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Naoki Mori - One of the best experts on this subject based on the ideXlab platform.

  • retraction molecular characterization of legionella pneumophila induced Interleukin 8 expression in t cells
    BMC Microbiology, 2011
    Co-Authors: Reika Takamatsu, Naofumi Mukaida, Hiromitsu Teruya, Eriko Takeshima, Chie Ishikawa, Kunihiro Matsumoto, Klaus Heuner, Futoshi Higa, Jiro Fujita, Naoki Mori
    Abstract:

    Article Retracted Retraction After lengthy investigation by the editors, the original article [1] has been retracted because of inappropriate duplication of images from previously published articles. The last author, Naoki Mori takes full responsibility and apologizes for any inconvenience caused. Author details Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan. Division of Control and Prevention of Infectious Diseases, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 9030215, Japan. Transdisciplinary Research Organization for Subtropics and Island Studies, University of the Ryukyus, 1 Senbaru, Nishihara, Okinawa 9030215, Japan. Department of Molecular Biology, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan. Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-0934, Japan. Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, New York 14642, USA. Project group 26 “Nosocomial Infections of the Elderly”, Robert Koch-Institut, 20 Nordufer, Berlin 13353, Germany. Received: 27 January 2011 Accepted: 2 June 2011 Published: 2 June 2011 Reference 1. Takamatsu R, Teruya H, Takeshima E, Ishikawa C, Matsumoto K, Mukaida N, Li J-D, Heuner K, Higa F, Fujita J, Mori N: Molecular characterization of Legionella pneumophila-induced Interleukin-8 expression in T cells. BMC Microbiol 2010, 10:1. doi:10.1186/1471-2180-11-127 Cite this article as: Takamatsu et al.: Retraction: Molecular characterization of Legionella pneumophila-induced Interleukin-8 expression in T cells. BMC Microbiology 2011 11:127. Submit your next manuscript to BioMed Central and take full advantage of: • Convenient online submission • Thorough peer review • No space constraints or color figure charges • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit * Correspondence: n-mori@med.u-ryukyu.ac.jp Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan Full list of author information is available at the end of the article Takamatsu et al. BMC Microbiology 2011, 11:127 http://www.biomedcentral.com/1471-2180/11/127 © 2011 Takamatsu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • molecular characterization of legionella pneumophila induced Interleukin 8 expression in t cells
    BMC Microbiology, 2010
    Co-Authors: Reika Takamatsu, Naofumi Mukaida, Hiromitsu Teruya, Eriko Takeshima, Chie Ishikawa, Kunihiro Matsumoto, Klaus Heuner, Futoshi Higa, Jiro Fujita, Naoki Mori
    Abstract:

    Background Legionella pneumophila is the causative agent of human Legionnaire's disease. During infection, the bacterium invades macrophages and lung epithelial cells, and replicates intracellularly. However, little is known about its interaction with T cells. We investigated the ability of L. pneumophila to infect and stimulate the production of Interleukin-8 (IL-8) in T cells. The objective of this study was to assess whether L. pneumophila interferes with the immune system by interacting and infecting T cells.

Naofumi Mukaida - One of the best experts on this subject based on the ideXlab platform.

  • retraction molecular characterization of legionella pneumophila induced Interleukin 8 expression in t cells
    BMC Microbiology, 2011
    Co-Authors: Reika Takamatsu, Naofumi Mukaida, Hiromitsu Teruya, Eriko Takeshima, Chie Ishikawa, Kunihiro Matsumoto, Klaus Heuner, Futoshi Higa, Jiro Fujita, Naoki Mori
    Abstract:

