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• W2022031507 abstract "We report the use of non-invasive tape stripping to sample psoriatic lesional and non-lesional skin in 96 patients. The procedure was well tolerated with any discomfort described as mild; we did not observe any cases of Koebner phenomena at any non-lesional tape-stripped sites. Tape-harvested epidermis was extracted for RNA, which was profiled by semiquantitative reverse transcriptase-PCR. This analysis revealed that mRNAs for tumor necrosis factor α, IFNγ, Krt-16, CD2, IL-23A, IL-12B, and vascular endothelial growth factor are overexpressed in the “average” psoriatic lesion in a majority of patients. In addition, 10 of these patients were biopsied at lesional and non-lesional sites and the expression data compared to tape-stripping data. This comparison shows that five of seven mRNA are more highly expressed in cells captured by tape stripping than biopsy, suggesting that the upper aspect of a lesion contains cells very active in the disease. The tape-harvesting data reveal that approximately 46% of lesions have at least one pathogenic mRNA within non-lesional skin limits. Data demonstrate that tape stripping reveals mRNA markers not detected in biopsy samples and thus the method may be a useful supplement to biopsy. We report the use of non-invasive tape stripping to sample psoriatic lesional and non-lesional skin in 96 patients. The procedure was well tolerated with any discomfort described as mild; we did not observe any cases of Koebner phenomena at any non-lesional tape-stripped sites. Tape-harvested epidermis was extracted for RNA, which was profiled by semiquantitative reverse transcriptase-PCR. This analysis revealed that mRNAs for tumor necrosis factor α, IFNγ, Krt-16, CD2, IL-23A, IL-12B, and vascular endothelial growth factor are overexpressed in the “average” psoriatic lesion in a majority of patients. In addition, 10 of these patients were biopsied at lesional and non-lesional sites and the expression data compared to tape-stripping data. This comparison shows that five of seven mRNA are more highly expressed in cells captured by tape stripping than biopsy, suggesting that the upper aspect of a lesion contains cells very active in the disease. The tape-harvesting data reveal that approximately 46% of lesions have at least one pathogenic mRNA within non-lesional skin limits. Data demonstrate that tape stripping reveals mRNA markers not detected in biopsy samples and thus the method may be a useful supplement to biopsy. tumor necrosis factor α vascular endothelial growth factor Psoriasis is a common inflammatory skin disorder, estimated to affect 1–3% of the world's population and is characterized by lesions exhibiting erythema, induration, and scaling (Peters et al., 2000Peters B.P. Weissman F.G. Gill M.A. Pathophysiology and treatment of psoriasis.Am J Health Syst Pharm. 2000; 57 (quiz 660–661): 645-659PubMed Google Scholar). At the physiological and molecular level, psoriasis is a complex disease highlighted by hyperproliferative keratinocytes, defective differentiation and barrier formation, dermal and epidermal infiltration by diverse leukocytes, and profoundly altered gene expression (Lew et al., 2004Lew W. Bowcock A.M. Krueger J.G. Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and “Type 1” inflammatory gene expression.Trends Immunol. 2004; 25: 295-305Abstract Full Text Full Text PDF PubMed Scopus (226) Google Scholar). Much of our knowledge concerning the pathophysiology of psoriatic skin lesions has been derived from biopsies of lesional and non-lesional control skin (also referred to as uninvolved skin) of a psoriatic patient. While biopsy data have been invaluable in characterizing psoriatic skin, the invasive nature of biopsy makes it much less practical as a method for repetitive clinical investigation of psoriatic lesions. Repetitive non-invasive monitoring of this skin disease would be of considerable value if the information obtained reflected the pathophysiological state of the lesion. Tape stripping or tape harvesting is a non-invasive method that allows recovery of cells comprising and associated with the upper epidermis (Morhenn et al., 1999Morhenn V.B. Chang E.Y. Rheins L.A. A noninvasive method for quantifying and distinguishing inflammatory skin reactions.J Am Acad Dermatol. 