Suction Blister Device for Separation of Viable Epidermis from Dermis*

Kiistala, U

doi:10.1038/jid.1968.15

Cited by 434 publications

(227 citation statements)

References 8 publications

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“…A number of other models of aseptic inflammation in humans have been developed, including: 'skin windows', involving removal of the stratum corneum by a blade [28], drill [29], or by tape stripping [30]; suction blisters [31]; and blisters induced by cantharidin [32]. In addition, some of these techniques have involved the collection of recruited cells in a chamber containing a chemoattractant [29,31,33]. The method we used here, involving abrasion of the skin with sand paper, is similar to the other 'skin window' models, but with the benefit that it is simple and easy to perform and contains fewer contaminating erythrocytes [29].…”

Section: Discussionmentioning

confidence: 99%

“…[32]. In addition, some of these techniques have involved the collection of recruited cells in a chamber containing a chemoattractant [29,31,33]. The method we used here, involving abrasion of the skin with sand paper, is similar to the other 'skin window' models, but with the benefit that it is simple and easy to perform and contains fewer contaminating erythrocytes [29].…”

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confidence: 99%

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Human MICL (CLEC12A) is differentially glycosylated and is down‐regulated following cellular activation

Willment¹,

Pyż²,

Dennehy³

et al. 2006

Eur J Immunol

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C-type lectins are the most diverse and prevalent lectin family in immunity. Particular interest has recently been attracted by the C-type lectin-like receptors on NK cells, which appear to regulate the activation/inhibitory balance of these cells, controlling cytotoxicity and cytokine production. We previously identified a human C-type lectin-like receptor, closely related to both the beta-glucan receptor and the lectin-like receptor for oxidized-LDL, named MICL (myeloid inhibitory C-type lectin-like receptor), which we had shown using chimeric analysis to function as an inhibitory receptor. Using a novel MICL-specific monoclonal antibody, we show here that human MICL is expressed primarily on myeloid cells, including granulocytes, monocytes, macrophages, and dendritic cells. Although MICL was highly N-glycosylated in primary cells, the level of glycosylation was found to vary between cell types. MICL surface expression was down-regulated during inflammatory/activation conditions in vitro, as well as during an in vivo model of acute inflammation, which we characterize here. This suggests that human MICL may be involved in the control of myeloid cell activation during inflammation. IntroductionIn order to execute their immune (and non-immune) functions, leukocytes must interact with a broad range of endogenous and exogenous ligands and must be able to respond to these interactions appropriately. This requires a wide and flexible, yet specific and regulated, repertoire of cell surface molecules. One large family of such molecules, which are particularly important to immunity, are the C-type lectin and lectin-like receptors. C-type lectin-like receptors were first identified as dimeric molecules on NK cells. On these cells, much attention has been drawn toward their ability to regulate the balance between cellular activation and inhibition, such as cytotoxicity and cytokine production. This is achieved through signalling via intracellular ITIM present in the cytoplasmic tails of these receptors or via ITAM, of which the majority are located in the cytoplasmic tails of associated molecules, such as DAP12. The study of these activationand inhibitory NK cell receptorshas generated a number of interesting hypotheses, including immune privilege [1], the recognition of 'missing self', 'non-self' and 'induced self' [2][3][4][5], as well elucidating the underlying mechanisms of some of the immune responses to viruses [6] and malignancy [7]. Others and we have demonstrated that C-type lectinlike receptors are not restricted to NK cells, but are expressed by many other cell types including myeloid cells [8][9][10]. This introduces the novel concept that the myeloid paralogs of NK cell receptors might govern myeloid cell activation/inhibition in the same manner as those on NK cells. The genes of most C-type lectin-like molecules are located within the 'natural killer complex' (NKC), but many of those expressed by myeloid and other cells are found in a distinct cluster of genes within the NKC [10]. This cluster includes Decti...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Human MICL (CLEC12A) is differentially glycosylated and is down‐regulated following cellular activation

Willment¹,

Pyż²,

Dennehy³

et al. 2006

Eur J Immunol

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“…The vessels remain intact and proteins flow into the blister compartment according to their molecular size (Vermeer et al, 1979). The induction takes 1-2 h, does not cause pain and the blister sites heal rapidly without scar formation (Kiistala, 1968).…”

