Tumour necrosis factor stimulates human skin mast cells to release histamine and tryptase

Overveld, F. J. van; Jorens, P. G.; Rampart, M.; Backer, Wilfried De; Vermeire, P.

doi:10.1111/j.1365-2222.1991.tb03200.x

Cited by 69 publications

(30 citation statements)

References 12 publications

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“…Significant levels of TNF-a have been measured in blister fluids of patients with pemphigoid or toxic epidermal necrolysis [Paquet and Pierard, 1998;Rhodes et al, 1999]. It is noteworthy that TNF-a itself can induce mast cell activation and mediator release [Overveld van et al, 1991], and TNF-a production can be induced in keratinocytes themselves [Luger and Schwarz, 1990]. Therefore, heparin derived from mast cells may interact with TNF-a derived not only from mast cells but also from keratinocytes or other cells.…”

Section: Discussionmentioning

confidence: 96%

Heparin modulates the growth and adherence and augments the growth‐inhibitory action of TNF‐α on cultured human keratinocytes

Harvima

Lappalainen

Hirvonen³

et al. 2004

J of Cellular Biochemistry

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Previous works suggest the involvement of mast cells in the epithelialization of chronic wounds. Since heparin is a major mediator stored in the secretory granules of mast cells, the purpose of this work was to elucidate the function of heparin in epithelialization using in vitro culture models. For this, low- and high-calcium media in monolayer and epithelium cultures of keratinocytes were used. Also, an assay based on keratinocyte adherence onto plastic surface was used as well. Heparin (0.02-200 microg/ml) inhibited keratinocyte growth in a non-cytotoxic and dose-dependent manner in low- and high-calcium media, Keratinocyte-SFM and DMEM, in the absence of growth factors and serum. Also, heparin inhibited the growth of keratinocyte epithelium in the presence of 10% fetal calf serum and DMEM. Instead, in the presence of Keratinocyte-SFM and growth factors, heparin at 2 microg/ml inhibited the growth by 18% but at higher heparin concentrations the inhibition was reversed to baseline. TNF-alpha is another preformed mediator in mast cell granules and it inhibited keratinocyte growth in monolayer and epithelium cultures. Interestingly, heparin at 2-20 microg/ml augmented or even potentiated this growth-inhibitory effect of TNF-alpha. The association of TNF-alpha with heparin was shown by demonstrating that TNF-alpha bound tightly to heparin-Sepharose chromatographic material. However, heparin could not augment TNF-alpha-induced cell cycle arrest at G0/G1 phase or intercellular adhesion molecule-1 expression in keratinocytes. In the cell adherence assay, heparin at 2 microg/ml inhibited significantly by 12-13% or 33% the adherence of keratinocytes onto the plastic surface coated with fibronectin or collagen, respectively, but this inhibition was reversed back to baseline at 20 or 200 microg/ml heparin. Also, heparin affected the cell membrane rather than the protein coat on the plastic surface. In conclusion, heparin not only inhibits or modulates keratinocyte growth and adherence but it also binds and potentiates the growth-inhibitory function of TNF-alpha.

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Section: Discussionmentioning

confidence: 96%

Heparin modulates the growth and adherence and augments the growth‐inhibitory action of TNF‐α on cultured human keratinocytes

Harvima

Lappalainen

Hirvonen³

et al. 2004

J of Cellular Biochemistry

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“…The ability of these receptors to transduce signals is dependent upon the recruitment of TNFR-associated factors (30) which initiate a number of downstream events, including the activation of NF-B-inducing kinases (31,32). TNF-␣ has been reported to induce histamine release from human skin mast cells (33,34) and to enhance IgE-dependent histamine release from sensitized lung mast cells (35). Furthermore, the sustained release of preformed and newly synthesized TNF-␣ following appropriate stimulation represents a mechanism by which mast cell-derived TNF-␣ can exert its actions on leukocyte migration and activation and the initiation of late-phase allergic inflammation.…”

Section: Discussionmentioning

confidence: 99%

NF-κB and TNF-α: A Positive Autocrine Loop in Human Lung Mast Cells?