1999; 41: 687-692Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar; Wong et al., 2004Wong R. Tran V. Morhenn V. Hung S.P. Andersen B. Ito E. et al.Use of RT-PCR and DNA microarrays to characterize RNA recovered by non-invasive tape harvesting of normal and inflamed skin.J Invest Dermatol. 2004; 123: 159-167Crossref PubMed Scopus (48) Google Scholar). Recently, it has been demonstrated that the sequential application of four small adhesive tape strips to a normal or inflamed skin site is sufficient to recover a skin sample whose RNA population can be profiled by quantitative reverse transcriptase-PCR or DNA microarray (Wong et al., 2004Wong R. Tran V. Morhenn V. Hung S.P. Andersen B. Ito E. et al.Use of RT-PCR and DNA microarrays to characterize RNA recovered by non-invasive tape harvesting of normal and inflamed skin.J Invest Dermatol. 2004; 123: 159-167Crossref PubMed Scopus (48) Google Scholar). The application of this method to dermatological disease – in concert with RNA profiling – could allow for more precise diagnosis and facilitate the pharmacogenomic characterization of skin diseases by allowing large amounts of informative molecular data to be gathered; which because it can be gathered in a non-invasive manner would otherwise be unavailable. Herein we describe the use of tape harvesting as a method for routinely recovering pathologic information in messenger RNA from the surface of psoriatic and non-lesional skin. We show that the tape harvesting of psoriatic patients gives relatively large quantities of total RNA and that RNA profiles contained within the recovered RNA are consistent with the body of biopsy data in the literature. In a subset of patients, we directly compare biopsy and tape-stripping results. We observe that biopsy and tape-strip RNA samples provide largely similar but also individually unique data suggesting that tape stripping is an important addition to biopsy as a sampling technique. In this study, we tape stripped 96 patients at one lesional site and three non-lesional control sites. From lesions, an average of 116±19.5 ng of RNA was recovered; from the combined three control skin sites an average of 83±17.3 ng of total RNA was isolated (median recoveries were 46.2 and 25.3 ng, respectively). As the control sample was a pool of three separate skin sites (described in Materials and Methods) and the lesion samples were from a single site, it is clear that substantially more RNA was harvested from lesional skin than control skin. Gene expression has been well characterized in lesional and non-lesional skin by both immunohistochemistry and quantitative reverse transcriptase-PCR, using incisional skin biopsies to procure samples (Yawalkar et al., 1998Yawalkar N. Karlen S. Hunger R. Brand C.U. Braathen L.R. Expression of interleukin-12 is increased in psoriatic skin.J Invest Dermatol. 1998; 111: 1053-1057Crossref PubMed Scopus (194) Google Scholar; Trepicchio et al., 1999Trepicchio W.L. Ozawa M. Walters I.B. Kikuchi T. Gilleaudeau P. Bliss J.L. et al.Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions.J Clin Invest. 1999; 104: 1527-1537Crossref PubMed Scopus (204) Google Scholar; Bhawan et al., 2004Bhawan J. Bansal C. Whren K. Schwertschlag U. K16 expression in uninvolved psoriatic skin: a possible marker of pre-clinical psoriasis.J Cutan Pathol. 2004; 31: 471-476Crossref PubMed Scopus (23) Google Scholar; Lee et al., 2004Lee E. Trepicchio W.L. Oestreicher J.L. Pittman D. Wang F. Chamian F. et al.Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris.J Exp Med. 2004; 199: 125-130Crossref PubMed Scopus (721) Google Scholar). To determine if tape harvesting could yield data consistent with this body of work, we assayed the samples described above for the mRNAs listed in Table 1. These mRNAs (with the exception of tumor necrosis factor (TNF)α) are known to be elevated in lesional skin and characteristic of psoriatic disease. Table 1 shows the average fold increase of the (gene/β-actin) mRNA ratio in lesion samples relative to non-lesional control skin. The table shows that, on average, all of the mRNAs are significantly (95% confidence interval) overexpressed in lesional skin. This result indicates that RNA recovered using the tape-harvesting method yields data qualitatively identical to biopsy-recovered RNA (Yawalkar et al., 1998Yawalkar N. Karlen S. Hunger R. Brand C.U. Braathen L.R. Expression of interleukin-12 is increased in psoriatic skin.J Invest Dermatol. 