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• W2014286054 abstract "Mast cells and their mediator, histamine, are well-recognized effectors in immediate allergy, but their role in tissue remodeling and chronic inflammation has also been the focus of intense research during the past decade. Gschwandtner et al. (2008, this issue) report that histamine can induce MMP-9 expression in keratinocytes, promote collagen type IV degradation in the basement membrane, and stimulate keratinocytes, leading to increased T-cell transmigration through an artificial basement membrane. Mast cells and their mediator, histamine, are well-recognized effectors in immediate allergy, but their role in tissue remodeling and chronic inflammation has also been the focus of intense research during the past decade. Gschwandtner et al. (2008, this issue) report that histamine can induce MMP-9 expression in keratinocytes, promote collagen type IV degradation in the basement membrane, and stimulate keratinocytes, leading to increased T-cell transmigration through an artificial basement membrane. Mast cells are strategically located in the upper dermis of normal skin, where host tissue is exposed to external antigens and microbes. For many years, mast cells and especially their well-known mediator, histamine, have been known to be effectors of immediate allergy, but during the past decade numerous reports have shown that mast cells are intimately involved in the innate and acquired immune system (reviewed in Harvima et al., 2008Harvima I.T. Nilsson G. Suttle M.-M. Naukkarinen A. Is there a role for mast cells in psoriasis?.Arch Dermatol Res. 2008; 300: 461-478Crossref PubMed Scopus (93) Google Scholar). Upon activation by a range of different stimuli, mast cells can produce, store, and release mediators that can affect the immune system and promote inflammation. These mediators can be divided into preformed and newly synthesized mediators. Preformed mediators stored in the secretory granules include histamine, tryptase, chymase, carboxypeptidase, a cathepsin G-like proteinase, proteoglycans, acidic hydrolases, and various cytokines and growth factors. Newly synthesized mediators include prostaglandin D2, leukotriene C4, and varying amounts of other lipid-derived mediators. Mast cells can be induced to synthesize de novo a range of cytokines, chemokines, growth factors, and cell membrane molecules, all of which are crucial in inflammatory reactions (Harvima et al., 2008Harvima I.T. Nilsson G. Suttle M.-M. Naukkarinen A. Is there a role for mast cells in psoriasis?.Arch Dermatol Res. 2008; 300: 461-478Crossref PubMed Scopus (93) Google Scholar). Although mast cells can only rarely be seen in close association with the epidermis in healthy skin, soluble mediators (e.g., histamine and tryptase), stored in large quantities in mast cell secretory granules, can diffuse through the dermal matrix and reach the basement membrane zone and basal keratinocytes. Furthermore, the number of mast cells increases markedly in the upper dermal skin and becomes closely associated with the epidermis in skin diseases that are characterized by chronic inflammation and epidermal hyperplasia, such as psoriasis, chronic leg ulcers, pseudoepitheliomatous diseases, and epithelial skin cancers (Harvima et al., 2008Harvima I.T. Nilsson G. Suttle M.-M. Naukkarinen A. Is there a role for mast cells in psoriasis?.Arch Dermatol Res. 2008; 300: 461-478Crossref PubMed Scopus (93) Google Scholar). These morphological findings further support the hypothesis that mast cells communicate with the epidermis in chronic skin inflammation. A central role for histamine in the symptoms of immediate allergy is largely accepted. However, the immunomodulatory function of histamine is clearly less recognized. Histamine has previously been reported to affect dendritic cell maturation and activation. For example, histamine receptor H1 and H3 stimulation of dendritic cells results in proinflammatory cytokine production, T helper 1 priming, and increased antigen-presenting activity, whereas H2 stimulation leads to IL-10 induction and T helper 2 or tolerance priming (reviewed by Akdis and Blaser, 2003Akdis C.A. Blaser K. Histamine in the immune regulation of allergic inflammation.J Allergy Clin Immunol. 