Mast Cell Interactions and Crosstalk in Regulating Allergic Inflammation

Velez, Tania Estefania; Bryce, Paul J.; Hulse, Kathryn E.

doi:10.1007/s11882-018-0786-6

Cited by 20 publications

(11 citation statements)

References 55 publications

(59 reference statements)

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“…Mast cells, which serve as key effector cells in allergic disease were shown to be under control of the SCN and to have a circadian expression and release of their mediators in response to activation. Being ubiquitously distributed throughout connective and mucosal tissues and near blood vessels, mast cells are uniquely able to affect other immune cells and serve as a transition point from innate to adaptive immune response ( 46 , 62 ). Hence, disrupted mast cell clocks could impair the subsequent adaptive immune responses and trigger or fortify allergic symptoms.…”

Section: Discussionmentioning

confidence: 99%

The Circadian Clock Drives Mast Cell Functions in Allergic Reactions

Christ

Sowa

Froy³

et al. 2018

Front. Immunol.

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Allergic diseases are known to vary in the severity of their symptoms throughout the day/night cycle. This rhythmicity is also observed in mast cell function and responsiveness. Mast cells are key effector cells of allergic reactions and release cytokines, chemokines, and important inflammatory mediators such as histamine, which have been shown to display diurnal variation. Recent research clarified that mast cells are controlled by their internal clock—which is regulated by a specific set of clock genes—as well as external factors such as light sensed by the suprachiasmatic nuclei, hormonal status, or diet. Here, we give an overview of the connections between circadian clock, mast cells, and allergic disease. Further work aimed at studying the role of chronotherapy/chronomedicine should take into account this rhythmic nature of not only mast cells but also the immune responses generated by mast cell signaling.

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Section: Discussionmentioning

confidence: 99%

The Circadian Clock Drives Mast Cell Functions in Allergic Reactions

Christ

Sowa

Froy³

et al. 2018

Front. Immunol.

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“…15,16 In brief, fresh samples were prepared using a diagnostic lyse-no-wash protocol with commercial Trucount tubes (BD Biosciences, San Jose, Calif) for absolute counts of total T cells, B cells, and natural killer (NK) cells. Because mast cells are known to induce type 2 inflammation, for instance in allergy and helminth infections, 17,18 we hypothesized that an imbalance in T H 1 and T H 2 subsets might be present. T-helper cell subsets were therefore also analyzed.…”

Section: Flow Cytometrymentioning

confidence: 99%

Altered leukocyte subsets and immune proteome indicate proinflammatory mechanisms in mastocytosis

Hermans¹,

Heeringa²,

Swagemakers³

et al. 2022

Journal of Allergy and Clinical Immunology

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“…Mast cells have been long recognized to play a critical role in allergic airway inflammation and asthma (32,33); however, their contributions to innate immunity and host defense during acute respiratory infections have also been increasingly recognized (34,35). Unlike circulating white blood cells, mast cells mature in tissues and the local microenvironment plays a critical role in the differentiation of mast cells and the establishment of their phenotype.…”

Section: Discussionmentioning

confidence: 99%

Respiratory Syncytial Virus Infection of Human Lung Fibroblasts Induces a Hyaluronan-Enriched Extracellular Matrix That Binds Mast Cells and Enhances Expression of Mast Cell Proteases

Reeves

Barrow²,

Rich³

et al. 2020

Front. Immunol.

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Human lung fibroblasts (HLFs) treated with the viral mimetic polyinosine-polycytidylic acid (poly I:C) form an extracellular matrix (ECM) enriched in hyaluronan (HA) that avidly binds monocytes and lymphocytes. Mast cells are important innate immune cells in both asthma and acute respiratory infections including respiratory syncytial virus (RSV); however, the effect of RSV on HA dependent mast cell adhesion and/or function is unknown. To determine if RSV infection of HLFs leads to the formation of a HA-enriched ECM that binds and enhances mast cell activity primary HLFs were infected with RSV for 48 h prior to leukocyte binding studies using a fluorescently labeled human mast cell line (LUVA). Parallel HLFs were harvested for characterization of HA production by ELISA and size exclusion chromatography. In separate experiments, HLFs were infected as above for 48 h prior to adding LUVA cells to HLF wells. Co-cultures were incubated for 48 h at which point media and cell pellets were collected for analysis. The role of the hyaladherin tumor necrosis factor-stimulated gene 6 (TSG-6) was also assessed using siRNA knockdown. RSV infection of primary HLFs for 48 h enhanced HA-dependent LUVA binding assessed by quantitative fluorescent microscopy. This coincided with increased HLF HA synthase (HAS) 2 and HAS3 expression and decreased hyaluronidase (HYAL) 2 expression leading to increased HA accumulation in the HLF cell layer and the presence of larger HA fragments. Separately, LUVAs co-cultured with RSV-infected HLFs for 48 h displayed enhanced production of the mast cell proteases, chymase, and tryptase. Pre-treatment with the HA inhibitor 4-methylumbelliferone (4-MU) and neutralizing antibodies to CD44 (HA receptor) decreased mast cell protease expression in co-cultured LUVAs implicating a direct role for HA. TSG-6 expression was increased over the 48-h infection. Inhibition of HLF TSG-6 expression by siRNA knockdown led Reeves et al.RSV-Induced ECM and Mast Cells to decreased LUVA binding suggesting an important role for this hyaladherin for LUVA adhesion in the setting of RSV infection. In summary, RSV infection of HLFs contributes to inflammation via HA-dependent mechanisms that enhance mast cell binding as well as mast cell protease expression via direct interactions with the ECM.

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Mast Cell Interactions and Crosstalk in Regulating Allergic Inflammation

Cited by 20 publications

References 55 publications

The Circadian Clock Drives Mast Cell Functions in Allergic Reactions

The Circadian Clock Drives Mast Cell Functions in Allergic Reactions

Altered leukocyte subsets and immune proteome indicate proinflammatory mechanisms in mastocytosis

Respiratory Syncytial Virus Infection of Human Lung Fibroblasts Induces a Hyaluronan-Enriched Extracellular Matrix That Binds Mast Cells and Enhances Expression of Mast Cell Proteases

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