1998; 111: 1053-1057Crossref PubMed Scopus (194) Google Scholar; Trepicchio et al., 1999Trepicchio W.L. Ozawa M. Walters I.B. Kikuchi T. Gilleaudeau P. Bliss J.L. et al.Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions.J Clin Invest. 1999; 104: 1527-1537Crossref PubMed Scopus (204) Google Scholar; Bhawan et al., 2004Bhawan J. Bansal C. Whren K. Schwertschlag U. K16 expression in uninvolved psoriatic skin: a possible marker of pre-clinical psoriasis.J Cutan Pathol. 2004; 31: 471-476Crossref PubMed Scopus (23) Google Scholar; Lee et al., 2004Lee E. Trepicchio W.L. Oestreicher J.L. Pittman D. Wang F. Chamian F. et al.Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris.J Exp Med. 2004; 199: 125-130Crossref PubMed Scopus (721) Google Scholar). In later sections, we confirm this observation with analysis of a subset of patients for which we have biopsy samples and address the observation of increased TNFα mRNA in tape samples.Table 1Average fold change in (gene/β-actin) mRNA ratio in lesional relative to non-lesional psoriatic skinAverage fold change1The average fold change in lesional psoriatic skin relative to non-lesional control skin is calculated as described in Materials and Methods using the data in Table S1. The >95% confidence interval is given in parenthesis below the fold change.TNFαIFNγ2These confidence intervals are large because mRNA for these markers could only be detected in two (IFN) and four (IL-12B) control skin samples.CD2Krt-16IL-12B2These confidence intervals are large because mRNA for these markers could only be detected in two (IFN) and four (IL-12B) control skin samples.IL-23AVEGF7 (5–7.5)6 (1.6–20)2.5 (1.8–2.7)2 (1.6–2.1)6.2 (1–63)6.8 (3.5–9.2)5 (4–5.3)1 The average fold change in lesional psoriatic skin relative to non-lesional control skin is calculated as described in Materials and Methods using the data in Table S1. The >95% confidence interval is given in parenthesis below the fold change.2 These confidence intervals are large because mRNA for these markers could only be detected in two (IFN) and four (IL-12B) control skin samples. Open table in a new tab Table 1 shows that in our sample of 96 patients, lesional skin contains, on average, elevated levels of pathogenic mRNAs. However, inspection of individual patient data reveals that there is heterogeneity in specific (gene/β-actin) mRNA ratios (data not shown). To reveal this heterogeneity in lesion gene expression we refer to the ΔCt value, an experimental measure of the (gene/β-actin) mRNA ratio in a sample (described in Materials and Methods). By comparing individual (gene/actin) mRNA ratios (i.e. ΔCt values) to average values from our 96 patients, we can classify a sample as being “lesion-like” or “non-lesion-like”. For reference, the average lesion and non-lesion ΔCt data is shown in Table S1. Download .pdf (.12 MB) Help with pdf files Table S1Average ΔCt values for lesional and control skin in tape and biopsy samples. By comparison of individual patient ΔCt values (data not shown) to the average values shown in Table S1, we can determine if individual lesions overexpress each of the mRNAs shown in Table 1. We have carried out such a comparison for all 96 patients and summarize the results in Table 2. The table shows the number of lesion samples with specific gene expression characteristic of non-lesional skin. For instance, of the 95 lesion samples with quantifiable TNFα mRNA, there were five ΔCt, TNF values that were characteristic of average control skin. Similarly, of 92 lesion samples with quantifiable CD2 mRNA, 22 samples were determined to have ΔCt, CD2 values characteristic of control skin. Furthermore, if one asks how many of the 96 lesion samples have significant increases in all the mRNAs, we find that 52 samples have increased expression of all mRNAs (K16 is not included in this analysis for reasons discussed later). Thus, 44 