scholarly journals The Bcl10–Malt1 complex segregates FcεRI-mediated nuclear factor κB activation and cytokine production from mast cell degranulation

2006 ◽  
Vol 172 (4) ◽  
pp. i7-i7
Author(s):  
Stefanie Klemm ◽  
Jan Gutermuth ◽  
Lothar Hültner ◽  
Tim Sparwasser ◽  
Heidrun Behrendt ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cytokine Production ◽  
Nuclear Factor Κb ◽  
Mast Cell Degranulation ◽  
Nuclear Factor

scholarly journals ELKS1 controls mast cell degranulation by regulating the transcription of Stxbp2 and Syntaxin 4 via Kdm2b stabilization

2020 ◽  
Vol 6 (31) ◽  
pp. eabb2497
Author(s):  
Hiu Yan Lam ◽  
Surendar Arumugam ◽  
Han Gyu Bae ◽  
Cheng Chun Wang ◽  
Sangyong Jung ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cytokine Production ◽  
Nuclear Factor Κb ◽  
Mast Cell Degranulation ◽  
Nuclear Factor ◽  
Regulated Exocytosis ◽  
Lysine Specific Demethylase ◽  
Syntaxin 4

ELKS1 is a protein with proposed roles in regulated exocytosis in neurons and nuclear factor κB (NF-κB) signaling in cancer cells. However, how these two potential roles come together under physiological settings remain unknown. Since both regulated exocytosis and NF-κB signaling are determinants of mast cell (MC) functions, we generated mice lacking ELKS1 in connective tissue MCs (Elks1f/f Mcpt5-Cre) and found that while ELKS1 is dispensable for NF-κB–mediated cytokine production, it is essential for MC degranulation both in vivo and in vitro. Impaired degranulation was caused by reduced transcription of Syntaxin 4 (STX4) and Syntaxin binding protein 2 (Stxpb2), resulting from a lack of ELKS1-mediated stabilization of lysine-specific demethylase 2B (Kdm2b), which is an essential regulator of STX4 and Stxbp2 transcription. These results suggest a transcriptional role for active-zone proteins like ELKS1 and suggest that they may regulate exocytosis through a novel mechanism involving transcription of key exocytosis proteins.

scholarly journals The Bcl10–Malt1 complex segregates FcεRI-mediated nuclear factor κB activation and cytokine production from mast cell degranulation

2006 ◽  
Vol 203 (2) ◽  
pp. 337-347 ◽  
Author(s):  
Stefanie Klemm ◽  
Jan Gutermuth ◽  
Lothar Hültner ◽  
Tim Sparwasser ◽  
Heidrun Behrendt ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Cytokine Production ◽  
De Novo ◽  
Late Phase ◽  
B Cell Lymphoma ◽  
Nuclear Factor Κb ◽  
Mast Cell Activation ◽  
Nuclear Factor

Mast cells are pivotal effector cells in IgE-mediated allergic inflammatory diseases. Central for mast cell activation are signals from the IgE receptor FcεRI, which induce cell degranulation with the release of preformed mediators and de novo synthesis of proinflammatory leukotrienes and cytokines. How these individual mast cell responses are differentially controlled is still unresolved. We identify B cell lymphoma 10 (Bcl10) and mucosa-associated lymphoid tissue 1 (Malt1) as novel key regulators of mast cell signaling. Mice deficient for either protein display severely impaired IgE-dependent late phase anaphylactic reactions. Mast cells from these animals neither activate nuclear factor κB (NF-κB) nor produce tumor necrosis factor α or interleukin 6 upon FcεRI ligation even though proximal signaling, degranulation, and leukotriene secretion are normal. Thus, Bcl10 and Malt1 are essential positive mediators of FcεRI-dependent mast cell activation that selectively uncouple NF-κB–induced proinflammatory cytokine production from degranulation and leukotriene synthesis.

scholarly journals Extract of Boehmeria nivea Suppresses Mast Cell-Mediated Allergic Inflammation by Inhibiting Mitogen-Activated Protein Kinase and Nuclear Factor-κB