    Article Retracted Retraction After lengthy investigation by the editors, the original article [1] has been retracted because of inappropriate duplication of images from previously published articles. The last author, Naoki Mori takes full responsibility and apologizes for any inconvenience caused. Author details Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan. Division of Control and Prevention of Infectious Diseases, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 9030215, Japan. Transdisciplinary Research Organization for Subtropics and Island Studies, University of the Ryukyus, 1 Senbaru, Nishihara, Okinawa 9030215, Japan. Department of Molecular Biology, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan. Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-0934, Japan. Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, New York 14642, USA. Project group 26 “Nosocomial Infections of the Elderly”, Robert Koch-Institut, 20 Nordufer, Berlin 13353, Germany. Received: 27 January 2011 Accepted: 2 June 2011 Published: 2 June 2011 Reference 1. Takamatsu R, Teruya H, Takeshima E, Ishikawa C, Matsumoto K, Mukaida N, Li J-D, Heuner K, Higa F, Fujita J, Mori N: Molecular characterization of Legionella pneumophila-induced Interleukin-8 expression in T cells. BMC Microbiol 2010, 10:1. doi:10.1186/1471-2180-11-127 Cite this article as: Takamatsu et al.: Retraction: Molecular characterization of Legionella pneumophila-induced Interleukin-8 expression in T cells. BMC Microbiology 2011 11:127. Submit your next manuscript to BioMed Central and take full advantage of: • Convenient online submission • Thorough peer review • No space constraints or color figure charges • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit * Correspondence: n-mori@med.u-ryukyu.ac.jp Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan Full list of author information is available at the end of the article Takamatsu et al. BMC Microbiology 2011, 11:127 http://www.biomedcentral.com/1471-2180/11/127 © 2011 Takamatsu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • molecular characterization of legionella pneumophila induced Interleukin 8 expression in t cells
    BMC Microbiology, 2010
    Co-Authors: Reika Takamatsu, Naofumi Mukaida, Hiromitsu Teruya, Eriko Takeshima, Chie Ishikawa, Kunihiro Matsumoto, Klaus Heuner, Futoshi Higa, Jiro Fujita, Naoki Mori
    Abstract:

    Background Legionella pneumophila is the causative agent of human Legionnaire's disease. During infection, the bacterium invades macrophages and lung epithelial cells, and replicates intracellularly. However, little is known about its interaction with T cells. We investigated the ability of L. pneumophila to infect and stimulate the production of Interleukin-8 (IL-8) in T cells. The objective of this study was to assess whether L. pneumophila interferes with the immune system by interacting and infecting T cells.

  • essential involvement of Interleukin 8 il 8 in acute inflammation
    Journal of Leukocyte Biology, 1994
    Co-Authors: Akihisa Harada, Tohru Akahoshi, Nobuaki Sekido, Takashi Wada, Naofumi Mukaida, Kouji Matsushima
    Abstract:

    Neutrophil infiltration into inflammatory sites is one of the hallmarks of acute inflammation. Lo- cally produced chemotactic factors are presumed to medi- ate the sequence of events leading to the infiltration at inflammatory sites. Interleukin-8 (IL-8), a novel leuko- cyte chemotactic activating cytokine (chemokine), is pro- duced by various types of cells upon stimulation with inflammatory stimuli and exerts a variety of functions on leukocytes, particularly, neutrophils in vitro. However, no definitive evidence has been presented on its role in recruiting and activating neutrophils in the lesions of various types of inflammatory reactions. We admin- istered a highly specific neutralizing antibody against IL-8 in several types of acute inflammatory reactions, in- cluding lipopolysaccharide (LPS)-induced dermatitis, LPS/IL-1-induced arthritis, lung reperfusion injury, and acute immune complex-type glomerulonephritis. Anti- IL-8 treatment prevented neutrophil-dependent tissue damage as well as neutrophil infiltration in these condi- tions. These results suggest that IL-8 plays a causative role in acute inflammation by recruiting and activating neutrophils. J. Leukoc Biol. 56: 559-564; 1994.

