Human Mast Cell Activation with Viruses and Pathogen Products

Haidl, Ian D.; Marshall, Jean S.

doi:10.1007/978-1-4939-1568-2_12

Cited by 6 publications

(5 citation statements)

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“…Mast cell differentiation, phenotypes and functions in tissues are largely determined by the microenvironment (e.g., cytokines, activating and inhibitory stimuli, chemokines) (Mukai et al, 2018). Mast cells are canonically implicated in allergic disorders (Liccardi et al, 2003; Fujisawa et al, 2014; Bradding and Arthur, 2016; Canonica et al, 2016; Subramanian et al, 2016; Mukai et al, 2018), but also in several non allergic conditions including autoimmune disorders (de Paulis et al, 1996; Brown and Weinberg, 2018; Rivellese et al, 2018; Yu et al, 2018), cardiovascular diseases (Patella et al, 1996, 1998; Theoharides et al, 2011; Shi et al, 2015; Ngkelo et al, 2016), bacterial (Piliponsky and Romani, 2018) and viral diseases (Haidl and Marshall, 2015), neurological disorders (Skaper et al, 2014; Theoharides et al, 2016; Skaper et al, 2017; Conti et al, 2018), and cancer (Galdiero et al, 2016; Varricchi et al, 2017). Increasing evidence supports the role of mast cells and their mediators in neurogenic inflammation leading to pain and itch (Gupta and Harvima, 2018; Steinhoff et al, 2018; Yosipovitch et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Heterogeneity of Human Mast Cells With Respect to MRGPRX2 Receptor Expression and Function

Varricchi

Pecoraro

Loffredo

et al. 2019

Front. Cell. Neurosci.

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Mast cells and their mediators play a role in the control of homeostasis and in the pathogenesis of several disorders. The concept of rodent mast cell heterogeneity, initially established in the mid-1960s has been extended in humans. Human mast cells isolated and purified from different anatomic sites can be activated via aggregation of cell surface high affinity IgE receptors (FcεRI) by antigens, superantigens, anti-IgE, and anti-FcεRI. MAS-related G protein-coupled receptor-X2 (MRGPRX2) is expressed at high level in human skin mast cells (MCs) (HSMCs), synovial MCs (HSyMCs), but not in lung MCs (HLMCs). MRGPX2 can be activated by neuropeptide substance P, several opioids, cationic drugs, and 48/80. Substance P (5 × 10 −7 M – 5 × 10 −6 M) induced histamine and tryptase release from HSMCs and to a lesser extent from HSyMCs, but not from HLMCs and human cardiac MCs (HHMCs). Morphine (10 −5 M – 3 × 10 −4 M) selectively induced histamine and tryptase release from HSMCs, but not from HLMCs and HHMCs. SP and morphine were incomplete secretagogues because they did not induce the de novo synthesis of arachidonic acid metabolites from human mast cells. In the same experiments anti-IgE (3 μg/ml) induced the release of histamine and tryptase and the de novo synthesis of prostaglandin D 2 (PGD 2 ) from HLMCs, HHMCs, HSyMCs, and HSMCs. By contrast, anti-IgE induced the production of leukotriene C 4 (LTC 4 ) from HLMCs, HHMCs, HSyMCs, but not from HSMCs. These results are compatible with the heterogeneous expression and function of MRGPRX2 receptor on primary human mast cells isolated from different anatomic sites.

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Section: Introductionmentioning

confidence: 99%

Heterogeneity of Human Mast Cells With Respect to MRGPRX2 Receptor Expression and Function

Varricchi

Pecoraro

Loffredo

et al. 2019

Front. Cell. Neurosci.