Section: Discussionmentioning

confidence: 99%

“…Here, we used a sensitive, direct and non-invasive method, based on the use of the suction blister technique (Kiistala, 1968) and on the radioimmunoassays of procollagen propeptides (Risteli et al, 1988;Melkko et al, 1990Melkko et al, , 1996 to study local ongoing type I and III collagen synthesis (Oikarinen et al, 1992) in the irradiated and unirradiated skin of breast cancer patients 1-5 years after the radiation therapy. (Risteli et al, 1988;Melkko et al, 1990Melkko et al, , 1996.…”

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confidence: 99%

Demonstration of increased collagen synthesis in irradiated human skin in vivo

Autio

Saarto²,

Tenhunen³

et al. 1998

Br J Cancer

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Summary Fibrosis is a common side-effect of radiation therapy. As a complex network of cytokines and other mediators plays a central role in the process leading to fibrosis, we used an in vivo method to measure skin collagen synthesis, taking into account the physiological conditions. We determined suction blister (i.e. interstitial) fluid concentrations of types and IlIl procollagen propeptides, reflecting types I and Ill collagen synthesis, in irradiated and unirradiated skin of breast cancer patients 1-5 years after surgery and radiation therapy, hence using the patients as their own controls. The mean concentrations of the measured collagen markers were approximately two times higher in the irradiated skin than in the unirradiated contralateral breast skin. The difference slowly diminishes with time. These results indicate that abundant collagen synthesis in the irradiated skin continues several years after discontinuation of the radiation therapy, leading to fibrosis.The method outlined here offers a new in vivo perspective to study events leading to radiation fibrosis.

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“…To study cefotiam concentrations at the site of bacterial infections in skin and soft-tissue infections following cefotiam hexetil (SCE2174), skin blister fluid [11,12] and serum levels have been determined in healthy volunteers. The drug levels following a single oral dose have been compared to those after an intravenous injection.…”

Section: Concentration In the Skinmentioning

confidence: 99%

Skin tissue fluid levels of cefotiam in healthy man following oral cefotiam hexetil

Körting¹,

Schäfer‐Korting

Kees

et al. 1990

Eur J Clin Pharmacol

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Summary.Cefotiam hexetil is a pro-drug of cefotiam available for oral administration. To evaluate cefotiam concentrations at the active site in skin and soft-tissue infections, drug levels in skin suction blister fluid (SBF), cantharides blister fluid (CBF) and serum were determined. Six healthy subjects received oral cefotiam 400 mg as cefotiam hexetil. On an other day 200 mg was injected intravenously.Following the oral dose, the bioavailability of cefotiam was 45.5%, and the maximum concentration in serum of 2.6mg-1 -~ was obtained at 2.1 h. Peak concentrations in both types of blister fluid (0.9 mg. 1-1) were significantly lower than after the iv dose (SBF 1.4 mg.1 -I, CBF 1.5 mg. 1 -1), and the peak levels occurred later (3.3 versus 1.5 h in CBF). Despite the delay, the extent of penetration was about 100% following either mode of administration (SBE iv dose 112%, oral dose 117%). The cefotiam level in skin blister fluids declined significantly more slowly than the serum level. Following the oral dose, the mean terminal half life was serum 0.8 h, SBF 2.6 h and CBF 4.6h.Cefotiam concentrations in the blister fluids were close to the MIC90 of Staphylococcus aureus, S. epidermis and H. influenzae and exceeded the MIC90 of Streptococci, E. coli and Proteus mirabilis.Thus, the oral administration of cefotiam 400 mg t. i. d. should be curative in the majority of bacterial infections of the skin and soft-tissues.

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Suction Blister Device for Separation of Viable Epidermis from Dermis*

Cited by 434 publications

References 8 publications

Human MICL (CLEC12A) is differentially glycosylated and is down‐regulated following cellular activation

Human MICL (CLEC12A) is differentially glycosylated and is down‐regulated following cellular activation

Demonstration of increased collagen synthesis in irradiated human skin in vivo

Skin tissue fluid levels of cefotiam in healthy man following oral cefotiam hexetil

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