  • essential involvement of Interleukin 8 il 8 in acute inflammation
    Journal of Leukocyte Biology, 1994
    Co-Authors: Akihisa Harada, Tohru Akahoshi, Nobuaki Sekido, Takashi Wada, Naofumi Mukaida, Kouji Matsushima
    Abstract:

    Neutrophil infiltration into inflammatory sites is one of the hallmarks of acute inflammation. Locally produced chemotactic factors are presumed to mediate the sequence of events leading to the infiltration at inflammatory sites. Interleukin-8 (IL-8), a novel leukocyte chemotactic activating cytokine (chemokine), is produced by various types of cells upon stimulation with inflammatory stimuli and exerts a variety of functions on leukocytes, particularly, neutrophils in vitro. However, no definitive evidence has been presented on its role in recruiting and activating neutrophils in the lesions of various types of inflammatory reactions. We administered a highly specific neutralizing antibody against IL-8 in several types of acute inflammatory reactions, including lipopolysaccharide (LPS)-induced dermatitis, LPS/IL-1-induced arthritis, lung reperfusion injury, and acute immune complex-type glomerulonephritis. Anti-IL-8 treatment prevented neutrophil-dependent tissue damage as well as neutrophil infiltration in these conditions. These results suggest that IL-8 plays a causative role in acute inflammation by recruiting and activating neutrophils.

Steven L. Kunkel - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of Interleukin 8 attenuates angiogenesis in bronchogenic carcinoma
    Journal of Experimental Medicine, 1994
    Co-Authors: Daniel R Smith, Steven L. Kunkel, Peter J Polverini, Mark B Orringer, Richard I Whyte, Marie D Burdick, Carol A Wilke, Robert M. Strieter
    Abstract:

    We investigated the role of Interleukin 8 (IL-8) in mediating angiogenesis in human bronchogenic carcinoma. Increased quantities of IL-8 were detected in tumor tissue as compared with normal lung tissue. Immunohistochemical staining of tumors revealed primary localization of IL-8 to individual tumor cells and demonstrated the capacity of tumor to elaborate IL-8. Functional studies that used tissue homogenates of tumors demonstrated the induction of both in vitro endothelial cell chemotaxis and in vivo corneal neovascularization. It is important to note that the addition of neutralizing antisera to IL-8 to these assays resulted in the marked and specific attenuation of these responses. Our observations definitively establish IL-8 as a primary mediator of angiogenesis in bronchogenic carcinoma and offer a potential target for immunotherapies against solid malignancies.

  • Interleukin 8 and development of adult respiratory distress syndrome in at risk patient groups
    The Lancet, 1993
    Co-Authors: Seamas C. Donnelly, Christopher Haslett, Robert M. Strieter, Steven L. Kunkel, Alfred Walz, C R Robertson, D C Carter, A Pollok, I S Grant
    Abstract:

    Abstract Neutrophils have been implicated in the pathogenesis of the adult respiratory distress syndrome (ARDS). We have measured concentrations of the neutrophil attractant Interleukin-8 in blood and bronchoalveolar lavage fluid (BAL) from patients at risk of ARDS. We studied 29 patients from three groups at risk of developing ARDS: multiple trauma (n=16), perforated bowel (n=6), and pancreatitis (n=7). ARDS developed in 7 of these patients. Interleukin-8 in BAL and blood samples taken on initial hospital presentation was measured by a sandwich enzyme-linked immunosorbent assay. The mean BAL Interleukin-8 concentration was significantly higher for the patients who subsequently progressed to ARDS than for the non-ARDS group (3·06 [SE 2·64] vs 0·053 [0·010] ng/mL, p=0·0006). There was no difference between the groups in plasma Interleukin-8 (6·23 [2·60] vs 5·12 [2·22] ng/mL, p=0·31). Immunocytochemistry suggested that the alveolar macrophage is an important source of Interleukin-8 at this early stage in ARDS development. This study provides evidence of a relation between the presence of Interleukin-8 in early BAL samples and the development of AR DS. The early appearance of Interleukin-8 in BAL of patients at risk of ARDS may be an important prognostic indicator for the development of the disorder and reinforces the likely importance of neutrophils and the effects of their accumulation and activation in the pathogenesis of many cases of ARDS.

