Cold Urticaria Patients Exhibit Normal Skin Levels of Functional Mast Cells and Histamine after Tolerance Induction

Dermatology ◽  
2012 ◽  
Vol 224 (2) ◽  
pp. 101-105 ◽  
Author(s):  
Line Kring Tannert ◽  
Per Stahl Skov ◽  
Louise Bjerremann Jensen ◽  
Marcus Maurer ◽  
Carsten Bindslev-Jensen
Keyword(s):  
Mast Cells ◽  
Normal Skin ◽  
Tolerance Induction ◽  
Cold Urticaria

Effects of Skin Mast Cells on Bleeding Time and Coagulation Activation at the Site of Platelet Plug Formation

1998 ◽  
Vol 79 (04) ◽  
pp. 843-847 ◽  
Author(s):  
Petteri Kauhanen ◽  
Petri Kovanen ◽  
Timo Reunala ◽  
Riitta Lassila
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Thrombin Generation ◽  
Bleeding Time ◽  
Normal Skin ◽  
Urticaria Pigmentosa ◽  
Primary Hemostasis ◽  
Cell Accumulation ◽  
The Mean ◽  
Cutaneous Mast Cell

SummaryWe studied the effects of stimulated skin mast cells on bleeding time and thrombin generation which was measured using prothrombin fragment F 1+2 (F 1+2) and thrombin-antithrombin-III-complex (TAT). In 10 patients with urticaria pigmentosa (chronic cutaneous mast cell accumulation) the mean bleeding time was significantly prolonged in wounds made on urticaria pigmentosa lesions vs. normal skin (460 ± 34 vs. 342 ± 27 s, p = 0.005). In 10 atopic subjects skin incisions were made on prick-tested sites 30, 60, 120 and 240 min after administration of an allergen (acute mast cell stimulation), histamine or vehicle. The mean bleeding time was significantly prolonged at all time points, being maximal at 120 min (60% prolonged) in wounds made on allergen-stimulated skin areas (p <0.01) compared with histamine or vehicle sites. Administration of allergen or histamine lowered the TAT concentration in the bleeding-time blood. Furthermore, TAT and F 1+2 levels in the bleeding-time blood were lower at 60, 120 and 240 min after allergen or histamine application in comparison with samples collected at 30 min. We conclude that skin mast cells can regulate primary hemostasis by prolonging bleeding time and by inhibiting thrombin generation.

Mast Cells in Hemangiomas and Vascular Malformations

PEDIATRICS ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 48-51
Author(s):  
Julie Glowacki ◽  
John B. Mulliken
Keyword(s):  
Mast Cells ◽  
High Power ◽  
Vascular Malformations ◽  
Normal Skin ◽  
High Power Field ◽  
Proliferative Phase ◽  
Large Numbers ◽  
Endothelial Proliferation ◽  
Vascular Birthmarks

Common pediatric vascular birthmarks, classified as hemangiomas or malformations, were analyzed for the presence of mast cells. Hemangiomas in the proliferative phase contained large numbers of mast cells (27 ± 15 cells/high-power field [HPF]) in comparison with hemangiomas in the involuting phase (2.6 ± 2.9), vascular malformations (1.7 ± 3.2), and normal skin (5.0 ± 1.0). Inasmuch as hemangiomas are characterized by endothelial proliferation and increased numbers of mast cells, these data raise the possibility that mast cells may have an important role in the formation and/or maintenance of these lesions.

Human cutaneous mast cells–a study of fixative and staining reactions in normal skin

1989 ◽  
Vol 120 (5) ◽  
pp. 625-631 ◽  
Author(s):  
A.C. MARKEY ◽  
LINDA J. CHURCHILL ◽  
D.M. MACDONALD
Keyword(s):  
Mast Cells ◽  
Normal Skin

scholarly journals Development of large numbers of mast cells at sites of idiopathic chronic dermatitis in genetically mast cell-deficient WBB6F1-W/Wv mice

Blood ◽  
1987 ◽  
Vol 69 (6) ◽  
pp. 1661-1666 ◽  
Author(s):  
SJ Galli ◽  
N Arizono ◽  
T Murakami ◽  
AM Dvorak ◽  
JG Fox
Keyword(s):  
Mast Cell ◽  
Cell Differentiation ◽  
Mast Cells ◽  
Peritoneal Cavity ◽  
Local Development ◽  
Normal Skin ◽  
Large Numbers ◽  
And Function

