No abstract available.
Leukemia, Mast-Cell* ; Mast Cells*

No abstract available.
Diagnosis* ; Leukemia, Mast-Cell* ; Mast Cells*

OBJECTIVETo investigate the role of mast cells and interleukin-9 (IL-9) in B-cell non-Hodgkin lymphoma (B-NHL) development and its clinical significance.

METHODSThe expression level of CD117 in tumor tissues of 32 B-NHL patients was determined by Western blot. The infiltration of CD117⁺ mast cells (MCs) in human B-NHL tumor tissues was observed by immunohistochemistry staining. To evaluate the correlations between the data from CD117⁺ MCs and biological markers of human B-NHL, a Spearman correlation coefficient (rs) was calculated. IL-9 levels in sera of B-NHL patients were measured by ELISA. Effects of IL-9 on expressions of functional genes of mouse bone marrow-derived mast cells (BMMCs) were detected by real-time quantitative RT-PCR.

RESULTSThe expression of CD117 was upregulated significantly in human B-cell NHL involved tissues when compared with that of controls (0.0551±0.0064 vs 0.0192±0.0072, P<0.01). Infiltration of more CD117⁺ MCs was found in tissues from B-cell NHL subjects compared with that of controls. IL-9 level in serum samples from patients with B-cell NHL was higher than that from healthy controls. Addition of rIL-9 to the culture gave rise to increase in the purity of mouse BMMCs in the first three weeks. In vitro culture experiments showed that the addition of IL-9 could induce the differentiation of mouse BMMC and the expressions of MC-related genes, including CD117, Fcer1α, Mcpt1 and Mcpt5.

CONCLUSIONOur study showed that IL-9 promoted immune response mediated by MCs, and probably played important roles in B-NHL growth. Pharmacological or targeted inhibition of mast cells or IL-9 activity may provide new strategy for B-cell NHL therapy.

Animals ; Cells, Cultured ; Humans ; Interleukin-9 ; blood ; Lymphoma, B-Cell ; pathology ; Male ; Mast Cells ; immunology ; Mice

In spontaneous hair loss of C57BL/6N mice model, we investiged the factors related to hair loss by microscopic and immunocytochemical methods. The results were as follows; Microsopic observation of sebaceous gland was developed, and subcutaneous layer was thin in SA and AU group. Number of mast cells in SA and AU group was more increased than that of other groups. Number and immunoreactive density of CD4/CD8 lymphocytes was more increased than that of other groups. Immunoreactivity of substance P and CRF was weakly stained in stem cell region of SA and AU group. Immunoreactivity of CRF-R and CRF-BP was weakly stained in stem cell and bulge regions of SA and AU group. Immunoreactivity of stem cell factor was weakly stained in stem cell, bulge region and dermal papilla of SA and AU group. These experiment suggest that factors related to hair loss in spontaneous hair loss C57BL/6N mice models are increased of mast cell, CD4 and CD8 lymphocytes, and decreased of cytokine and neuropeptide in stem cell, bulge region and dermal papilla.
Animals ; Hair* ; Lymphocytes ; Mast Cells ; Mice* ; Neuropeptides ; Sebaceous Glands ; Stem Cell Factor ; Stem Cells ; Substance P

Ca2+-signals in endothelial cells are determined by release from intracellular stores and entry through the plasma membrane. In this review, the nature of Ca2+ entry and mechanisms of its control are reviewed. The following ion channels play a pivotal role in regulation of the driving force for Ca2+ entry: an inwardly rectifying K+ channel, identified as Kir2.1, a big-conductance, Ca2+-activated K+ channel (hslo) and at least two Cl- channels (a volume regulated Cl- channel, VRAC, and a Ca2+ activated Cl- channel, CaCC). At least two different types of Ca2+-entry channels exist: 1. A typical CRAC-like, highly selective Ca2+ channel is described. Current density for this Ca2+ entry is approximately 0.1 pA/pF at 0 mV and thus 10 times smaller than in Jurkat or mast cells. 2. Another entry pathway for Ca2+ entry is a more non-selective channel, which might be regulated by intracellular Ca2+. Although detected in endothelial cells, the functional role of trp1,3,4 as possible channel proteins is unclear. Expression of trp3 in macrovascular endothelial cells from bovine pulmonary artery induced non-selective cation channels which are probably not store operated or failed to induce any current. Several features as well as a characterisation of Ca2+ -oscillations in endothelial cells is also presented.
Cell Membrane ; Endothelial Cells* ; Endothelium ; Ion Channels* ; Mast Cells ; Potassium Channels ; Pulmonary Artery

BACKGROUND: There has been no general agreement in classifying basal cell carcinoma (BCC), and little is known about the immunohistochemical profiles in each subtypes of BCC. BCC is a locally-invasive tumor, but its aggressive forms tend to recur and metastasize. OBJECTIVE: In this study, we have compared the histolopathological subtypes of BCC by immunohistochemical study. We also focused on identifying representative markers of growth in the aggressive forms of BCC by assessing VEGF, p53 and alpha-SMA expression. METHODS: A total of 87 BCC specimens were collected at the 7 branch hospitals of The Catholic University of Korea from July 1997 to June 2003. For multiple immunohistochemical staining, a tissue microarray technique was used. The 87 samples were divided into 6 subtypes: 18 nodular, 19 nodular infiltrative, 12 micronodular, 14 infiltrative, 11 morphea and 13 basosquamous. Overall, 18 samples were classified as non-aggressive and the remaining 69 as aggressive. RESULTS: The following results were obtained after immunohistochemical staining with antibodies alpha-SMA, VEGF and p53. A significant increase of alpha-SMA expression was observed in aggressive forms of BCC, whereas the expression of p53, VEGF, the number of mast cells remained the same. The representative markers of tumor growth such as alpha-SMA were most highly expressed in the basosquamous type, and least expressed in the micronodular type compared to the nodular type. CONCLUSION: alpha-SMA was considered as an appropriate immunohistochemical marker in BCC to represent aggressiveness.
Antibodies ; Carcinoma, Basal Cell* ; Hospitals, Satellite ; Immunohistochemistry ; Korea ; Mast Cells ; Scleroderma, Localized ; Vascular Endothelial Growth Factor A

