Anti-allergic Effect of Methanol Extract from Polysiphonia morrowii Harveyin IgE/BSA-stimulated Bone Marrow-derived Cultured Mast Cells anda Passive Cutaneous Anaphylaxis Mouse Model

2019 ◽  
Vol 24 (2) ◽  
pp. 99-104
Author(s):  
Eui Jeong Han ◽  
Eun-Ji Shin ◽  
Min Ju Kim ◽  
Soo-Jin Heo ◽  
Eun-A Kim ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Mouse Model ◽  
Methanol Extract ◽  
Passive Cutaneous Anaphylaxis ◽  
Allergic Effect

Anti-Inflammatory and Anti-Allergic Effect of Agaricus blazei Extract in Bone Marrow-Derived Mast Cells

2012 ◽  
Vol 40 (05) ◽  
pp. 1073-1084 ◽  
Author(s):  
Hyuk-Hwan Song ◽  
Hee-Sung Chae ◽  
Sei-Ryang Oh ◽  
Hyeong-Kyu Lee ◽  
Young-Won Chin
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Mouse Bone Marrow ◽  
Agaricus Blazei ◽  
Soluble Extract ◽  
Anti Inflammatory ◽  
Allergic Effect

In this study, the anti-inflammatory and anti-allergic effects of the chloroform-soluble extract of Agaricus blazei in mouse bone marrow-derived mast cells (BMMCs) were investigated. The chloroform-soluble extract inhibited IL-6 production in PMA plus A23187-stimulated BMMCs, and down-regulated the phosphorylation of Akt. In addition, this extract demonstrated inhibition of the degranulation of β-hexosaminidase and the production of IL-6, prostaglandin D2 and leukotriene C4 in PMA plus A23187-induced BMMCs. In conclusion, the chloroform-soluble extract of Agaricus blazei exerted anti-inflammatory and anti-allergic activities mediated by influencing IL-6, prostaglandin D2, leukotriene C4, and the phosphorylation of Akt.

Gomisin N has anti-allergic effect and inhibits inflammatory cytokine expression in mouse bone marrow-derived mast cells

2011 ◽  
Vol 33 (4) ◽  
pp. 709-713 ◽  
Author(s):  
Hee-Sung Chae ◽  
Ok-Hwa Kang ◽  
You-Chang Oh ◽  
Jang-Gi Choi ◽  
Joon-Ho Keum ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Mouse Bone Marrow ◽  
Gomisin N ◽  
Allergic Effect

Anti-allergic effect of a chloroform-soluble extract ofCinnamomum cambodianumin bone marrow-derived mast cells

2012 ◽  
Vol 34 (4) ◽  
pp. 639-644 ◽  
Author(s):  
Hee-Sung Chae ◽  
Piseth Khiev ◽  
Hyeong-Kyu Lee ◽  
Sei-Ryang Oh ◽  
Young-Won Chin
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Soluble Extract ◽  
Allergic Effect

Anti-allergic Effect of Eckolona cava Ethyl Acetate Fraction of on IgE/BSA-stimulated Bone Marrow-derived Cultured Mast Cells

2018 ◽  
Vol 23 (4) ◽  
pp. 277-284
Author(s):  
Eui Jeong Han ◽  
Hyun Soo Kim ◽  
Eun Ji Shin ◽  
Min Ju Kim ◽  
Hee-jin Han ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Ethyl Acetate ◽  
Ethyl Acetate Fraction ◽  
Allergic Effect

scholarly journals IL13 Contributes to Fibrotic Progression of the Myeloproliferative Neoplasms

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 60-60
Author(s):  
Johanna Melo-Cardenas ◽  
Lavanya Bezavada ◽  
Jeremy Chase Crawford ◽  
Sandeep Gurbuxani ◽  
Anitria Cotton ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Mouse Model ◽  
Single Cell ◽  
Research Funding ◽  
Bone Marrow Cells ◽  
Myeloproliferative Neoplasms ◽  
Disease Process ◽  
Wild Type ◽  
Marrow Cells

