Effect of IL-33 on de novo synthesized mediators from human mast cells

Theoharides, Theoharis C.; Leeman, Susan E.

doi:10.1016/j.jaci.2018.09.014

Cited by 19 publications

(15 citation statements)

References 7 publications

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“…Identification of other mast cell mediators which might have utility in diagnosing MCAS is an area of active investigation (e.g. [84,85]), but questions remain regarding whether such mediators (e.g. interleukin-1β [84] and interleukin-6, interleukin-31, tumor necrosis factor, or vascular endothelial growth factor [85]) are "sufficiently" specific to the MC to warrant their having significance visà-vis a diagnosis as important as MCAS.…”

Section: Discussionmentioning

confidence: 99%

“…[84,85]), but questions remain regarding whether such mediators (e.g. interleukin-1β [84] and interleukin-6, interleukin-31, tumor necrosis factor, or vascular endothelial growth factor [85]) are "sufficiently" specific to the MC to warrant their having significance visà-vis a diagnosis as important as MCAS. It is possible that some MC mediators, while being of insufficient specificity for diagnostic purposes, may nevertheless eventually demonstrate utility for therapeutic efficacy monitoring purposes in at least some MCAS patients, i.e.…”

Section: Discussionmentioning

confidence: 99%

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Diagnosis of mast cell activation syndrome: a global “consensus-2”

Ackerley²,

et al. 2020

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The concept that disease rooted principally in chronic aberrant constitutive and reactive activation of mast cells (MCs), without the gross MC neoplasia in mastocytosis, first emerged in the 1980s, but only in the last decade has recognition of “mast cell activation syndrome” (MCAS) grown significantly. Two principal proposals for diagnostic criteria have emerged. One, originally published in 2012, is labeled by its authors as a “consensus” (re-termed here as “consensus-1”). Another sizable contingent of investigators and practitioners favor a different approach (originally published in 2011, newly termed here as “consensus-2”), resembling “consensus-1” in some respects but differing in others, leading to substantial differences between these proposals in the numbers of patients qualifying for diagnosis (and thus treatment). Overdiagnosis by “consensus-2” criteria has potential to be problematic, but underdiagnosis by “consensus-1” criteria seems the far larger problem given (1) increasing appreciation that MCAS is prevalent (up to 17% of the general population), and (2) most MCAS patients, regardless of illness duration prior to diagnosis, can eventually identify treatment yielding sustained improvement. We analyze these proposals (and others) and suggest that, until careful research provides more definitive answers, diagnosis by either proposal is valid, reasonable, and helpful.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Diagnosis of mast cell activation syndrome: a global “consensus-2”

Ackerley²,

et al. 2020

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“…IL-1 stimulates human MCs to selectively release IL-6 without degranulation, via a unique process utilizing 40-80 nm vesicles unrelated to the length of secretory granules (800-1,000 nm) ( 62 ). IL-33 may serve as a potent activator of MCs and was reported to promote MC survival, maturation, migration and adhesion, and to selectively produce a variety of pro-inflammatory cytokines, including IL-4, IL-5, IL-6, IL-8 and IL-13 and chemokines including macrophage inflammatory protein-1α and monocyte chemoattractant protein 1 (MCP-1) ( 63 , 64 ). IL-33 enhances the role of the pro-inflammatory peptide substance P in stimulating human MCs to secrete high levels of VEGF and TNF via the interaction of neurokinin 1 and ST2 receptors without concomitant secretion of tryptase ( 65 ).…”

Section: Overview and Activation Of Mcsmentioning

confidence: 99%

Mast cell‑mediated neuroinflammation may have a role in attention deficit hyperactivity disorder (Review)

Song

Huang

et al. 2020

Exp Ther Med

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Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental and behavioral disorder with a serious negative impact on the quality of life from childhood until adulthood, which may cause academic failure, family disharmony and even social unrest. The pathogenesis of ADHD has remained to be fully elucidated, leading to difficulties in the treatment of this disease. Genetic and environmental factors contribute to the risk of ADHD development. Certain studies indicated that ADHD has high comorbidity with allergic and autoimmune diseases, with various patients with ADHD having a high inflammatory status. Increasing evidence indicated that mast cells (MCs) are involved in the pathogenesis of brain inflammation and neuropsychiatric disorders. MCs may cause or aggravate neuroinflammation via the selective release of inflammatory factors, interaction with glial cells and neurons, activation of the hypothalamic-pituitary adrenal axis or disruption of the blood-brain barrier integrity. In the present review, the notion that MC activation may be involved in the occurrence and development of ADHD through a number of ways is discussed based on previously published studies. The association between MCs and ADHD appears to lack sufficient evidence at present and this hypothesis is considered to be worthy of further study, providing a novel perspective for the treatment of ADHD.

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“…Following stimulation, mast cells release proinflammatory mediators 117 such as histamine, tryptase, chemokines (e.g., CCL2, CCXL8) 118 and cytokines (IL-6, 119 IL-1β , 120 and tumor necrosis factor [TNF] 114 ), especially when primed by IL-33. 121,122 Histamine can stimulate macrophages to release IL-1, 123 which stimulates mast cells to release IL-6. 119 Mast cells can also secrete mitochondrial DNA (mtDNA), 124 which was recently reported to be increased in the serum of COVID-19 patients and correlated with disease severity.…”

Section: Inflammation Of the Brainmentioning

confidence: 99%

Long‐COVID syndrome‐associated brain fog and chemofog: Luteolin to the rescue

Cholevas²,

Polyzoidis³

et al. 2021

BioFactors

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164

140

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COVID-19 leads to severe respiratory problems, but also to long-COVID syndrome associated primarily with cognitive dysfunction and fatigue. Long-COVID syndrome symptoms, especially brain fog, are similar to those experienced by patients undertaking or following chemotherapy for cancer (chemofog or chemobrain), as well in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or mast cell activation syndrome (MCAS). The pathogenesis of brain fog in these illnesses is presently unknown but may involve neuroinflammation via mast cells stimulated by pathogenic and stress stimuli to release mediators that activate microglia and lead to inflammation in the hypothalamus. These processes could be mitigated by phytosomal formulation (in olive pomace oil) of the natural flavonoid luteolin.

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Effect of IL-33 on de novo synthesized mediators from human mast cells

Cited by 19 publications

References 7 publications

Diagnosis of mast cell activation syndrome: a global “consensus-2”

Diagnosis of mast cell activation syndrome: a global “consensus-2”

Mast cell‑mediated neuroinflammation may have a role in attention deficit hyperactivity disorder (Review)

Long‐COVID syndrome‐associated brain fog and chemofog: Luteolin to the rescue

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