serially sectioned human TGs were prepared for CD34 and mast cell tryptase immunostaining. The following quantifications were performed in microscopic fields of three parts of the TG: microvessel density (MVD), mast cell density (MCD) and ganglionic cell count. The density of CD34-positive microvessels was not significantly different in any of the three observed parts of the TG. The distribution of neurons showed no significant statistical difference in three parts of the TG. There was no difference in the density of tryptase-positive mast cells within the TG, but there was an abundant presence of mast cells in the periganglionic dural and subdural tissues, a finding hitherto not reported. We can say that there is a homogenous vascular pattern within the TG which excludes local predominance in pathogenesis of trigeminal neuralgia. Second, and more important, the finding of peri-trigeminal mast cells indicates their important role in migraine pain and confirms their degranulation as the main therapeutic goal for this condition.

scholarly journals Basophils preferentially express mouse mast cell protease 11 among the mast cell tryptase family in contrast to mast cells

2009 ◽  
Vol 86 (6) ◽  
pp. 1417-1425 ◽  
Author(s):  
Tsukasa Ugajin ◽  
Toshiyuki Kojima ◽  
Kaori Mukai ◽  
Kazushige Obata ◽  
Yohei Kawano ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Mast Cell Tryptase ◽  
Mast Cell Protease ◽  
Mouse Mast Cell

scholarly journals Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

Blood ◽  
2006 ◽  
Vol 109 (9) ◽  
pp. 3640-3648 ◽  
Author(s):  
Susumu Nakae ◽  
Hajime Suto ◽  
Gerald J. Berry ◽  
Stephen J. Galli
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Th17 Cell ◽  
Neutrophil Infiltration ◽  
Cell Receptor ◽  
Neutrophil Recruitment ◽  
T Helper 17 ◽  
Ifn Γ

AbstractBoth mast cells and IL-17 can contribute to host defense and pathology in part by orchestrating neutrophil recruitment, but the possible role of mast cells in IL-17–induced inflammation remains to be defined. We found that mast cells and IL-17, but neither IFN-γ nor FcRγ signaling, contributed significantly to the antigen (Ag)–dependent airway neutrophilia elicited in ovalbumin-specific T-cell receptor (TCR)–expressing C57BL/6-OTII mice, and that IFN-γ significantly suppressed IL-17–dependent airway neutrophilia in this setting. IL-18, IL-1β, and TNF each contributed significantly to the development of Ag- and T helper 17 (Th17 cell)–mediated airway neutrophilia. Moreover, IL-17 enhanced mast cell TNF production in vitro, and mast cell–associated TNF contributed significantly to Ag- and Th17 cell–mediated airway neutrophilia in vivo. By contrast, we detected no significant role for the candidate mediators histamine, PGD2, LTB4, CXCL10, or IL-16, each of which can be produced by mast cells and other cell types, in the neutrophil infiltration elicited in this model. These findings establish that mast cells and mast cell–derived TNF can significantly enhance, by FcRγ-independent mechanisms, the Ag- and Th17 cell–dependent development of a neutrophil-rich inflammatory response at a site of Ag challenge.

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