of the lesions (46%) have at least one mRNA with expression characteristic of non-lesional skin.Table 2Identification of lesions with levels of pathological mRNA within control skin limitsNumber of patients displaying a lesion with gene expression characteristic of control skin1The number of patients presenting a lesion with mRNA expression characteristic of non-lesional skin. For example, five of 95 lesions with assayable TNFα mRNA had a ΔCt, TNF >8.2 (average control ΔCt, TNF minus 1 SEM; Table S1; see Materials and Methods for a full explanation of how lesions were evaluated), demonstrating that these five lesions do not overexpress TNFα mRNA; one out of the 96 samples could not be evaluated for TNFα because of low RNA yield. The total number of lesions considered is in parentheses; some lesion samples did not have sufficient RNA to be evaluated for some markers.TNFαIFNγCD2Krt-16IL-12BIL-23AVEGF5 (95)17 (82)22 (93)30 (96)22 (85)10 (93)3 (96)1 The number of patients presenting a lesion with mRNA expression characteristic of non-lesional skin. For example, five of 95 lesions with assayable TNFα mRNA had a ΔCt, TNF >8.2 (average control ΔCt, TNF minus 1 SEM; Table S1; see Materials and Methods for a full explanation of how lesions were evaluated), demonstrating that these five lesions do not overexpress TNFα mRNA; one out of the 96 samples could not be evaluated for TNFα because of low RNA yield. The total number of lesions considered is in parentheses; some lesion samples did not have sufficient RNA to be evaluated for some markers. Open table in a new tab In 10 of our 97 patients, we obtained 4 mm punch biopsies from lesional and non-lesional skin directly adjacent to sites which had been tape stripped. The biopsies were further divided into epidermal and dermal sections and RNA prepared from each section. Table 3 shows the comparison of average change in gene expression in lesional relative to control skin in biopsy and tape samples from these patients. In this table, each sample of tape, biopsy-epidermis, and biopsy-dermis from lesional skin is calibrated to the same sample type from non-lesional skin. Thus, the average RNA expression in tape-strip samples of lesions is calibrated to average expression in tape-strip samples of non-lesional skin; lesion epidermis-biopsy samples are calibrated to control epidermis-biopsy samples, etc.Table 3Average fold change of inflammatory mRNAs from 10 matched tape and biopsy samples in lesional psoriatic skin relative to control skinGeneStatistic1Calculation of fold change and 95% confidence interval (95% CI) is described in Materials and Methods; N is the number of lesion and control samples upon which the fold-change calculations are based and are shown as (no. of lesion, no. of control).Sample source and fold change in gene expressionTape2Data from the 10 tape-strip samples for which we have accompanying biopsy samples, for fold-change calculations of IFNγ and CD2 mRNAs only one of the 10 control tape samples had detectable IFN or CD2 mRNA, thus the fold change is based on that single sample and no 95% CI is presented.Biopsy3Data for lesion and control biopsy samples split into epidermal and dermal fractions. Data for 10 control samples and nine lesion samples are presented. The average fold change for IFNγ, IL-12B, and IL-23A (gene/actin) mRNA ratio in lesions is calibrated on the single control sample in which specific mRNA could be assayed (specific mRNA could not be detected in nine control samples), therefore, no 95% CI given for these mRNAs.EpidermisDermisTNFαFold change90.80.795% CI(5.4–15)(0.4–1.5)(0.4–1.1)N(10, 4)(9, 10)(9, 10)IFNFold change3.12195% CI———N(7, 1)(9, 1)(9, 1)CD2Fold change2.73.91.795% CI—(1.8–8.6)(0.9–3.3)N(9, 1)(9, 10)(9, 10)K16Fold change1.3712695% CI(0.7–2.5)(18–280)(8.5–79)N(10, 9)(9, 10)(9, 10)IL-12BFold change4.64In this subset of 10 tape-strip samples of control skin IL-12B mRNA could not be detected, therefore in order to calculate a fold change for IL-12B mRNA we used the average ΔCt, IL12B value of the four of 96 tape samples where IL-12B mRNA could be assayed (taken from Table S1).9.43.195% CI———N(8, 0)(9, 1)(8, 1)IL-23AFold change2.73.90.8495% CI(0.7–11)——N(10, 2)(9, 1)(9, 1)VEGFFold