2003; 112: 15-22Abstract Full Text Full Text PDF PubMed Scopus (181) Google Scholar). Histamine has also been reported to stimulate human keratinocytes through the H1 receptor for increased expression of IL-6, IL-8, GM-CSF, tumor necrosis factor (TNF)-α, ICAM-1, and different matrix metalloproteinases (MMP-1, MMP-3, MMP-9, and MMP-13), and histamine can even augment TNF-α-induced GM-CSF, IL-8, and IL-6 expression (Matsubara et al., 2005Matsubara M. Tamura T. Ohmori K. Hasegawa K. Histamine H1 receptor antagonist blocks histamine-induced proinflammatory cytokine production through inhibition of Ca2+-dependent protein kinase C, Raf/MEK/ERK and IKK/IκB/NF-κB signal cascades.Biochem Pharmacol. 2005; 69: 433-449Crossref PubMed Scopus (106) Google Scholar). Furthermore, histamine can augment, through the H1 receptor, IFN-γ-induced expression of major histocompatibility complex class I, ICAM-1, GM-CSF, CCL-5/RANTES, CCL-2/MCP-1, CCL-20/MIP-3α, and CXCL-10/IP-10 in human keratinocytes (Giustizieri et al., 2004Giustizieri M.L. Albanesi C. Fluhr J. Gisondi P. Norgauer J. Girolomoni G. H1 histamine receptor mediates inflammatory responses in human keratinocytes.J Allergy Clin Immunol. 2004; 114: 1176-1182Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar). On the other hand, histamine has been thought to control the growth of the epidermis, because histamine can inhibit the growth of monolayer keratinocytes and keratinocyte epithelium, and this effect is potentiated even to cytolysis when histamine affects keratinocytes together with TNF-α (Diaconu et al., 2008Diaconu N.-C. Rummukainen J. Mättö M. Naukkarinen A. Harvima R.J. Pelkonen J. et al.Cervical squamous carcinoma cells are resistant to the combined action of tumor necrosis factor-α and histamine whereas normal keratinocytes undergo cytolysis.BMC Cancer. 2008; 8: 46Crossref PubMed Scopus (5) Google Scholar). Histamine induces MMP-9 in keratinocytes. Histamine induces MMP-9 in keratinocytes. MMP-9 is an interesting enzyme in skin pathology. Its main function is thought to be the regulation of cell-matrix composition, and the enzyme cleaves gelatin, collagen type IV, fibronectin, elastin, laminin, and several other protein substrates (Ram et al., 2006Ram M. Sherer Y. Shoenfeld Y. Matrix metalloproteinase-9 and autoimmune diseases.J Clin Immunol. 2006; 26: 299-307Crossref PubMed Scopus (204) Google Scholar). Hence, the cleavage of the components in the basement membrane allows cells of the immune system, such as T cells, to transmigrate across the vascular basement membrane or enter the epidermal compartment in skin inflammation. MMP-9 has been associated with a range of pathologic processes, such as autoimmune diseases and psoriasis (Ram et al., 2006Ram M. Sherer Y. Shoenfeld Y. Matrix metalloproteinase-9 and autoimmune diseases.J Clin Immunol. 2006; 26: 299-307Crossref PubMed Scopus (204) Google Scholar; Cordiali-Fei et al., 2006Cordiali-Fei P. Trento E. D’Agosto G. Bordignon V. Mussi A. Ardig M. et al.Decreased levels of metalloproteinase-9 and angiogenic factors in skin lesions of patients with psoriatic arthritis after therapy with anti-TNF-α.J Autoimmune Dis. 2006; 3: 5Crossref PubMed Scopus (41) Google Scholar), and anti-TNF-α therapy with infliximab has been found to decrease the expression of MMP-9 in psoriatic lesions (Cordiali-Fei et al., 2006Cordiali-Fei P. Trento E. D’Agosto G. Bordignon V. Mussi A. Ardig M. et al.Decreased levels of metalloproteinase-9 and angiogenic factors in skin lesions of patients with psoriatic arthritis after therapy with anti-TNF-α.J Autoimmune Dis. 2006; 3: 5Crossref PubMed Scopus (41) Google Scholar). In addition to several other cell types, mast cells have been shown to produce MMP-9. Furthermore, incubation of human mast cells with cell membranes isolated from activated T cells leads to MMP-9 expression and release in vitro, an effect that appears to be dependent on mast cell–derived TNF-α and cell–cell contact (Baram et al., 2001Baram D. Vaday G.G. Salamon P. Drucker I. Hershkoviz R. Mekori Y.A. Human mast cells release metalloproteinase-9 on contact with activated T cells: juxtacrine regulation by TNF-α.J Immunol. 