  • Interleukin 8 as a macrophage derived mediator of angiogenesis
    Science, 1992
    Co-Authors: Alisa E Koch, Steven L. Kunkel, Peter J Polverini, Lisa A Harlow, Luisa A Dipietro, Victor M Elner, Susan G Elner, Robert M. Strieter
    Abstract:

    Angiogenic factors produced by monocytes-macrophages are involved in the pathogenesis of chronic inflammatory disorders characterized by persistent angiogenesis. The possibility was tested that Interleukin-8 (IL-8), which is a cytokine that is chemotactic for lymphocytes and neutrophils, is also angiogenic. Human recombinant IL-8 was potently angiogenic when implanted in the rat cornea and induced proliferation and chemotaxis of human umbilical vein endothelial cells. Angiogenic activity present in the conditioned media of inflamed human rheumatoid synovial tissue macrophages or lipopolysaccharide-stimulated blood monocytes was equally blocked by antibodies to either IL-8 or tumor necrosis factor-alpha. An IL-8 antisense oligonucleotide specifically blocked the production of monocyte-induced angiogenic activity. These data suggest a function for macrophage-derived IL-8 in angiogenesis-dependent disorders such as rheumatoid arthritis, tumor growth, and wound repair.

  • kupffer cell derived cytokines induce the synthesis of a leukocyte chemotactic peptide Interleukin 8 in human hepatoma and primary hepatocyte cultures
    Hepatology, 1991
    Co-Authors: Amanda J Thornton, John M Ham, Steven L. Kunkel
    Abstract:

    Communication circuits operating between activated monocytes/macrophages and adjacent hepatocytes in the liver effect important alterations in hepatocyte function. We demonstrate here that primary human hepatocytes and hepatoma cells are able to function as effector cells in the recruitment of inflammatory cells in hepatic disease and inflammatory states by synthesizing a neutrophil/lymphocyte chemotactic factor, Interleukin-8. We have further investigated the possibility that endogenous factors elaborated by activated peripheral blood monocytes and Kupffer cells in the liver are mediators of hepatocyte-derived Interleukin-8 expression. Twenty-four-hour conditioned medium from lipopolysaccharide-stimulated peripheral blood monocytes and nonparenchymal human liver cells enriched for Kupffer cells induced a time-dependent increase in Interleukin-8 messenger RNA levels in SK-hepatoma cells over a 24-hr period, similar to that seen for tumor necrosis factor-alpha or Interleukin-1 beta induction of Interleukin-8 in primary hepatocytes. Exogenously added lipopolysaccharide or recombinant Interleukin-6 had no effect. Cell-associated Interleukin-8 antigen was present in SK-hepatoma and primary hepatocytes that had been incubated with macrophage-conditioned medium, tumor necrosis factor or Interleukin-1 beta. Similarly, neutrophil chemotactic activity was secreted by SK-hepatoma cells, a significant proportion of which could be blocked with Interleukin-8--specific antiserum. Preincubation of macrophage-conditioned medium with neutralizing antibodies to tumor necrosis factor-alpha or Interleukin-1 beta reduced its Interleukin-8 messenger RNA-inducing capacity. Exposure of SK-hepatoma to conditioned medium followed by removal of the stimulus resulted in a rapid down-regulation of Interleukin-8 messenger RNA to 50% of the maximum level within the first hour. These data suggest that products derived from activated Kupffer cells can modulate hepatoma cells and primary hepatocyte Interleukin-8 gene expression. In addition, macrophage/monocyte-derived tumor necrosis factor-alpha and Interleukin-1 beta have major roles in the positive regulatory component of this modulation.

  • regulation of transendothelial neutrophil migration by endogenous Interleukin 8
    Science, 1991
    Co-Authors: Andreas R Huber, Steven L. Kunkel, Robert F Todd, Stephen J Weiss
    Abstract:

    Movement of neutrophils from the bloodstream to inflamed tissue depends on the activation of both the neutrophil and the endothelial cell. Endothelial cells lining the postcapillary venule respond to proinflammatory mediators by expressing adhesion molecules and synthesizing a variety of neutrophil-activating factors. Endothelial cell production of a 77-amino acid variant of Interleukin-8 (IL-8) was found to be a requirement for the invasion of neutrophils through a vessel wall model. IL-8 secreted by cytokine- or lipopolysaccharide-stimulated endothelial cells induced the rapid shedding of neutrophil lectin adhesion molecule-1, the up-regulation of leukocyte beta 2 integrins, and the attachment and transmigration of the neutrophils. Thus, endogenous endothelial IL-8 regulates transvenular traffic during acute inflammatory responses.

