Modulation of IL-6 Production of IL-1 Activity by Keratinocyte-Fibroblast Interaction View Full Text


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Article Info

DATE

1993-09

AUTHORS

I Boxman, C Löwik, L Aarden, M Ponec

ABSTRACT

The present study was undertaken to investigate whether modulation of interleukin-6 and interleukin-1 production occurs owing to keratinocyte-fibroblast interaction. Normal human keratinocytes or squamous carcinoma cells were cultured either alone or in the presence of human foreskin fibroblasts or murine 3T3 cells. All cells tested produced interleukin-6, and interleukin-6 levels were markedly increased when normal or malignant keratinocytes were co-cultured with fibroblasts. The bioassay (species independent) and enzyme-linked immunosorbent assay (specific for human interleukin-6) together with use of complementary DNA probes specific for human or murine interleukin-6 revealed that fibroblasts are responsible for increased interleukin-6 levels. Moreover, interleukin-6 levels were increased when fibroblasts were cultured in conditioned media derived from normal human keratinocytes and squamous carcinoma cells-4 cultures. Interleukin-1 alpha secreted by normal human keratinocytes and squamous carcinoma cells-4 cells was mainly responsible for the increased interleukin-6 production in fibroblasts. Although interleukin-1 activity increased linearly with the incubation time in squamous carcinoma cells-4 monocultures, interleukin-1 activity was low and remained unchanged in squamous carcinoma cells-4/3T3 co-cultures. Low interleukin-1 activity was most probably not due to inhibition of interleukin-1 alpha production in squamous carcinoma cells-4/3T3 co-cultures because interleukin-1 alpha messenger RNA expression in squamous carcinoma cells-4 cells remained unchanged in the presence of 3T3 cells. Furthermore, when 3T3 cells were incubated in conditioned medium derived from squamous carcinoma cells-4 cells, high interleukin-1 activity decreased to an undetectable level, suggesting that fibroblasts are involved in the suppression of interleukin-1 activity. The remaining interleukin-1 activity, however, was sufficient for maximal induction of interleukin-6 production in fibroblasts. These results suggest that the interaction between epithelial and mesenchymal cells is at least partly initiated by interleukin-1 alpha secreted by the activated epithelial cell during skin injury or tumor invasion. Interleukin-1 in turn can induce modulation of the synthesis of various pro-inflammatory mediators and proteases in surrounding fibroblasts. An enhanced proteolytic activity and/or a possible induced production of an interleukin-1 inhibitor in fibroblasts and/or a receptor-mediated interleukin-1 consumption by fibroblasts will cause a decrease in interleukin-1 activity and thus exert a negative feedback. More... »

PAGES

316-324

References to SciGraph publications

  • 1991-11. In Vitro Reconstitution of Skin: Fibroblasts Facilitate Keratinocyte Growth and Differentiation on Acellular Reticular Dermis in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1991-05. Production of Interleukin-1 and Interleukin-6 by Human Keratinocytes and Squamous Cell Carcinoma Cell Lines in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1990-06. Interleukin-6: Molecular Pathophysiology in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1992-05. Co-Culture of Human Keratinocytes on Post-Mitotic Human Dermal Fibroblast Feeder Cells: Production of Large Amounts of Interleukin 6 in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1991-04. Regulation of Epidermal Cell Interleukin-6 production by UV Light and Corticosteroids in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1990-06. The Activated Keratinocyte: A Model for Inducible Cytokine Production by Non-Bone-Marrow-Derived Cells in Cutaneous Inflammatory and Immune Responses in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1992-09. Human Dermal Fibroblast Interleukin-1 Receptor Antagonist (IL-1ra) and Interleukin-1β (IL-1β) mRNA and Protein Are Co-Stimulated by Phorbol Ester: Implication for a Homeostatic Mechanism in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1990-11. Interleukin-1 in Human Skin: Dysregulation in Psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1992-01. Interleukin-1 Receptor antagonist Production by Human Keratinocytes in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • 1992-02. Regulation of Parathyroid Hormonelike Protein Production in Cultured Normal and Malignant Keratinocytes in JOURNAL OF INVESTIGATIVE DERMATOLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1111/1523-1747.ep12365474

    DOI

    http://dx.doi.org/10.1111/1523-1747.ep12365474

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/8370968


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    59 schema:description The present study was undertaken to investigate whether modulation of interleukin-6 and interleukin-1 production occurs owing to keratinocyte-fibroblast interaction. Normal human keratinocytes or squamous carcinoma cells were cultured either alone or in the presence of human foreskin fibroblasts or murine 3T3 cells. All cells tested produced interleukin-6, and interleukin-6 levels were markedly increased when normal or malignant keratinocytes were co-cultured with fibroblasts. The bioassay (species independent) and enzyme-linked immunosorbent assay (specific for human interleukin-6) together with use of complementary DNA probes specific for human or murine interleukin-6 revealed that fibroblasts are responsible for increased interleukin-6 levels. Moreover, interleukin-6 levels were increased when fibroblasts were cultured in conditioned media derived from normal human keratinocytes and squamous carcinoma cells-4 cultures. Interleukin-1 alpha secreted by normal human keratinocytes and squamous carcinoma cells-4 cells was mainly responsible for the increased interleukin-6 production in fibroblasts. Although interleukin-1 activity increased linearly with the incubation time in squamous carcinoma cells-4 monocultures, interleukin-1 activity was low and remained unchanged in squamous carcinoma cells-4/3T3 co-cultures. Low interleukin-1 activity was most probably not due to inhibition of interleukin-1 alpha production in squamous carcinoma cells-4/3T3 co-cultures because interleukin-1 alpha messenger RNA expression in squamous carcinoma cells-4 cells remained unchanged in the presence of 3T3 cells. Furthermore, when 3T3 cells were incubated in conditioned medium derived from squamous carcinoma cells-4 cells, high interleukin-1 activity decreased to an undetectable level, suggesting that fibroblasts are involved in the suppression of interleukin-1 activity. The remaining interleukin-1 activity, however, was sufficient for maximal induction of interleukin-6 production in fibroblasts. These results suggest that the interaction between epithelial and mesenchymal cells is at least partly initiated by interleukin-1 alpha secreted by the activated epithelial cell during skin injury or tumor invasion. Interleukin-1 in turn can induce modulation of the synthesis of various pro-inflammatory mediators and proteases in surrounding fibroblasts. An enhanced proteolytic activity and/or a possible induced production of an interleukin-1 inhibitor in fibroblasts and/or a receptor-mediated interleukin-1 consumption by fibroblasts will cause a decrease in interleukin-1 activity and thus exert a negative feedback.
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