Different potency of bacterial antigens TLR2 and TLR4 ligands in stimulating mature mast cells to cysteinyl leukotriene synthesis

Bąbolewska, Edyta; Witczak, Piotr; Pietrzak, Anna; Brzezińska‐Błaszczyk, Ewa

doi:10.1111/j.1348-0421.2012.00426.x

Cited by 10 publications

(7 citation statements)

References 66 publications

(76 reference statements)

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“…Recent reports have highlighted that other cells such as alveolar epithelial cells play an important role in innate defense to produce the chemokine CCL2 and also in the pathogenesis of mycobacterial infection (Chuquimia et al, 2012). Additionally, mast cells are activated by mycobacterial LAM to induce the generation of cysteinyl leukotriene through TLR2-NF-κB-dependent signaling (Bąbolewska et al, 2012). Together, these studies suggest that TLRs have a crucial role in the host immune responses against mycobacterial infection and that they are involved in not only immune cells but also other cells.…”

Section: Overview Of Tlrs In Mycobacterial Infectionmentioning

confidence: 99%

Mycobacterial signaling through toll-like receptors

Basu¹,

Shin²,

Jo³

2012

Front. Cell. Inf. Microbio.

109

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Studies over the past decade have helped to decipher molecular networks dependent on Toll-like receptor (TLR) signaling, in mycobacteria-infected macrophages. Stimulation of TLRs by mycobacteria and their antigenic components rapidly induces intracellular signaling cascades involved in the activation of nuclear factor-κB and mitogen-activated protein kinase pathways, which play important roles in orchestrating proinflammatory responses and innate defense through generation of a variety of antimicrobial effector molecules. Recent studies have provided evidence that mycobacterial TLR-signaling cross talks with other intracellular antimicrobial innate pathways, the autophagy process and functional vitamin D receptor (VDR) signaling. In this article we describe recent advances in the recognition, responses, and regulation of mycobacterial signaling through TLRs.

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Section: Overview Of Tlrs In Mycobacterial Infectionmentioning

confidence: 99%

Mycobacterial signaling through toll-like receptors

Basu¹,

Shin²,

Jo³

2012

Front. Cell. Inf. Microbio.

109

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“…MCs are well accepted as highly competent cells for host defense against bacteria. For instance, several microbial products have been shown to stimulate MCs through TLR2 and TLR4 to generate various proinflammatory humoral factors, including lipid mediators, cytokines, and chemokines [11][12][13][14][15][16][17]. Mainly, these cells exert several mechanisms of direct bacterial killing like the ability to phagocytose and intracellular digestion via oxidative and nonoxidative route [18] or, irrespective of phagocytosis, to form extracellular traps (MCETs), which can entrap and eliminate various bacterial materials [19].…”

Section: Introductionmentioning

confidence: 99%

The Response of Tissue Mast Cells to TLR3 Ligand Poly(I:C) Treatment

Witczak

Brzezińska‐Błaszczyk

Agier

2020

Journal of Immunology Research

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Mast cells (MCs) are found mainly at the anatomical sites exposed to the external environment; thus, they are localized close to blood vessels, lymphatic vessels, and a multitude of immune cells. Moreover, those cells can recognize invading pathogens through a range of surface molecules known as pathogen recognition receptors (PRRs), mainly Toll-like receptors (TLRs). MCs are extensively engaged in the control and clearance of bacterial infections, but much less is known about their contribution to antiviral host response as well as pathomechanisms of virus-induced diseases. In the study, we employed in vivo differentiated mature tissue mast cells freshly isolated from rat peritoneal cavity. Here, we demonstrated that rat peritoneal mast cells (rPMCs) express viral dsRNA-specific TLR3 molecule (intracellularly and on the cell surface) as well as other proteins associated with cellular antiviral response: IRF3, type I and II IFN receptors, and MHC I. We found that exposure of rPMCs to viral dsRNA mimic, i.e., poly(I:C), induced transient upregulation of surface TLR3 (while temporarily decreased TLR3 intracellular expression), type II IFN receptor, and MHC I. TLR3 ligand-stimulated rPMCs did not degranulate but generated and/or released type I IFNs (IFN-α and IFNβ) as well as proinflammatory lipid mediators (cysLTs), cytokines (TNF, IL-1β), and chemokines (CCL3, CXCL8). We documented that rPMC priming with poly(I:C) did not affect FcεRI-dependent degranulation. However, their costimulation with TLR3 agonist and anti-IgE led to a significant increase in cysLT and TNF secretion. Our findings confirm that MCs may serve as active participants in the antiviral immune response. Presented data on modulated FcεRI-mediated MC secretion of mediators upon poly(I:C) treatment suggests that dsRNA-type virus infection could influence the severity of allergic reactions.

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“…TLR ligation by its agonists induces the highly selective mast cell response. A number of studies have indicated that neither TLR2 nor TLR4 stimulation resulted in mast cell degranulation and preformed mediator release [5][6][7][8][9][10] but it induces synthesis of newly generated lipid mediators, including cysteinyl leukotrienes (cysLTs) [5,[7][8][9][10][11][12][13]. TLR2 and TLR4 ligation can activate mast cells to synthesize many different cytokines and chemokines, as well [5,7,[14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%