scholarly journals Nonlethal Plasmodium yoelii Infection Drives Complex Patterns of Th2-Type Host Immunity and Mast Cell-Dependent Bacteremia

2020 ◽  
Vol 88 (12) ◽  
Author(s):  
Nora Céspedes ◽  
Erinn Donnelly ◽  
Sarah Garrison ◽  
Lori Haapanen ◽  
Judy Van De Water ◽  
...  
Keyword(s):  
Mast Cell ◽  
Intestinal Permeability ◽  
Cell Activation ◽  
Plasmodium Yoelii ◽  
Mast Cell Activation ◽  
Interleukin 4 ◽  
Content Type ◽  
Th1 And Th2 Cytokines ◽  
Circulating Levels ◽  
Gastrointestinal Permeability

ABSTRACT Malaria strongly predisposes to bacteremia, which is associated with sequestration of parasitized red blood cells and increased gastrointestinal permeability. The mechanisms underlying this disruption are poorly understood. Here, we evaluated the expression of factors associated with mast cell activation and malaria-associated bacteremia in a rodent model. C57BL/6J mice were infected with Plasmodium yoelii yoelli 17XNL, and blood and tissues were collected over time to assay for circulating levels of bacterial 16S DNA, IgE, mast cell protease 1 (Mcpt-1) and Mcpt-4, Th1 and Th2 cytokines, and patterns of ileal mastocytosis and intestinal permeability. The anti-inflammatory cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early after P. yoelii yoelii 17XNL infection. This was followed by the appearance of IL-9 and IL-13, cytokines known for their roles in mast cell activation and growth-enhancing activity as well as IgE production. Later increases in circulating IgE, which can induce mast cell degranulation, as well as Mcpt-1 and Mcpt-4, were observed concurrently with bacteremia and increased intestinal permeability. These results suggest that P. yoelii yoelii 17XNL infection induces the production of early cytokines that activate mast cells and drive IgE production, followed by elevated IgE, IL-9, and IL-13 that maintain and enhance mast cell activation while disrupting the protease/antiprotease balance in the intestine, contributing to epithelial damage and increased permeability.

scholarly journals SNAP23-Dependent Surface Translocation of Leukotriene B4 (LTB4) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB4

2016 ◽  
Vol 85 (1) ◽  
Author(s):  
Arim Min ◽  
Young Ah Lee ◽  
Kyeong Ah Kim ◽  
Jamel El-Benna ◽  
Myeong Heon Shin
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Trichomonas Vaginalis ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Ros Generation ◽  
Physical Interaction ◽  
Content Type ◽  
Receptor Complexes ◽  
Human Mast Cells

ABSTRACT Trichomonas vaginalis is a sexually transmitted parasite that causes vaginitis in women and itself secretes lipid mediator leukotriene B4 (LTB4). Mast cells are important effector cells of tissue inflammation during infection with parasites. Membrane-bridging SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complexes are critical for fusion during exocytosis. Although T. vaginalis-derived secretory products (TvSP) have been shown to induce exocytosis in mast cells, information regarding the signaling mechanisms between mast cell activation and TvSP is limited. In this study, we found that SNAP23-dependent surface trafficking of LTB4 receptor 1 (BLT1) is required for nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2)-mediated exocytotic degranulation of mast cells induced by TvSP. First, stimulation with TvSP induced exocytotic degranulation and reactive oxygen species (ROS) generation in HMC-1 cells. Next, TvSP-induced ROS generation and exocytosis were strongly inhibited by transfection of BLT1 small interfering RNA (siRNA). TvSP induced trafficking of BLT1 from the cytosol to the plasma membrane. We also found that knockdown of SNAP23 abrogated TvSP-induced ROS generation, exocytosis, and surface trafficking of BLT1 in HMC-1 cells. By coimmunoprecipitation, there was a physical interaction between BLT1 and SNAP23 in TvSP-stimulated HMC-1 cells. Taken together, our results suggest that SNAP23-dependent surface trafficking of BLT1 is essential for exocytosis in human mast cells induced by T. vaginalis-secreted LTB4. Our data collectively demonstrate a novel regulatory mechanism for SNAP23-dependent mast cell activation of T. vaginalis-secreted LTB4 involving surface trafficking of BLT1. These results can help to explain how the cross talk mechanism between parasite and host can govern deliberately tissue inflammatory responses.

scholarly journals Anaplasma phagocytophilum Infects Mast Cells via α1,3-Fucosylated but Not Sialylated Glycans and Inhibits IgE-Mediated Cytokine Production and Histamine Release