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4178
Author(s):  
Ji-Ye Lim ◽  
Ji-Hyun Lee ◽  
Bo-Ri Lee ◽  
Mi Ae Kim ◽  
Young-Mi Lee ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Protein Kinase ◽  
Allergic Inflammation ◽  
Nuclear Factor Κb ◽  
Mitogen Activated Protein Kinase ◽  
Nuclear Factor ◽  
Boehmeria Nivea ◽  
Mitogen Activated Protein ◽  
Ige Mediated

Mast cells are effector cells that initiate allergic inflammatory immune responses by inducing inflammatory mediators. Boehmeria nivea (Linn.) Gaudich is a natural herb in the nettle family Urticaceae that possesses numerous pharmacological properties. Despite the various pharmacological benefits of Boehmeria nivea, its effects on allergic inflammation have not yet been determined. Here, we investigated the effect of the ethanol extract of Boehmeria nivea (BNE) on degranulation rat basophilic leukemia (RBL)-2H3 mast cells stimulated with anti-dinitrophenyl (anti-DNP) and bovine serum albumin (BSA) during immunoglobulin E (IgE)-mediated allergic immune response. The results showed inhibition of the release of β-hexosaminidase and histamine from the cells. BNE suppressed pro-inflammatory cytokines (Tumor necrosis factor (TNF)-α, Interleukin (IL)-1β, and IL-6) and reduced T helper (Th)2 cytokine IL-4 expression and/or secretion correlated with the downregulation of p38, extracellular signal-regulated kinases (ERK) mitogen-activated protein kinase (MAPK), and nuclear factor-κB (NF-κB) signaling pathways in treated RBL-2H3 mast cells. In passive cutaneous anaphylaxis, treatment with BNE during IgE-mediated local allergic reaction triggered a reduction in mouse ear pigmentation and thickness. Taken together, these results indicated that BNE suppressed mast cell-mediated inflammation, suggesting that BNE might be a candidate for the treatment of various allergic disorders.

scholarly journals TLR2 Regulates Mast Cell IL-6 and IL-13 Production During Listeria monocytogenes Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Rodolfo Soria-Castro ◽  
Ángel R. Alfaro-Doblado ◽  
Gloria Rodríguez-López ◽  
Marcia Campillo-Navarro ◽  
Yatsiri G. Meneses-Preza ◽  
...  
Keyword(s):  
Mast Cell ◽  
Listeria Monocytogenes ◽  
Cytokine Production ◽  
Bacterial Load ◽  
Mast Cell Degranulation ◽  
Signaling Proteins ◽  
Ros Production ◽  
Tnf Α ◽  
Listeria Monocytogenes Infection ◽  
Activation Pathways

Listeria monocytogenes (L.m) is efficiently controlled by several cells of the innate immunity, including the Mast Cell (MC). MC is activated by L.m inducing its degranulation, cytokine production and microbicidal mechanisms. TLR2 is required for the optimal control of L.m infection by different cells of the immune system. However, little is known about the MC receptors involved in recognizing this bacterium and whether these interactions mediate MC activation. In this study, we analyzed whether TLR2 is involved in mediating different MC activation responses during L.m infection. We found that despite MC were infected with L.m, they were able to clear the bacterial load. In addition, MC degranulated and produced ROS, TNF-α, IL-1β, IL-6, IL-13 and MCP-1 in response to bacterial infection. Interestingly, L.m induced the activation of signaling proteins: ERK, p38 and NF-κB. When TLR2 was blocked, L.m endocytosis, bactericidal activity, ROS production and mast cell degranulation were not affected. Interestingly, only IL-6 and IL-13 production were affected when TLR2 was inhibited in response to L.m infection. Furthermore, p38 activation depended on TLR2, but not ERK or NF-κB activation. These results indicate that TLR2 mediates only some MC activation pathways during L.m infection, mainly those related to IL-6 and IL-13 production.

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