Abstract The normal skin and other tissues of adult mast cell-deficient WBB6F1- W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. As a result, genetically mast cell-deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice are widely used for studies of mast cell differentiation and function. We found that mast cells developed at sites of idiopathic chronic dermatitis in WBB6F1-W/Wv mice and that the number of mast cells present in the skin of WBB6F1-W/Wv mice was proportional to the severity of the dermatitis (in ear skin, there were 33 +/- 4 mast cells/mm2 of dermis at sites of severe dermatitis v 9 +/- 3 at sites of mild dermatitis, 0.8 +/- 0.3 in skin without dermatitis, and 100 +/- 7 in the normal skin of congenic WBB6F1-+/+ mice; in back skin, the corresponding values were 2.0 +/- 0.6, 1.1 +/- 0.9, 0.025 +/- 0.025, and 26.2 +/- 3.2). The development of mast cells was a local, not systemic, consequence of the dermatitis. Thus, WBB6F1-W/Wv mice with severe dermatitis lacked mast cells in skin not showing signs of dermatitis and also in the peritoneal cavity, stomach, cecum, and tongue. Idiopathic chronic dermatitis was not associated with the local development of mast cells in WCB6F1-Sl/Sld mice, a mutant whose mast cell deficiency is due to a mechanism distinct from that of WBB6F1-W/Wv mice. These findings may have implications for understanding the nature of the mast cell deficiency in WBB6F1-W/Wv and WCB6F1-Sl/Sld mice and for the use of these mutants to analyze mast cell differentiation and function.

scholarly journals Activated Protein C Protects against Murine Contact Dermatitis by Suppressing Protease-Activated Receptor 2

2022 ◽  
Vol 23 (1) ◽  
pp. 516
Author(s):  
Meilang Xue ◽  
Haiyan Lin ◽  
Ruilong Zhao ◽  
Callum Fryer ◽  
Lyn March ◽  
...  
Keyword(s):  
Mast Cells ◽  
Barrier Function ◽  
Protein C ◽  
Normal Skin ◽  
Activated Protein C ◽  
Contact Hypersensitivity ◽  
Skin Barrier Function ◽  
Lower Survival Rate ◽  
Therapeutic Benefits

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with excessive inflammation and defective skin barrier function. Activated protein C (APC) is a natural anticoagulant with anti-inflammatory and barrier protective functions. However, the effect of APC on AD and its engagement with protease activated receptor (PAR)1 and PAR2 are unknown. Methods: Contact hypersensitivity (CHS), a model for human AD, was induced in PAR1 knockout (KO), PAR2KO and matched wild type (WT) mice using 2,4-dinitrofluorobenzene (DNFB). Recombinant human APC was administered into these mice as preventative or therapeutic treatment. The effect of APC and PAR1KO or PARKO on CHS was assessed via measurement of ear thickness, skin histologic changes, inflammatory cytokine levels, Th cell phenotypes and keratinocyte function. Results: Compared to WT, PAR2KO but not PAR1KO mice displayed less severe CHS when assessed by ear thickness; PAR1KO CHS skin had less mast cells, lower levels of IFN-γ, IL-4, IL-17 and IL-22, and higher levels of IL-1β, IL-6 and TGF-β1, whereas PAR2KO CHS skin only contained lower levels of IL-22 and IgE. Both PAR1KO and PAR2KO spleen cells had less Th1/Th17/Th22/Treg cells. In normal skin, PAR1 was present at the stratum granulosum and spinosum, whereas PAR2 at the upper layers of the epidermis. In CHS, however, the expression of PAR1 and PAR2 were increased and spread to the whole epidermis. In vitro, compared to WT cells, PAR1KO keratinocytes grew much slower, had a lower survival rate and higher para permeability, while PAR2KO cells grew faster, were resistant to apoptosis and para permeability. APC inhibited CHS as a therapeutic but not as a preventative treatment only in WT and PAR1KO mice. APC therapy reduced skin inflammation, suppressed epidermal PAR2 expression, promoted keratinocyte growth, survival, and barrier function in both WT and PAR1KO cells, but not in PAR2KO cells. Conclusions: APC therapy can mitigate CHS. Although APC acts through both PAR1 and PAR2 to regulate Th and mast cells, suppression of clinical disease in mice is achieved mainly via inhibition of PAR2 alone. Thus, APC may confer broad therapeutic benefits as a disease-modifying treatment for AD.