2001; 167: 4008-4016Crossref PubMed Scopus (186) Google Scholar). In addition to TNF-α, mast cells can express CD30 ligand, OX40 ligand, and ICAM-1, which can interact with their respective receptors, CD30, OX40, and LFA-1, respectively, on T cells (Harvima et al., 2008Harvima I.T. Nilsson G. Suttle M.-M. Naukkarinen A. Is there a role for mast cells in psoriasis?.Arch Dermatol Res. 2008; 300: 461-478Crossref PubMed Scopus (93) Google Scholar). It therefore seems plausible that mast cells, T cells, and keratinocytes are all in close relationship with one another in the uppermost dermis of inflamed skin (Figure 1). It was previously demonstrated that MMP-9 production can be induced in keratinocytes by TNF-α and transforming growth factor (TGF)-β, and a combination of both factors gives rise to a synergistic induction of MMP-9 in keratinocytes and fibroblasts (Han et al., 2001Han Y.-P. Tuan T.-L. Hughes M. Wu H. Garner W.L. Transforming growth factor-β- and tumor necrosis factor-α-mediated induction and proteolytic activation of MMP-9 in human skin.J Biol Chem. 2001; 276: 22341-22350Crossref PubMed Scopus (139) Google Scholar). Preliminary results by Matsubara et al. (Matsubara et al., 2005Matsubara M. Tamura T. Ohmori K. Hasegawa K. Histamine H1 receptor antagonist blocks histamine-induced proinflammatory cytokine production through inhibition of Ca2+-dependent protein kinase C, Raf/MEK/ERK and IKK/IκB/NF-κB signal cascades.Biochem Pharmacol. 2005; 69: 433-449Crossref PubMed Scopus (106) Google Scholar) have shown that histamine can also induce MMPs in keratinocytes, including MMP-9. Gschwandtner et al. (Gschwandtner et al., 2008Gschwandtner M. Purwar R. Wittmann M. Bäumer W. Kietzmann M. Werfel T. et al.Histamine upregulates keratinocyte MMP-9 production via the histamine H1 receptor.J Invest Dermatol. 2008; 128: 2783-2791Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar, this issue) have considerably expanded on the previous preliminary findings on histamine-induced MMP-9 expression in human keratinocytes. The authors demonstrate comprehensively that histamine, or the H1 receptor agonist β-histine, can stimulate, in a dose- and time-dependent manner, cultured human keratinocytes to express MMP-9 mRNA, immunoreactive protein (MMP-9/TIMP-1 complex), and gelatinolytic activity. Ten micrometers of histamine produced maximal stimulation, and this concentration is relevant and achievable in the pericellular microenvironment in vivo because histamine concentrations in mast cell secretory granules approximate 100 mM. The stimulatory effect is mediated via the H1 receptor, a conclusion that is supported by the results obtained with the agonists or antagonists of three other histamine receptors and experiments with the H1 inverse agonist clemastine or levocetirizine. Interestingly, the authors found that the combination of 10 μM histamine and 1 ng ml−1 TGF-β resulted in an additive effect on MMP-9/TIMP-1 production. This result thus further extends the previous findings about histamine–TNF-α and histamine–IFN-γ combinations in keratinocyte stimulation (Matsubara et al., 2005Matsubara M. Tamura T. Ohmori K. Hasegawa K. Histamine H1 receptor antagonist blocks histamine-induced proinflammatory cytokine production through inhibition of Ca2+-dependent protein kinase C, Raf/MEK/ERK and IKK/IκB/NF-κB signal cascades.Biochem Pharmacol. 2005; 69: 433-449Crossref PubMed Scopus (106) Google Scholar; Giustizieri et al., 2004Giustizieri M.L. Albanesi C. Fluhr J. Gisondi P. Norgauer J. Girolomoni G. H1 histamine receptor mediates inflammatory responses in human keratinocytes.J Allergy Clin Immunol. 2004; 114: 1176-1182Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar; Diaconu et al., 2008Diaconu N.-C. Rummukainen J. Mättö M. Naukkarinen A. Harvima R.J. Pelkonen J. et al.Cervical squamous carcinoma cells are resistant to the combined action of tumor necrosis factor-α and histamine whereas normal keratinocytes undergo cytolysis.BMC Cancer. 