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“…[1][2][3] Mast cells express an array of receptors that allow these cells to recognize and respond to a wide spectrum of infectious pathogens and endogenous molecules produced by damaged or inflamed tissues. Thus, in addition to the high-affinity receptor of IgE, FcεRI, and other immunoglobulin Fc receptors, mast cells express the microbial pattern recognition receptors Toll-like receptor (TLRs) and NOD-like receptor 4 and the more recently described Mas-related G protein-coupled receptor X2 (MRGPRX2 [human subjects]), which recognizes cationic neuropeptides, antimicrobial peptides, and insect venom peptides. 5 Similarly, mast cells recognize molecules associated with tissue inflammation or damage through receptors such as complement receptors and the IL-33 receptor, also called ST2 long-form (ST2L).…”

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confidence: 99%

Mast cells signal their importance in health and disease

Olivera

Beaven

Metcalfe

2018

Journal of Allergy and Clinical Immunology

189

131

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FcεRI is the primary receptor in mast cells that mediates allergic reactions by inducing rapid release of mediators, an adaptive immune response that might have evolved as a host defense against parasites and venoms. Yet it is apparent that mast cells are also activated through non-IgE receptors, the significance of which is just beginning to be understood. This includes the Mas-related G protein-coupled receptor X2, which might contribute to reactions to diverse antimicrobials and polybasic compounds, and the adhesion G protein-coupled receptor E2, variants of which are associated with familial vibratory urticaria and are activated by mechanical vibration. Similarly, mast cells have long been recognized as the main repository for histamine, heparin, and proteases. Recent evidence also points to new functions, modes of delivery, and mechanisms of action of mast cell proteases that add new dimensions to the roles of mast cells in human biology. In addition, exposure of mast cells to environmental cues can quantitatively and qualitatively modulate their responses and thus their effect on allergic inflammation. Illustrating this paradigm, we summarize a number of recent studies implicating the injury/tissue damage cytokine IL-33 as a modulator of allergen-induced mast cell responses. We also discuss the discovery of markers associated with transformed mast cells and new potential directions in suppressing mast cell activity.

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“…MCs play a key role in the fight against bacterial infection and viral infection 28 , 29 , however their role remains poorly understood in the process of corneal fungal infection. This research found that MCs, which are mainly distributed in the corneal limbus, play a dominant role in controlling the fungus infection of the cornea by several mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Mast Cell Activation Protects Cornea by Promoting Neutrophil Infiltration via Stimulating ICAM-1 and Vascular Dilation in Fungal Keratitis

Xie

Zhang

Liu

et al. 2018

Sci Rep

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The role of mast cells (MCs) in fungal infection is largely unknown. This study was to explore a protective role and mechanism of MCs in fungal keratitis. Experimental fungal keratitis (FK) mouse model was developed. Mice untreated (UT) or receiving corneal wound without fungal infection (Mock) were used as controls. Large number of connective tissue MCs was found in normal mice. MC activation with degranulation was largely observed, and the percentage of degranulated/total cells was high in FK. Dilated limbal vasculature with increased permeability, as well as largely infiltrated neutrophils with stimulated ICAM-1 protein levels were observed in corneas of FK mice, when compared with Mock and UT mice. Interestingly, pretreatment with cromolyn sodium (Block) significantly blocked MC degranulation, dramatically suppressed vascular dilation and permeability, and markedly reduced neutrophil infiltration with lower ICAM-1 levels in FK mice at 6–24 hours. Furthermore, the Block mice manifested prolonged disease course, increased pathological damage, and vigorous fungus growth, with much higher corneal perforation rate than FK mice at 72 h. These findings reveal a novel phenomenon that MCs play a vital role in protecting cornea against fungal infection through degranulation that promotes neutrophil infiltration via stimulating ICAM-1 production and limbal vascular dilation and permeability.

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Human Mast Cell Activation with Viruses and Pathogen Products

Cited by 6 publications

References 105 publications

Heterogeneity of Human Mast Cells With Respect to MRGPRX2 Receptor Expression and Function

Heterogeneity of Human Mast Cells With Respect to MRGPRX2 Receptor Expression and Function

Mast cells signal their importance in health and disease

Mast Cell Activation Protects Cornea by Promoting Neutrophil Infiltration via Stimulating ICAM-1 and Vascular Dilation in Fungal Keratitis

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