Coward

Okayama

Sagara

et al. 2002

The Journal of Immunology

123

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The generation of cytokines, particularly TNF-α, by mast cells is crucial for the initiation of the allergic response. A key transcription factor involved in the synthesis of TNF-α is NF-κB. Using a mAb specific for the activated form of NF-κB, immunocytochemistry, confocal microscopy, and gel shift assays have been used in conjunction to localize this transcription factor to human lung mast cells and to study its activation. Activation of mast cells with stem cell factor (10 ng/ml) and anti-IgE (1 μg/ml) induced maximal activation of NF-κB at 4 and 2 h, respectively. In contrast, with TNF-α (5 ng/ml) maximal activation occurred within 15 min. Parallel falls in IκB were demonstrated. Confocal microscopy demonstrated the localization of the activated form of NF-κB to the nuclei of activated mast cells. NF-κB activation was verified using a gel shift assay. A supershift assay showed mast cell NF-κB to be composed primarily of p50 with smaller amounts of p65. No interaction with Abs for Rel-A, c-Rel, Rel-B, and p52 was seen. Immunocytochemistry and ELISAs showed TNF-α to be stored within mast cells and released into the extracellular environment following activation. The possible participation of TNF-α generated by mast cells in NF-κB activation by anti-IgE was investigated using a blocking Ab for TNF-α. The blocking Ab reduced NF-κB activation by anti-IgE by >50%, suggesting that the release of preformed mast cell-associated TNF-α acts as a positive autocrine feedback signal to augment NF-κB activation and production of further cytokine, including GM-CSF and IL-8.

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“…Recently, mast cells have been reported to express a range of toll-like receptors which can be activated by microbial products [29]. Mast cells can also be activated for mediator release by numerous endogenous peptides and proteins, including complement products C3a and C5a [38], neuropeptides, such as substance P (SP) and vasoactive intestinal peptide (VIP) [23], stem cell factor (SCF) [35], tumor necrosis factor (TNF) [192], tryptase [122], and -melanocyte-stimulating hormone [56]. Corticotropin-releasing hormone has been found to induce selective release of vascular endothelial growth factor (VEGF) from human mast cells [17], a factor which is essentially involved in angiogenesis and capillary growth.…”

Section: Introductionmentioning

confidence: 99%

Is there a role for mast cells in psoriasis?

et al. 2008

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Mast cells have traditionally been considered as eVector cells in allergy but during the last decade it has been realized that mast cells are essentially involved in the mechanisms of innate and acquired immunity. Upon activation by anaphylactic, piecemeal degranulation or degranulation-independent mechanisms mast cells can secrete rapidly or slowly a number of soluble mediators, such as serine proteinases, histamine, lipid-derived mediators, cytokines, chemokines and growth factors. Mast cells can express cell surface co-stimulatory receptors and ligands, and they can express MHC class II molecules and thereby present antigens. These soluble factors and cell surface molecules can interact with other cells, such as endothelial cells, keratinocytes, sensory nerves, neutrophils, T cell subsets and antigen presenting cells which are essential eVectors in the development of skin inXammation. Besides promoting inXammation, mast cells may attempt in some circumstances to suppress the inXammation and epidermal growth but the regulation between suppressive and proinXammatory mechanisms is unclear. Psoriasis is characterized by epidermal hyperplasia and chronic inXammation where tryptase-and chymase-positive MC TC mast cells are activated early in the developing lesion and later the cells increase in number in the upper dermis with concomitant expression of cytokines and TNF superfamily ligands as well as increased contacts with neuropeptide-containing sensory nerves. Due to the intimate involvement of mast cells in immunity and chronic inXammation the role of mast cells in psoriasis is discussed in this review.

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Tumour necrosis factor stimulates human skin mast cells to release histamine and tryptase

Cited by 69 publications

References 12 publications

Heparin modulates the growth and adherence and augments the growth‐inhibitory action of TNF‐α on cultured human keratinocytes

Heparin modulates the growth and adherence and augments the growth‐inhibitory action of TNF‐α on cultured human keratinocytes

NF-κB and TNF-α: A Positive Autocrine Loop in Human Lung Mast Cells?

Is there a role for mast cells in psoriasis?

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