2011 ◽  
Vol 79 (7) ◽  
pp. 2717-2726 ◽  
Author(s):  
Nore Ojogun ◽  
Brian Barnstein ◽  
Bernice Huang ◽  
Carole A. Oskeritzian ◽  
Jonathon W. Homeister ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Anaplasma Phagocytophilum ◽  
Defense Mechanisms ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Murine Bone Marrow ◽  
Granulocytic Anaplasmosis

ABSTRACTMast cells are sentinels for infection. Upon exposure to pathogens, they release their stores of proinflammatory cytokines, chemokines, and histamine. Mast cells are also important for the control of certain tick-borne infections.Anaplasma phagocytophilumis an obligate intracellular tick-transmitted bacterium that infects neutrophils to cause the emerging disease granulocytic anaplasmosis.A. phagocytophilumadhesion to and infection of neutrophils depend on sialylated and α1,3-fucosylated glycans. We investigated the hypotheses thatA. phagocytophiluminvades mast cells and inhibits mast cell activation. We demonstrate thatA. phagocytophilumbinds and/or infects murine bone marrow-derived mast cells (BMMCs), murine peritoneal mast cells, and human skin-derived mast cells.A. phagocytophiluminfection of BMMCs depends on α1,3-fucosylated, but not sialylated, glycans.A. phagocytophilumbinding to and invasion of BMMCs do not elicit proinflammatory cytokine secretion. Moreover,A. phagocytophilum-infected cells are inhibited in the release of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-13, and histamine following stimulation with IgE or antigen. Thus,A. phagocytophilummitigates mast cell activation. These findings potentially represent a novel means by whichA. phagocytophilumusurps host defense mechanisms and shed light on the interplay between mast cells and vector-borne bacterial pathogens.

scholarly journals Trichinella spiralis Secreted Enzymes Regulate Nucleotide-Induced Mast Cell Activation and Release of Mouse Mast Cell Protease 1

2012 ◽  
Vol 80 (11) ◽  
pp. 3761-3767 ◽  
Author(s):  
Holly C. Afferson ◽  
Emily Eleftheriou ◽  
Murray E. Selkirk ◽  
Kleoniki Gounaris
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Trichinella Spiralis ◽  
Critical Role ◽  
Extracellular Nucleotides ◽  
Mast Cell Activation ◽  
Content Type ◽  
Mast Cell Protease ◽  
Mouse Mast Cell

ABSTRACTExtracellular nucleotides are important triggers of innate immunity, acting on a wide variety of cells via signaling through purinergic receptors. Mucosal mast cells contribute to expulsion of a number of gastrointestinal nematode parasites, and mouse mast cell protease 1 has been shown to have a critical role in clearance ofTrichinella spiralisfrom the intestinal tract. We show here that adenosine, ADP, ATP, UDP, and UTP all stimulate calcium mobilization in bone marrow-derived mast cells with a mucosal phenotype. Secreted proteins fromT. spiralisinfective larvae inhibit nucleotide-induced mast cell activation, and that induced by ADP and UDP is specifically blocked by parasite secretory 5′-nucleotidase. Release of mouse mast cell protease 1 is stimulated by ADP and ATP. Both parasite secreted products and the 5′-nucleotidase inhibit ADP-induced release of mast cell protease, whereas that stimulated by ATP is partially inhibited by secreted products alone. This indicates that the 5′-nucleotidase contributes to but is not solely responsible for inhibition of nucleotide-mediated effects on mast cell function. Secretion of nucleotide-metabolizing enzymes by parasitic nematodes most likely evolved as a strategy for suppression of innate immune responses and is discussed in this context.

Depression, psychosocial correlates, and psychosocial resources in individuals with mast cell activation syndrome

2021 ◽  
pp. 135910532110145
Author(s):  
Jennifer Nicoloro SantaBarbara ◽  
Marci Lobel
Keyword(s):  
Mast Cell ◽  
Depressive Symptoms ◽  
Cell Activation ◽  
Physical Symptoms ◽  
Mast Cell Activation ◽  
Emotional States ◽  
Mast Cell Activation Syndrome ◽  
Disease Experience ◽  
Clinically Significant ◽  
Activation Syndrome

Individuals with Mast Cell Activation Syndrome (MCAS), a rare chronic disease, experience unpredictable physical symptoms and diagnostic challenges resulting in poor emotional states. The prevalence and correlates of depressive symptoms were examined among 125 participants who completed the CES-D and relevant instruments. The majority reported a clinically-significant level of depression which was especially common among younger participants and those who reported greater loneliness or more disease-specific stressors. Greater magnitude of depressive symptoms was associated with greater illness intrusiveness, less social support, and lower optimism. Results highlight the value of interventions targeting loneliness and stressors unique to this population.

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