My research career has focused on the causes of asthma and its treatment. After establishing the key role that mast cells play in the inflammatory response in asthma, attention was turned towards understanding disease chronicity and variability across the lifecourse. Through a combination of studies on airway biopsies and primary cell cultures we have established that asthma is primarily an epithelial disease driven by increased environmental susceptibility to injury and an altered repair response as depicted by sustained activation of the epithelial mesenchymal trophic unit (EMTU) that is invoked in foetal branching morphogenesis. Varied activation of the EMTU connects the origins of asthma to its progression over time with involvement of epithelial susceptibility through impaired barrier and innate immune functions and altered mesenchymal susceptibility as exemplified by polymorphisms of the metalloprotease gene, ADAM33. Taken together these observations have led to a fundamental re-evaluation of asthma pathogenesis. Rather than placing allergic inflammation as the prime abnormality, it is proposed that the airway epithelium lies at the center of asthma pathogenesis, and that in conjunction with the underlying mesenchyme, it is the principle orchestrator of both the induction of asthma and its evolution over the lifecourse. This concept has provided 'the basis for a new preventative and therapeutic approach focused more on increasing the airways resistance to environmental insults rather than suppressing downstream inflammation once it is established.
Asthma ; Biopsy ; Epithelium ; Humans ; Inflammation ; Mast Cells ; Mesoderm ; Morphogenesis ; Primary Cell Culture

My research career has focused on the causes of asthma and its treatment. After establishing the key role that mast cells play in the inflammatory response in asthma, attention was turned towards understanding disease chronicity and variability across the lifecourse. Through a combination of studies on airway biopsies and primary cell cultures we have established that asthma is primarily an epithelial disease driven by increased environmental susceptibility to injury and an altered repair response as depicted by sustained activation of the epithelial mesenchymal trophic unit (EMTU) that is invoked in foetal branching morphogenesis. Varied activation of the EMTU connects the origins of asthma to its progression over time with involvement of epithelial susceptibility through impaired barrier and innate immune functions and altered mesenchymal susceptibility as exemplified by polymorphisms of the metalloprotease gene, ADAM33. Taken together these observations have led to a fundamental re-evaluation of asthma pathogenesis. Rather than placing allergic inflammation as the prime abnormality, it is proposed that the airway epithelium lies at the center of asthma pathogenesis, and that in conjunction with the underlying mesenchyme, it is the principle orchestrator of both the induction of asthma and its evolution over the lifecourse. This concept has provided 'the basis for a new preventative and therapeutic approach focused more on increasing the airways resistance to environmental insults rather than suppressing downstream inflammation once it is established.
Asthma ; Biopsy ; Epithelium ; Humans ; Inflammation ; Mast Cells ; Mesoderm ; Morphogenesis ; Primary Cell Culture

The potential role of topical valproate (VPA) in hair regrowth has been recently suggested. However, safety reports of VPA as a topical formulation are lacking. Therefore, in the present study, we investigated whether VPA causes skin irritation in humans. We first performed a cell viability test and showed that VPA did not exhibit toxicity toward HaCaT keratinocytes, fibroblasts, and RBL-3H mast cells. We then performed clinical patch test and skin irritation test through transdermal drug delivery with the help of microneedle rollers. No significant findings were obtained in the clinical patch test. In the skin irritation test, only 1 patient showed erythema at 1 hr, but the irritation reaction faded away within a few hours. Erythema and edema were not observed at 24 hr. We concluded that VPA has minimal potential to elicit skin irritation. Therefore, we consider that VPA can safely be applied to human skin.
Cell Survival ; Edema ; Erythema ; Fibroblasts ; Hair ; Humans ; Keratinocytes ; Mast Cells ; Patch Tests ; Skin ; Valproic Acid

BACKGROUND: Allergic disease is an inflammatory disease, whose main inflammatory cells are eosinophils, mast cells, and T lymphocytes. From that point, new therapeutic targets on allergic inflammation focusing on them are under investigation. We extracted four isoflavonoids from Sophorica japonica such as sophi, orobol, genistin, and genistein which has been known as PTK antagonist. We documented those three iso-flavonoids except genistein had an anti-inflammatory effect as potent as dexamethasone on carageen-induced ear model. Also they had antagonism on the Y-16 cell line, whose growth is dependent on IL-5. OBJECTIVES: From above results, in this experiment, we tried to find antagonistic effects of those compounds on IL-5 using the inhibition of eosinophil activation and survival in vitro and possibility of anti-allergic medicine. METHODS: LTC4 by RIA and ECP for degranulation by UniCAP(TM), which had been used previously were activation markers. RESULTS: Among those compounds, sophi was the most potent antagonist on IL-5 induced LTC4 release, degranulation, and survival. Orobol and genistin also had antagonism on them, but genistein, an antagonist of PTK didn't show any antagonistic effects. CONCLUSION: From these results, we concluded those three iso-flavonoids were IL-5 antagonist, and the mechanism of it might not be through PTK signaling.
Cell Line ; Dexamethasone ; Ear ; Eosinophils ; Genistein ; Inflammation ; Interleukin-5* ; Leukotriene C4 ; Mast Cells ; T-Lymphocytes