Abstract Pre-fibrotic-primary myelofibrosis PMF (Pre-PMF) is an indolent form of PMF that frequently progresses to overt-PMF. While both stages of the disease are characterized by the presence of dysplastic megakaryocytes, progression to fulminant disease is associated with significantly increased fibrosis in the bone marrow. We have previously shown that megakaryocyte maturation in overt-PMF is impaired due to a GATA1 deficiency. However, in Pre-PMF patients most megakaryocytes express GATA1. This raises the possibility that alterations in megakaryocyte development occur during the progression of the disease and may contribute to fibrosis. This progression in megakaryocyte defects is likely driven not only by the aberrant JAK/STAT signaling but also microenvironmental factors. To identify such factors, we performed studies in two mouse models of PMF (driven by JAK2V617 and MPLW515L mutations) before and after development of fibrosis. Using an unbiased approach, we measured the levels of different cytokines in the bone marrow, plasma, and spleen. In addition, we performed single cell RNAseq in bone marrow populations. We observed extensive changes in the level of cytokines in the bone marrow of the MPLW515L mouse model compared to the JAK2V617F model. We initially focused on those cytokines that are elevated in the bone marrow of both murine models, including IL13 (Figure 1A), because previous studies have shown that IL13 is elevated in PMF patients and that JAK2 inhibitors do not decrease IL13 (1-3). Moreover, elevated IL13 has been identified in patients who progress to secondary AML (2). How IL13 may contribute to the progression of the disease has not been investigated. We assayed the effect of IL13 on megakaryocytes in vitro and discovered that it promoted megakaryocyte differentiation in the absence of thrombopoietin (TPO) and potentiated the effect of TPO. This effect was observed in cultures of both wild-type and MPLW515L megakaryocytes. Next, we assayed for expression of the IL13 receptor (Il13ra1) in the bone marrow of JAK2V617F and MPLW515L mutant mice and found that it was highly upregulated compared to wild-type animals. IL13ra1 expression was particularly intense in the megakaryocyte lineage, and its expression increased with disease progression (Figure 1B). Next, we asked whether IL13 is essential for myeloproliferative neoplasm (MPN) development in vivo. To study this, we transplanted bone marrow cells from Il4/13 f/f Mx1-Cre mice expressing MPLW515L to irradiated recipients, waited until MPN developed, and then excised by pIpC injection. This experiment revealed that loss of IL13 and IL4 led to a profound reduction in disease burden (Figure 1C), decreased splenomegaly, and diminished degree of bone marrow fibrosis. Moreover, loss of IL13 and IL4 decreased the levels of pro-inflammatory cytokines in the bone marrow and spleen (Figure 1D). We attribute this effect to deletion of IL13 because IL4 was only moderately increased in the bone marrow of the MPLW515L mouse model, and because IL4 has been reported to not be altered in the MPNs. Finally, we performed single cell RNA-seq on bone marrow cells from mice transplanted with JAK2V617F or control progenitor cells early and late in the disease process (Figure 1E). Our results revealed that there was decreased myeloid progenitors but an enhancement in the mast cell lineage that tracked with the degree of fibrosis. We confirmed the presence of elevated numbers of mast cells in the bone marrow by immunohistochemistry (Figure 1F). Mast cells produce IL13, and therefore they are the likely source for the increased IL13. Finally, consistent with the observation that IL13 signaling is primarily mediated through STAT6, we found enrichment of STAT6 target genes in megakaryocyte progenitors from the late timepoint in our scRNAseq data (Figure 1G). In summary, our data demonstrate that IL13 is involved in the progression of PMF and that inhibition of the IL13 signaling pathway should be investigated as a therapeutic option in PMF. 1. Tefferi A, et al. J Clin Oncol (2011) 2. Fisher DAC, et al. Leukemia (2019) 3. Chen P, et al. Front Med (2021) Figure 1 Figure 1. Disclosures Crispino: Forma Therapeutics: Research Funding; Scholar Rock: Research Funding; MPN Research Foundation: Membership on an entity's Board of Directors or advisory committees; Sierra Oncology: Consultancy.

Isolation and Culture of Bone Marrow-derived Mast Cells

BIO-PROTOCOL ◽  
2014 ◽  
Vol 4 (4) ◽  
Author(s):  
Krisztina Vukman ◽  
Martin Metz ◽  
Marcus Maurer ◽  
Sandra O’Neill
Keyword(s):  
Bone Marrow ◽  
Mast Cells
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