Interleukin-6 potentiates FcεRI-induced PGD 2 biosynthesis and induces VEGF from human in situ -matured skin mast cells

McHale, Cody; Mohammed, Zahraa; Deppen, Juline; Gomez, Gregorio

doi:10.1016/j.bbagen.2018.01.020

Cited by 32 publications

(43 citation statements)

References 54 publications

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“…It also leads to recruitment and differentiation of mast cells, as well as monocytes, CD4+ and CD8+ T cells, and B lymphocytes, and it stimulates the production of VEGF by fibroblasts. IL-6 expression affects the homeostatic processes that is related to tissue injury and activation of stress-related responses [40][41][42][43]. Despite being an anti-inflammatory cytokine, the expression of IL-10 was increased in ZIKV-infected HMC-1 cells, which corroborates what was observed in another study, in the serum of Zika positive patients [44].…”

Section: Discussionsupporting

confidence: 82%

Zika Virus Infects Human Placental Mast Cells and the HMC-1 Cell Line, and Triggers Degranulation, Cytokine Release and Ultrastructural Changes

Rabelo

Gonçalves

Souza

et al. 2020

Cells

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Zika virus (ZIKV) is an emergent arthropod-borne virus whose outbreak in Brazil has brought major public health problems. Infected individuals have different symptoms, including rash and pruritus, which can be relieved by the administration of antiallergics. In the case of pregnant women, ZIKV can cross the placenta and infect the fetus leading to congenital defects. We have identified that mast cells in the placentae of patients who had Zika during pregnancy can be infected. This led to our investigation on the possible role of mast cells during a ZIKV infection, using the HMC-1 cell line. We analyzed their permissiveness to infection, release of mediators and ultrastructural changes. Flow cytometry detection of ZIKV-NS1 expression 24 h post infection in 45.3% of cells showed that HMC-1 cells are permissive to ZIKV infection. Following infection, β-hexosaminidase was measured in the supernatant of the cells with a notable release at 30 min. In addition, an increase in TNF-α, IL-6, IL-10 and VEGF levels were measured at 6 h and 24 h post infection. Lastly, different intracellular changes were observed in an ultrastructural analysis of infected cells. Our findings suggest that mast cells may represent an important source of mediators that can activate other immune cell types during a ZIKV infection, which has the potential to be a major contributor in the spread of the virus in cases of vertical transmission.

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Section: Discussionsupporting

confidence: 82%

Zika Virus Infects Human Placental Mast Cells and the HMC-1 Cell Line, and Triggers Degranulation, Cytokine Release and Ultrastructural Changes

Rabelo

Gonçalves

Souza

et al. 2020

Cells

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“…IL-6 is a pro-inflammatory molecule and mediates stroke-induced inflammation [40][41][42] and also increases MCs maturation [43]. IL-6 also upregulates histamine production and induces the FceR1 immunoglobulin receptor found on mast cells [44][45][46][47]. In addition, we found that mucus secreting fucosylated goblet cells were reduced after stroke in Ag mice.…”

Section: Discussionmentioning

confidence: 99%

“…stroke-induced inflammation [40][41][42]. IL-6 increases MCs maturation [43] by inducing the FceR1 receptor on MCs [44][45][46][47] and by upregulating HA production. In young mice, we found increased levels of plasma IL-6 at 6 hours post-stroke that normalized by 24 hours, when compared to age-matched shams.…”

Section: Stroke-induced Ha Release Is Associated With Increased Pro-imentioning

confidence: 99%

Age-dependent involvement of gut mast cells and histamine in post-stroke inflammation

