Histamine and TNF-α release by rat peritoneal mast cells stimulated with<i>Trichomonas vaginalis</i>

Im, Su Jeong; Ahn, Myoung-Hee; Han, Ik-Hwan; Song, Hyun-Ouk; Kim, Y.S.; Kim, H.M.; Ryu, Jae‐Sook

doi:10.1051/parasite/2011181049

Cited by 19 publications

(20 citation statements)

References 31 publications

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“…In particular, the release of stored inflammatory mediators from the cells contributes to the cascade of pathogenic events in the affected tissues. Our finding showing that TvSP have the ability to induce extracellular release of granular protein histamine from human mast cells is in line with a recent finding that TvSP can induce the extracellular release of prestored granular proteins such as histamine and TNF-␣ in rat peritoneal mast cells (49). Although it is evident that stimulation with T. vaginalis provokes mast cell degranulation, the mode of degranulation has not been elucidated.…”

Section: Discussionsupporting

confidence: 87%

“…Mast cells are predominant in the vaginal smears of patients infected with T. vaginalis (6). Activation of HMC-1 cells with T. vaginalis has been shown to result in an increased release of histamine and tumor necrosis factor alpha (TNF-␣), both of which are involved in the inflammatory response caused by the parasite (49). First, we stimulated HMC-1 cells with T. vaginalis-derived secretory products (TvSP) to clarify whether TvSP can induce degranulation in HMC-1 cells.…”

Section: Resultsmentioning

confidence: 99%

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SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

et al. 2017

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Trichomonas vaginalis is a sexually transmitted parasite that causes vaginitis in women and itself secretes lipid mediator leukotriene B 4 (LTB 4 ). 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 LTB 4 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 TvSPinduced 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 LTB 4 . Our data collectively demonstrate a novel regulatory mechanism for SNAP23-dependent mast cell activation of T. vaginalis-secreted LTB 4 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.KEYWORDS Trichomonas vaginalis, LTB 4 , human mast cells, SNAP23, NOX2, BLT1, surface trafficking, exocytotic degranulation T richomonas vaginalis is a lumen-dwelling protozoan parasite with flagella, which infects the genitourinary tract in humans via sexual intercourse (1, 2). Of note, in women it causes vaginitis or cervicitis leading to inflammatory and allergic symptoms, including vaginal discharge with a foul odor and an increased number of leukocytes, and vulvovaginal pruritus (3-6). During the infection, tight junctional proteins between

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Section: Discussionsupporting

confidence: 87%

Section: Resultsmentioning

confidence: 99%

SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

et al. 2017

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“…Although these observations suggest that mast cells are involved in the cellular reaction to vaginal trichomoniasis, mast cell infiltration and its role in immunity against trichomoniasis have not yet been clearly established. We only showed in a previous report that T. vaginalis induced rat peritoneal mast cells to migrate and to produce TNF‐α and histamine (11). Incidentally, there are a few reports of the migration of mast cells to epithelial sites; Niyonsaba et al.…”

Section: Discussionmentioning

confidence: 90%

“…They are dispersed throughout most tissues but are especially concentrated at interfaces with the environment, such as the skin and mucosae, which lends support to the view that they play a role in recognition of pathogens and other signs of infection (10). There is our evidence that rat peritoneal mast cells are involved in the inflammatory response to T. vaginalis (11). However, there are no reports that crosstalk (interaction) between VECs and mast cell influences the inflammation caused by T. vaginalis .…”

Section: Introductionmentioning

confidence: 95%

Involvement of mast cells in inflammation induced by Trichomonas vaginalis via crosstalk with vaginal epithelial cells