Reika Takamatsu - One of the best experts on this subject based on the ideXlab platform.

  • retraction molecular characterization of legionella pneumophila induced Interleukin 8 expression in t cells
    BMC Microbiology, 2011
    Co-Authors: Reika Takamatsu, Naofumi Mukaida, Hiromitsu Teruya, Eriko Takeshima, Chie Ishikawa, Kunihiro Matsumoto, Klaus Heuner, Futoshi Higa, Jiro Fujita, Naoki Mori
    Abstract:

    Article Retracted Retraction After lengthy investigation by the editors, the original article [1] has been retracted because of inappropriate duplication of images from previously published articles. The last author, Naoki Mori takes full responsibility and apologizes for any inconvenience caused. Author details Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan. Division of Control and Prevention of Infectious Diseases, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 9030215, Japan. Transdisciplinary Research Organization for Subtropics and Island Studies, University of the Ryukyus, 1 Senbaru, Nishihara, Okinawa 9030215, Japan. Department of Molecular Biology, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan. Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-0934, Japan. Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, New York 14642, USA. Project group 26 “Nosocomial Infections of the Elderly”, Robert Koch-Institut, 20 Nordufer, Berlin 13353, Germany. Received: 27 January 2011 Accepted: 2 June 2011 Published: 2 June 2011 Reference 1. Takamatsu R, Teruya H, Takeshima E, Ishikawa C, Matsumoto K, Mukaida N, Li J-D, Heuner K, Higa F, Fujita J, Mori N: Molecular characterization of Legionella pneumophila-induced Interleukin-8 expression in T cells. BMC Microbiol 2010, 10:1. doi:10.1186/1471-2180-11-127 Cite this article as: Takamatsu et al.: Retraction: Molecular characterization of Legionella pneumophila-induced Interleukin-8 expression in T cells. BMC Microbiology 2011 11:127. Submit your next manuscript to BioMed Central and take full advantage of: • Convenient online submission • Thorough peer review • No space constraints or color figure charges • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit * Correspondence: n-mori@med.u-ryukyu.ac.jp Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan Full list of author information is available at the end of the article Takamatsu et al. BMC Microbiology 2011, 11:127 http://www.biomedcentral.com/1471-2180/11/127 © 2011 Takamatsu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • molecular characterization of legionella pneumophila induced Interleukin 8 expression in t cells
    BMC Microbiology, 2010
    Co-Authors: Reika Takamatsu, Naofumi Mukaida, Hiromitsu Teruya, Eriko Takeshima, Chie Ishikawa, Kunihiro Matsumoto, Klaus Heuner, Futoshi Higa, Jiro Fujita, Naoki Mori
    Abstract:

    Background Legionella pneumophila is the causative agent of human Legionnaire's disease. During infection, the bacterium invades macrophages and lung epithelial cells, and replicates intracellularly. However, little is known about its interaction with T cells. We investigated the ability of L. pneumophila to infect and stimulate the production of Interleukin-8 (IL-8) in T cells. The objective of this study was to assess whether L. pneumophila interferes with the immune system by interacting and infecting T cells.

Vishva M Dixit - One of the best experts on this subject based on the ideXlab platform.