2008; 8: 46Crossref PubMed Scopus (5) Google Scholar). In the ex vivo experiments in skin biopsies, the authors demonstrated further that exogenously added 10 μM histamine induced MMP-9 in skin biopsies after incubation for 16 h, as detected with zymography of the extracted protein. Moreover, the effect of endogenous histamine was also investigated. In these experiments, the authors incubated skin biopsies with the mast cell degranulator, compound 48/80, with or without a 30-min pretreatment with clemastine. Again, MMP-9 was induced in the skin biopsies, and the effect was abolished with the clemastine pretreatment. Immunohistochemical studies also confirmed that MMP-9 immunoreactivity was increased in the epidermis as a result of 10 μM histamine stimulation for 16 h. Further, simultaneous with increased MMP-9, the immunoreactivity of collagen type IV was decreased in the basement membrane zone, and this effect by histamine was reversed by the addition of the MMP inhibitor GM6001 to the incubation mixture. Finally, the authors examined whether histamine-induced changes in keratinocytes could lead to increased transmigration of T cells through an artificial basement membrane using Matrigel transwells. In these experiments the investigators treated keratinocytes adhered to Matrigel with 10 μM histamine for 30 h in the presence or absence of galardin, a broad-spectrum MMP inhibitor. Thereafter, Jurkat T cells or freshly isolated CD4-positive T cells were added to the transwell for 16 h, and chemoattractants were added to the lower chamber. As expected, the histamine treatment led to increased T-cell transmigration, and this effect was inhibited by galardin, suggesting MMP involvement. The same authors recently published a study in which they demonstrated that IL-13, another mediator derived from mast cells and T helper 2 cells, can also induce MMP-9 in keratinocytes, promote collagen type IV degradation, and increase T-cell transmigration through Matrigel. However, neither additive nor synergistic MMP-9 expression could be detected when IL-13 acted together with TGF-β or TNF-α (Purwar et al., 2008Purwar R. Kraus M. Werfel T. Wittmann M. Modulation of keratinocyte-derived MMP-9 by IL-13: a possible role for the pathogenesis of epidermal inflammation.J Invest Dermatol. 2008; 128: 59-66Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar). The present study provides interesting insights into the role of histamine in skin inflammation and epidermal pathology. In fact, a variety of mast cell mediators, including histamine, IL-13, TNF-α, and TGF-β, can evidently stimulate keratinocytes for MMP-9 expression (Figure 1). Furthermore, different combinations of these mediators can even lead to enhanced proteinase expression. Nevertheless, it must be clarified whether this histamine-induced MMP-9 expression, and possibly also induction of other MMPs, together with subsequent basement membrane degradation and T-cell transmigration to the epidermis, actually take place in vivo in pathologic processes, such as psoriasis, eczema, or skin blistering, with resultant epidermal inflammation. It is noteworthy that histamine can also simultaneously induce numerous other molecules in keratinocytes and that these molecules can also impact immunopathogenesis. Because histamine can act together with TNF-α, IFN-γ, and TGF-β, leading to an enhanced biological effect, it is tempting to speculate that antihistamines might enhance the therapeutic effects of TNF-α-blocking drugs (Cordiali-Fei et al., 2006Cordiali-Fei P. Trento E. D’Agosto G. Bordignon V. Mussi A. Ardig M. et al.Decreased levels of metalloproteinase-9 and angiogenic factors in skin lesions of patients with psoriatic arthritis after therapy with anti-TNF-α.J Autoimmune Dis. 2006; 3: 5Crossref PubMed Scopus (41) Google Scholar). The author states no conflict of interest. The author thanks the Marie Curie EST Program within the 6th Framework Program of the European Commission, project 504926, “Mast Cells and Chronic Inflammatory Disease.” Marjukka Aronen is thanked for preparing the artwork." @default.
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• W2014286054 title "Induction of Matrix Metalloproteinase-9 in Keratinocytes by Histamine" @default.
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