change2.81.61.295% CI(1.4–5.6)(0.91–2.7)(0.95–1.5)N(10, 8)(9, 10)(9, 10)1 Calculation of fold change and 95% confidence interval (95% CI) is described in Materials and Methods; N is the number of lesion and control samples upon which the fold-change calculations are based and are shown as (no. of lesion, no. of control).2 Data from the 10 tape-strip samples for which we have accompanying biopsy samples, for fold-change calculations of IFNγ and CD2 mRNAs only one of the 10 control tape samples had detectable IFN or CD2 mRNA, thus the fold change is based on that single sample and no 95% CI is presented.3 Data for lesion and control biopsy samples split into epidermal and dermal fractions. Data for 10 control samples and nine lesion samples are presented. The average fold change for IFNγ, IL-12B, and IL-23A (gene/actin) mRNA ratio in lesions is calibrated on the single control sample in which specific mRNA could be assayed (specific mRNA could not be detected in nine control samples), therefore, no 95% CI given for these mRNAs.4 In this subset of 10 tape-strip samples of control skin IL-12B mRNA could not be detected, therefore in order to calculate a fold change for IL-12B mRNA we used the average ΔCt, IL12B value of the four of 96 tape samples where IL-12B mRNA could be assayed (taken from Table S1). Open table in a new tab In comparison of the average fold expression for all 96 subjects (Table 1) with the subset of 10 tape-strip patients for which we have biopsies (Table 3), we see that, with one exception, all of the (mRNA/actin) mRNA ratios are increased in the subset of 10 tape-strip lesion samples. The sole exception is K16 mRNA, whose average expression is not significantly overexpressed in the subset of 10 tape-strip lesion samples (K16 mRNA is significantly overexpressed in the larger set of 96 samples shown in Table 1). Thus, excepting the K16 data, the 10 tape-strip group is largely representative of the larger sample. In contrast, comparison of gene expression in tape-strip RNA versus epidermal- and dermal-biopsy RNA reveals some interesting differences, described below. Table 3 shows that the (TNFα/β-actin) mRNA ratio in our subset of 10 tape samples of psoriatic lesions is 9-fold elevated relative to control tape samples. In contrast, the epidermis- and dermal-biopsy mRNA ratios are not significantly different in lesional versus control samples. Our subset of 10 tape-strip data are in agreement with the larger sample set (Table 1) and our biopsy data are in agreement with published data. Therefore, we conclude that TNF mRNA is overexpressed in cells in the very upper epidermis of a psoriatic lesion; presumably, these cells are diluted out by the majority of other cells captured by a biopsy. This demonstrates that tape stripping is a more sensitive sampling method for assay of TNFα mRNA than is biopsy. Similar data are revealed for IL-23A expression. Although the average fold increase in expression in lesion versus control is 2.7- and 3.9-fold for tape and epidermis-biopsy samples, respectively, inspection of individual ΔCt data reveals that tape-strip samples have a much higher (IL-23A/β-actin) mRNA ratio than do epidermis-biopsy samples. The average ΔCt, IL23A in lesion tape samples was 5.9, while the average ΔCt, IL23A in the epidermal-biopsy fraction was 10.55 (for ΔCt values a lower number indicates higher expression); this difference in ΔCt values corresponds to a 2−(5.9–10.55) or 25-fold higher (IL-23A/actin) mRNA ratio in tape versus epidermal-biopsy lesion samples. For K16 mRNA expression, we see a slight, but not significant 1.3-fold increase in the (K16/actin) mRNA ratio in the subset of 10 tape samples of lesional relative to control skin (Table 3). However, epidermal- and dermal-biopsy lesion samples show, respectively, 71- and 26-fold increases relative to non-lesional skin. If we examine the average ΔCt values for tape-strip samples (Table S1; all 96 subjects) and epidermal-biopsy samples from control skin, we find that tape samples have a 2−(−1.46–3.81) or 38-fold higher (K16/actin) mRNA ratio than epidermal-biopsy samples (Table S1). Thus in non-lesional skin, there is active K16 expression in the very upper epidermis (revealed by tape stripping) that is not