scholarly journals Phorbol 12-myristate 13-acetate-induced development of functionally active mast cells in W/Wv but not Sl/Sld genetically mast cell- deficient mice

Blood ◽  
1990 ◽  
Vol 75 (8) ◽  
pp. 1637-1645
Author(s):  
JR Gordon ◽  
SJ Galli
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Normal Skin ◽  
Systemic Effect ◽  
Detectable Effect ◽  
Heparin Binding ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Deficient Mice ◽  
Convenient Model

The normal skin and other tissues of adult genetically mast cell- deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. We previously reported that mature dermal mast cells developed locally in the skin of W/Wv, but not Sl/Sld, mice at sites of chronic idiopathic dermatitis. We now report that the repeated application of phorbol 12-myristate 13-acetate (PMA) to the ear skin of either W/Wv or +/+ mice induces both dermatitis and a striking and dose-dependent increase in the number of dermal mast cells. The number of dermal mast cells at sites treated for 6 weeks with 5 micrograms PMA, three times per week, was 39 +/- 7/mm2 and 305 +/- 34/mm2 for W/Wv and +/+ mice, respectively; the corresponding values for vehicle-treated skin were 1.5 +/- 1.0/mm2 and 145 +/- 8/mm2, respectively. The PMA-induced dermal mast cells in W/Wv mice appeared mature by morphology, stained with the heparin-binding fluorescent dye, berberine sulfate, and were competent to express IgE-dependent passive cutaneous anaphylaxis responses. The development of mast cells was a local, not systemic, effect of PMA treatment. PMA treatment also induced dermatitis in both WCB6F1-Sl/Sld and +/+ mice, but was associated with increased numbers of dermal mast cells only in the WCB6F1(-)+/+ mice. PMA treatment had no detectable effect on the ability of bone marrow-derived cultured mast cells to survive in the skin of Sl/Sld mice. These findings establish a convenient model system for analyzing factors associated with the development of endogenous populations of mast cells in genetically mast cell-deficient W/Wv mice.

scholarly journals Phorbol 12-myristate 13-acetate-induced development of functionally active mast cells in W/Wv but not Sl/Sld genetically mast cell- deficient mice

Blood ◽  
1990 ◽  
Vol 75 (8) ◽  
pp. 1637-1645 ◽  
Author(s):  
JR Gordon ◽  
SJ Galli
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Normal Skin ◽  
Systemic Effect ◽  
Detectable Effect ◽  
Heparin Binding ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Deficient Mice ◽  
Convenient Model

Abstract The normal skin and other tissues of adult genetically mast cell- deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. We previously reported that mature dermal mast cells developed locally in the skin of W/Wv, but not Sl/Sld, mice at sites of chronic idiopathic dermatitis. We now report that the repeated application of phorbol 12-myristate 13-acetate (PMA) to the ear skin of either W/Wv or +/+ mice induces both dermatitis and a striking and dose-dependent increase in the number of dermal mast cells. The number of dermal mast cells at sites treated for 6 weeks with 5 micrograms PMA, three times per week, was 39 +/- 7/mm2 and 305 +/- 34/mm2 for W/Wv and +/+ mice, respectively; the corresponding values for vehicle-treated skin were 1.5 +/- 1.0/mm2 and 145 +/- 8/mm2, respectively. The PMA-induced dermal mast cells in W/Wv mice appeared mature by morphology, stained with the heparin-binding fluorescent dye, berberine sulfate, and were competent to express IgE-dependent passive cutaneous anaphylaxis responses. The development of mast cells was a local, not systemic, effect of PMA treatment. PMA treatment also induced dermatitis in both WCB6F1-Sl/Sld and +/+ mice, but was associated with increased numbers of dermal mast cells only in the WCB6F1(-)+/+ mice. PMA treatment had no detectable effect on the ability of bone marrow-derived cultured mast cells to survive in the skin of Sl/Sld mice. These findings establish a convenient model system for analyzing factors associated with the development of endogenous populations of mast cells in genetically mast cell-deficient W/Wv mice.

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