Human chymase is known to function as a chemoattractant for human leukocytes. To investigate the mechanism of the chymase-induced cell migration, change in intracellular calcium concentration ([Ca(2+)]i) was examined in human polymorphonuclear (PMN) cells using Fluo-3 as a fluorescent Ca(2+) indicator. Treatment of PMN cells with human chymase caused [Ca(2+)]i elevation in a concentration-dependent manner. Depletion of extracellular Ca(2+) from the medium partially attenuated the chymase-induced [Ca(2+)]i increase, showing that both Ca(2+) influx and Ca(2+) release from internal stores might be involved in the [Ca(2+)]i response. Pretreatment of the cells with pertussis toxin completely blocked the chymase-induced [Ca(2+)]i signal, suggesting an involvement of G protein in the chymase-mediated [Ca(2+)]i elevation. The data in the present study raise the possibility that the chymase-induced cell migration is mediated by the [Ca(2+)]i elevation, which might be caused by stimulation of a G-protein-coupled receptor such as protease-activated receptors (PARs).
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http://dx.doi.org/10.1016/s0165-2478(03)00129-9 | DOI Listing |
J Clin Invest
January 2025
Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Mast cells (MCs) expressing a distinctive protease phenotype (MCTs) selectively expand within the epithelium of human mucosal tissues during type 2 (T2) inflammation. While MCTs are phenotypically distinct from subepithelial MCs (MCTCs), signals driving human MCT differentiation and this subset's contribution to inflammation remain unexplored. Here, we have identified TGF-β as a key driver of the MCT transcriptome in nasal polyps.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Science of Allergy and Inflammation, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Mas-related G protein-coupled receptor b2 (Mrgprb2) binding to its cationic endogenous and exogenous ligands induces mast cell degranulation and promotes inflammation in mice. However, the physiological roles of its human homologue MRGPRX2 remain unclear. Here we aimed to elucidate the mechanisms by which MRGPRX2 regulates vascular permeability, and generated MRGPRX2 knock-in (MRGPRX2-KI) and Mrgprb2 knockout (Mrgprb2-KO) mice.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
Tick-Pathogen Transmission Unit, Laboratory of Bacteriology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, Hamilton, MT, USA. Electronic address:
Ticks obtain a blood meal by lacerating small blood vessels and ingesting the blood that flows to the feeding site, which triggers various host responses. However, ticks face the challenge of wound healing, a process involving hemostasis, inflammation, cell proliferation and migration, and remodeling, hindering blood acquisition. To overcome these obstacles, tick salivary glands produce an array of bioactive molecules.
View Article and Find Full Text PDFInt Immunopharmacol
December 2024
NMPA Key Laboratory for Research and Evaluation of Drug Metabolism, Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China. Electronic address:
bioRxiv
September 2024
The University of Chicago, Department of Microbiology, 920 East 58 Street, CLSC 1117, Chicago, IL 60637.
Tuberculosis (TB), caused by the bacterium (), infects approximately one-fourth of the world's population. While most infected individuals are asymptomatic, latent TB infection (LTBI) can progress to cause pulmonary TB (PTB). We recently reported an increased accumulation of mast cells (MCs) in lungs of macaques with PTB, compared with LTBI in macaques.
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