seen in the epidermal-biopsy sample (or the dermal sample). We also observe this high expression of K16 mRNA in tape-strip samples from normal healthy individuals (data not shown). In lesion samples, the activity of K16 expression in tape, epidermis, and dermis RNA samples is approximately equal (Table S1). Therefore, the large changes in K16 mRNA expression induced by psoriasis are occurring deeper in the skin, in layers of a lesion not sampled by tape stripping. For the remaining mRNAs, the average fold-change data in Table 3 show that changes revealed in tape-strip lesion samples are qualitatively mirrored by similar changes in epidermal-biopsy lesion samples. The data in Table 3 also show that in general the large changes in mRNA expression are restricted to the epidermis, since the dermal sections show few significant changes in lesional compared to control dermis, the sole exception being K16 expression which, as might be expected because of the acanthotic epidermis, is increased in psoriatic dermis compared to the control dermis. In this study, we demonstrate that mRNA can be recovered from the surface of lesional and non-lesional skin of psoriatics using a non-invasive tape-stripping method. Further, we have shown this RNA can be quantitatively assayed for specific mRNAs. This work expands the work of Wong et al., 2004Wong R. Tran V. Morhenn V. Hung S.P. Andersen B. Ito E. et al.Use of RT-PCR and DNA microarrays to characterize RNA recovered by non-invasive tape harvesting of normal and inflamed skin.J Invest Dermatol. 2004; 123: 159-167Crossref PubMed Scopus (48) Google Scholar who have generated similar data for normal skin and sodium lauryl sulfate-inflamed skin. In the course of tape-harvesting the superficial epidermis from lesional and non-lesional skin of 96 subjects with psoriasis, we observed no adverse events, including any evidence of the Koebner phenomenon. Previously, we reviewed the literature, reported our experience and noted that ≈30% of psoriatic subjects will develop psoriasis in areas receiving significant trauma (Eyre and Krueger, 1991Eyre R.W. Krueger G.G. The Koebner response in psoriasis.in: Roenigk H.H. Maibach H.I. Psoriasis. Marcel Dekker, New York1991: 135-147Google Scholar). In this review, it was noted that “deep” tape stripping has been reported as inducing the “Koebner reaction.” The fact that we have not seen psoriasis develop in any of the three control sites in the 96 subjects we report here nor in the over 300 patients we have treated since (data not presented) argues favorably for this method of sample collection as being minimally invasive and easily tolerated. There is mounting evidence that psoriasis is an immune-mediated disease, where activated T cells and activated dendritic cells are the principle effectors (Lew et al., 2004Lew W. Bowcock A.M. Krueger J.G. Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and “Type 1” inflammatory gene expression.Trends Immunol. 2004; 25: 295-305Abstract Full Text Full Text PDF PubMed Scopus (226) Google Scholar; Lowes et al., 2005Lowes M.A. Chamian F. Abello M.V. Fuentes-Duculan J. Lin S.L. Nussbaum R. et al.Increase in TNF-alpha and inducible nitric oxide synthase-expressing dendritic cells in psoriasis and reduction with efalizumab (anti-CD11a).Proc Natl Acad Sci USA. 2005; 102: 19057-19062Crossref PubMed Scopus (367) Google Scholar) and a hyperproliferative, poorly differentiated epidermis is the result. The mRNAs we have chosen to assay (Table 1) are well described in the literature with direct involvement in the pathogenesis of psoriasis, being markers of general inflammation, activated T cells or hyperproliferative keratinocytes. Our gene expression data from tape-harvested and biopsied lesions are – excepting K16 and TNFα mRNA expression – qualitatively in compete agreement with known gene expression profiles describing the “average” psoriatic lesion, data which is all based on biopsies (Yawalkar et al., 1998Yawalkar N. Karlen S. Hunger R. Brand C.U. Braathen L.R. Expression of interleukin-12 is increased in psoriatic skin.J Invest Dermatol. 1998; 111: 1053-1057Crossref PubMed Scopus (194) Google Scholar; Trepicchio et al., 1999Trepicchio W.L. Ozawa M. Walters I.B. Kikuchi T. Gilleaudeau P. Bliss J.L. et al.Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions.J Clin Invest. 1999; 104: 1527-1537Crossref PubMed Scopus (204) Google Scholar; Bowcock et al., 2001Bowcock A.M. Shannon W. Du F. Duncan J. Cao K. Aftergut K. et al.Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies.Hum Mol Genet. 2001; 10: 1793-1805Crossref PubMed Scopus (207) Google Scholar; Oestreicher et al., 2001Oestreicher J.L. Walters I.B. Kikuchi T. Gilleaudeau P. Surette J. Schwertschlag U. et al.Molecular classification of psoriasis disease-associated genes through pharmacogenomic expression profiling.Pharmacogenomics J. 2001; 1: 272-287Crossref PubMed Scopus (134) Google Scholar; Lee et al., 2004Lee E. Trepicchio W.L. Oestreicher J.L. Pittman D. Wang F. Chamian F. et al.Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris.J Exp Med. 2004; 199: 125-130Crossref PubMed Scopus (721) Google Scholar). In our comparison of lesion versus control skin gene expression in tape strip, epidermal-, and dermal-biopsy RNA samples, we have observed a general trend of higher expression in tape and epidermis-biopsy lesion samples and modest or no change in dermis-biopsy samples. Thus, generally speaking tape-strip RNA and epidermal-biopsy RNA gave equivalent results. Exceptions to these observations were the already noted changes in TNFα and K16 mRNA expression. While it is well established that TNFα protein is increased in psoriatic lesions, increases in TNFα mRNA have not been demonstrated (Zhou et al., 2003Zhou X. Krueger J.G. Kao M.C. Lee E. Du F. Menter A. et al.Novel mechanisms of T-cell and dendritic cell activation revealed by profiling of psoriasis on the 63,100-element oligonucleotide array.Physiol Genomics. 2003; 13: 69-78Crossref PubMed Scopus (246) Google Scholar; Johansen et al., 2006Johansen C. Funding A.T. Otkjaer K. Kragballe K. Jensen U.B. Madsen M. et al.Protein expression of TNF-{alpha} in psoriatic skin is regulated at a posttranscriptional level by MAPK-activated protein kinase 2.J Immunol. 2006; 176: 1431-1438Crossref PubMed Scopus (115) Google Scholar). The lack of increased TNFα mRNA in lesional skin has led to various post-translational TNF-activating mechanisms to account for the increases in protein (Kawaguchi et al., 2005Kawaguchi M. Mitsuhashi Y. Kondo S. Overexpression of tumour necrosis factor-alpha-converting enzyme in psoriasis.Br J Dermatol. 2005; 152: 915-919Crossref PubMed Scopus (40) Google Scholar; Johansen et al., 2006Johansen C. Funding A.T. Otkjaer K. Kragballe K. Jensen U.B. Madsen M. et al.Protein expression of TNF-{alpha} in psoriatic skin is regulated at a posttranscriptional level by MAPK-activated protein kinase 2.J Immunol. 2006; 176: 1431-1438Crossref PubMed Scopus (115) Google Scholar). We also did not observe increased TNFα mRNA in lesional skin biopsies (Table 3) but our tape-stripping data clearly show a significant increase in TNFα mRNA. As we see significant increases in TNFα mRNA in 90 of 95 lesion tape-strip samples (Table 2) there is little doubt that tape stripping is recovering cells with increased TNFα mRNA transcription. We hypothesize that these cells are in the very upper aspect of lesions and in a biopsy sample contribute little to the overall mRNA pool. Similar observations have been reported by Wong et al., 2004Wong R. Tran V. Morhenn V. Hung S.P. Andersen B. Ito E. et al.Use of RT-PCR and DNA microarrays to characterize RNA recovered by non-invasive tape harvesting of normal and inflamed skin.J Invest Dermatol. 2004; 123: 159-167Crossref PubMed Scopus (48) Google Scholar for IL-8 mRNA expression in tape versus biopsy samples of normal and irritated skin. The potential for tape samples to enrich for surface cells compared to biopsy samples is" @default.
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• W2022031507 date "2006-10-01" @default.
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• W2022031507 title "An Analysis of Select Pathogenic Messages in Lesional and Non-Lesional Psoriatic Skin Using Non-Invasive Tape Harvesting" @default.
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• W2022031507 doi "https://doi.org/10.1038/sj.jid.5700412" @default.
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