Han

Park

Ahn

et al. 2011

Parasite Immunology

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Vaginal epithelial cells (VECs) are thought to function as immune-responsive cells in trichomoniasis, and mast cells have been detected in vaginal smears and the vaginal wall in trichomoniasis. It therefore seemed possible that the VEC-trichomonad reaction might affect the activity of mast cells present in the lamina propria of the vaginal mucosa. In this study, we tested whether culture supernatants of VEC incubated with Trichomonas vaginalis (TCM) could stimulate mast cells. When VECs (MS74) were incubated with live trichomonads, IL-8, IL-6 and MCP-1 expressions increased in the TCM, and mast cells (HMC-1) and human neutrophils migrated more actively towards the TCM. Also, when the TCM was added to mast cells, β-hexosaminidase and cytokines (IL-8 and TNF-α) expressions were increased. Moreover, the culture supernatant of mast cells incubated with TCM (M-TCM) had more increased chemotactic activity for neutrophils than that of TCM. We conclude that inflammatory mediators made by VECs in response to activation by T. vaginalis activate and attract mast cells and then stimulate them to induce neutrophil migration. Our results indicate, for the first time, that VECs play a role in the infiltration of mast cells and neutrophils early in T. vaginalis infection.

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“…MCs are recognized as effector cells involved in clearance of diverse parasites, including Trichinella spiralis and Trichomonas vaginalis [10,11]. MC deﬁcient mice infected with Leishmania major develop larger lesion load with increased parasitemia [12].…”

Section: Introductionmentioning

confidence: 99%

Mast Cells Modulate Acute Toxoplasmosis in Murine Models

Huang

Chen

et al. 2013

PLoS ONE

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The role of mast cells (MCs) in Toxoplasma gondii infection is poorly known. Kunming outbred mice were infected intraperitoneally with RH strain T. gondii, either treated with compound 48/80 (C48/80, MC activator) or disodium cromoglycate (DSCG, MC inhibitor). Compared with infected controls, infected mice treated with C48/80 exhibited significantly increased inflammation in the liver (P < 0.01), spleen (P < 0.05), and mesentery (P < 0.05) tissues, higher parasite burden in the peritoneal lavage fluids (P < 0.01), and increased levels of mRNA transcripts of T. gondii tachyzoite surface antigen 1 (SAG1) gene in the spleen and liver tissues (P < 0.01), accompanied with significantly increased Th1 cytokine (IFN-γ, IL-12p40, and TNF-α) (P < 0.01) and decreased IL-10 (P < 0.01) mRNA expressions in the liver, and increased IFN-γ (P < 0.01) and IL-12p40 (P < 0.01) but decreased TNF-α (P < 0.01) and IL-4 (P < 0.01) in the spleens of infected mice treated with C48/80 at day 9-10 p.i. Whereas mice treated with DSCG had significantly decreased tissue lesions (P < 0.01), lower parasite burden in the peritoneal lavage fluids (P < 0.01) and decreased SAG1 expressions in the spleen and liver tissues (P < 0.01), accompanied with significantly increased IFN-γ (P < 0.01) and IL-12p40 (P < 0.05) in the liver, and decreased IFN-γ (P < 0.05) and TNF-α (P < 0.01) in the spleens; IL-4 and IL-10 expressions in both the spleen and liver were significantly increased (P < 0.01) in the infected mice treated with DSCG. These findings suggest that mediators associated with the MC activation may play an important role in modulating acute inflammatory pathogenesis and parasite clearance during T. gondii infection in this strain of mice. Thus, MC activation/inhibition mechanisms are potential novel targets for the prevention and control of T. gondii infection.

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Histamine and TNF-α release by rat peritoneal mast cells stimulated withTrichomonas vaginalis

Cited by 19 publications

References 31 publications

SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

Involvement of mast cells in inflammation induced by Trichomonas vaginalis via crosstalk with vaginal epithelial cells

Mast Cells Modulate Acute Toxoplasmosis in Murine Models

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Histamine and TNF-α release by rat peritoneal mast cells stimulated withTrichomonas vaginalis

Cited by 19 publications

References 31 publications

SNAP23-Dependent Surface Translocation of Leukotriene B 4 (LTB 4 ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB 4

SNAP23-Dependent Surface Translocation of Leukotriene B 4 (LTB 4 ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB 4

Involvement of mast cells in inflammation induced by Trichomonas vaginalis via crosstalk with vaginal epithelial cells

Mast Cells Modulate Acute Toxoplasmosis in Murine Models

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Product

Resources

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SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