  • aberrant production of Interleukin 8 and thrombospondin 1 by psoriatic keratinocytes mediates angiogenesis
    American Journal of Pathology, 1994
    Co-Authors: Brian J Nickoloff, Raj S Mitra, James Varani, Vishva M Dixit, Peter J Polverini
    Abstract:

    Psoriasis is a common inherited skin disease that is characterized by hyperproliferation of epidermal keratinocytes and excessive dermal angiogenesis. A growing body of evidence supports a key pathogenetic role for activated keratinocytes in the angiogenic response that accompanies psoriasis. We investigated the role of psoriatic epidermis in the aberrant expression of angiogenesis by examining the ability of pure populations of multipassaged keratinocytes obtained from the skin of normal individuals and psoriatic patients to induce angiogenesis in vivo in the rat corneal bioassay and endothelial cell chemotaxis in vitro. Media conditioned by keratinocytes from psoriatic patients, including both symptomless skin and psoriatic plaques, induced vigorous angiogenic responses in over 90% of corneas tested and potently stimulated directional migration of capillary endothelial cells in vitro. In contrast, conditioned medium from normal keratinocyte cultures was weakly positive in less than 10% of corneas assayed and failed to stimulate endothelial cell chemotaxis. Furthermore, keratinocytes from psoriatic skin exhibited a 10- to 20-fold increase in Interleukin-8 production and a seven-fold reduction in thrombospondin-1 production. The angiogenic activity present in keratinocyte-conditioned media from psoriatic patients was suppressed by adding either highly purified thrombospondin-1 (125 ng) or following the addition of either normal keratinocyte-conditioned media or neutralizing Interleukin-8 antibody. We conclude that psoriatic keratinocytes are phenotypically different from normal keratinocytes with respect to their angiogenic capacity and that this aberrant phenotype is attributable to a defect in the overproduction of Interleukin-8 and a deficiency in the production of the angiogenesis inhibitor thrombospondin-1.

  • cellular localization of Interleukin 8 and its inducer tumor necrosis factor alpha in psoriasis
    American Journal of Pathology, 1991
    Co-Authors: Brian J Nickoloff, Steven L. Kunkel, Vishva M Dixit, Gerald D Karabin, Jonathan N W N Barker, Christopher E M Griffiths, Vidya Sarma, R S Mitra, James T Elder
    Abstract:

    The importance of immunologic mechanisms in psoriasis has been deduced from the ability of immunosuppressive therapies to ameliorate this common and chronic skin disease. Certainly the histology of psoriatic lesions suggests a dialogue between the hyperplastic keratinocytes and infiltrating T lymphocytes and macrophages. To begin dissecting the cytokine network involved in the pathophysiology of psoriasis, the location, in both epidermal and dermal compartments, of tumor necrosis factor-alpha, Interleukin-8, intercellular adhesion molecule-1, and transforming growth factor-alpha at the protein and/or mRNA levels were identified. Tumor necrosis factor-alpha was selected as a potentially key regulatory cytokine, first because it induces cultured keratinocyte Interleukin-8, intercellular adhesion molecule-1, and transforming growth factor-alpha production, and second because intercellular adhesion molecule-1 expression by keratinocytes in psoriatic epidermis had been identified previously. Using immunohistochemical localization, tumor necrosis factor-alpha was identified in 12 psoriatic lesions as intense and diffuse expression by dermal dendrocytes (macrophages) in the papillary dermis (without significant staining of endothelial cells, mast cells, or dermal Langerhans cells), and focally by keratinocytes and intraepidermal Langerhans cells. Functional interaction between the dermal dendrocytes and keratinocytes was suggested by the presence of Interleukin-8 expression of suprabasal keratinocytes immediately above the tumor necrosis factor-alpha-positive dermal dendrocytes. Interleukin-8 mRNA and transforming growth factor-alpha mRNA were detectable in the epidermal roof of psoriatic lesions, but neither was detectable at the protein or mRNA levels in any normal skin specimens. Treatment of cultured human keratinocytes with phorbol ester (which experimentally produces psoriasiform changes on mouse skin) or tumor necrosis factor-alpha also increased Interleukin-8 and transforming growth factor-alpha mRNAs. Further elucidation of the cellular and molecular basis for the genesis and evolution of psoriasis will provide the framework for a better evaluation of the cause and treatment of this skin disease.