Blasco

Chauhan

Honarpisheh

et al. 2020

Preprint

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Background Risk of stroke-related morbidity and mortality increases significantly with age. Aging is associated with chronic, low-grade inflammation, which is thought to contribute to the poorer outcomes after stroke seen in the elderly. Histamine (HA) is a major molecular mediator of inflammation and mast cells residing in the gut are a primary source of histamine. Methods Stroke was induced in male C57BL/6J mice at 3 months (young) and 20 months (aged) of age. Role of histamine after stroke was examined using young (Yg) and aged (Ag) mice, mice underwent MCAO surgery and were euthanized at 6h, 24h and 7 days post-ischemia; sham mice received the same surgery but no MCAO. In this work, we evaluated whether worsened outcomes after experimental stroke in aged mice was associated with age-related changes in mast cells, histamine levels, and histamine receptor expression in the gut, brain, and plasma. Results We found increased numbers of mast cells in the gut and the brain with aging. Using the middle cerebral artery occlusion (MCAO) model of ischemic stroke, we demonstrate that stroke leads to increased numbers of mast cells and histamine receptors in the gut. These gut-centric changes are associated with elevated levels of HA and other pro-inflammatory cytokines including IL-6, G-CSF, TNF-α, and IFN-γ in the peripheral circulation. Our data also shows that post-stroke gut inflammation led to a significant reduction of mucin-producing goblet cells and a loss of gut barrier integrity. Lastly, gut inflammation after stroke is associated with changes in the composition of the gut microbiota as early as 24 hours post-stroke. Conclusion An important theme emerging from our results is that acute inflammatory events following ischemic insults in the brain persist longer in the aged mice when compared to younger animals. Taken together, our findings implicate mast cell activation and histamine signaling as a part of peripheral inflammatory response after ischemic stroke, which are profound in aged animals. Interfering with histamine signaling orally might provide translational value to improve stroke outcome.

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“…The high expression of PTGS2 can promote large amount of PGD2 synthesis and aggravate the in ammatory response in CSU patients. Besides, IL6 classical signaling can also enhance the expression of COX2 induced by FcεRI, which thereby enhances the production of IgEdependent PGD2 by human tissue-derived mast cells [36]. It is well known that endothelial dysfunction may increase vascular permeability, leading to a pro-in ammatory response.…”

Section: Discussionmentioning

confidence: 99%

Secondary Analysis of Microarray Data Reveals Immune-Related Key Genes and Pathways in Chronic Spontaneous Urticaria

Su¹,

Huang²,

Guan³

et al. 2020

Preprint

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Background: Lupus Nephritis (LN) in patients with Systemic Lupus Erythematosus (SLE) is one of the most serious and prevalent manifestations. The procedure of renal biopsy is harmful and accompanied by potential hazards. Therefore, introducing reliable biomarkers to predict LN is exceedingly worthwhile. In the current study, we compared the diagnostic values of circulating autoantibodies against dsDNA, C1q, C3b, SSA, SSB, and Sm alone or in combination to predict LN.Methods: This study evaluated abovementioned autoantibodies in 40 healthy controls (HCs) and 95 SLE patients with different kidney involvements, including absent (n = 40), inactive (n = 20), and active (n= 35) LN using EIA method.Result: The frequency and odds ratio of anti-dsDNA (71.4%, OR=4.2), anti-C1q (62.9%, OR= 5.1), and the simultaneous existence of anti-C1q and anti-dsDNA (51.4%, OR=6) antibodies were significantly higher in the active LN group compared with both inactive and absent LN groups. Moreover, the levels of anti-C1q and anti-dsDNA antibodies positively correlated with disease activity in patients with SLE. The prevalence of these autoantibodies was associated with the severity of LN biopsies. Conclusion: These data suggest that anti-C1q and anti-dsDNA antibodies and also the simultaneous presence of them may be valuable diagnostic biomarkers for LN prediction in patients with SLE.

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Interleukin-6 potentiates FcεRI-induced PGD 2 biosynthesis and induces VEGF from human in situ -matured skin mast cells

Abstract: These findings from this study indicate that IL-6 contributes to human allergic disease by enhancing the production of inflammatory PGD from tissue-resident mast cells. Moreover, the data suggest a novel role for IL-6 in mast cell-mediated angiogenesis.

Cited by 32 publications

References 54 publications

Zika Virus Infects Human Placental Mast Cells and the HMC-1 Cell Line, and Triggers Degranulation, Cytokine Release and Ultrastructural Changes

Zika Virus Infects Human Placental Mast Cells and the HMC-1 Cell Line, and Triggers Degranulation, Cytokine Release and Ultrastructural Changes

Age-dependent involvement of gut mast cells and histamine in post-stroke inflammation

Secondary Analysis of Microarray Data Reveals Immune-Related Key Genes and Pathways in Chronic Spontaneous Urticaria

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