1994FEBS LettersRequires access

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

Jean‐Marie Derocq, Michel Ségui, C. Poinot-Chaze, A Minty, Daniel Caput, Pascual Ferrara, Pierre Casellas

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Abstract

Interleukin-13 (IL-13) is a recently described human lymphokine which is produced by activated T-cells. Its effect on the production of IL-6 by normal keratinocytes and keratinocyte cell lines of human origin was studied and compared to that of IL-4. IL-13, similarly to IL-4, stimulated IL-6 expression by these cells in a dose- and time-dependent manner. Contamination with endotoxin was excluded by the use of polymyxin B and heat-inactivated cytokines. Further, we showed that IL-13, like IL-4, not only stimulated IL-6 production but also was able to induce overexpression of this cytokine in response to an inflammatory signal such as lipopolysaccharide (LPS). In a previous study, we demonstrated that IL-13, by inhibiting IL-6 and other cytokines produced by monocytes, exhibited an 'anti-inflammatory profile' comparable to that displayed by IL-4. In contrast, we show here that IL-13, by stimulating IL-6 production by keratinocytes, may favour the installation of an inflammatory process at a local level and, here again, it acted like IL-4. Therefore, according to the type of target cell these two 'TH2 type' cytokines induce similar opposing effects on IL-6 production and are likely to be important cytokines in the regulation of inflammation at both systemic and local levels.

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What this paper is about

Interleukin-13 (IL-13) is a recently described human lymphokine which is produced by activated T-cells. Its effect on the production of IL-6 by normal keratinocytes and keratinocyte cell lines of human origin was studied and compared to that of IL-4. IL-13, similarly to IL-4, stimulated IL-6 expression by these cells in a dose- and time-dependent manner. Contamination with endotoxin was excluded by the use of polymyxin B and heat-inactivated cytokines. Further, we showed that IL-13, like IL-4, not only stimulated IL-6 production but also was able to induce overexpression of this cytokine in response to an inflammatory signal such as lipopolysaccharide (LPS). In a previous study, we demonstrated that IL-13, by inhibiting IL-6 and other cytokines produced by monocytes, exhibited an 'anti-inflammatory profile' comparable to that displayed by IL-4. In contrast, we show here that IL-13, by stimulating IL-6 production by keratinocytes, may favour the installation of an inflammatory process at a local level and, here again, it acted like IL-4. Therefore, according to the type of target cell these two 'TH2 type' cytokines induce similar opposing effects on IL-6 production and are likely to be important cytokines in the regulation of inflammation at both systemic and local levels.

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Available abstract

Interleukin-13 (IL-13) is a recently described human lymphokine which is produced by activated T-cells. Its effect on the production of IL-6 by normal keratinocytes and keratinocyte cell lines of human origin was studied and compared to that of IL-4. IL-13, similarly to IL-4, stimulated IL-6 expression by these cells in a dose- and time-dependent manner. Contamination with endotoxin was excluded by the use of polymyxin B and heat-inactivated cytokines. Further, we showed that IL-13, like IL-4, not only stimulated IL-6 production but also was able to induce overexpression of this cytokine in response to an inflammatory signal such as lipopolysaccharide (LPS). In a previous study, we demonstrated that IL-13, by inhibiting IL-6 and other cytokines produced by monocytes, exhibited an 'anti-inflammatory profile' comparable to that displayed by IL-4. In contrast, we show here that IL-13, by stimulating IL-6 production by keratinocytes, may favour the installation of an inflammatory process at a local level and, here again, it acted like IL-4. Therefore, according to the type of target cell these two 'TH2 type' cytokines induce similar opposing effects on IL-6 production and are likely to be important cytokines in the regulation of inflammation at both systemic and local levels.

Key concepts: Interleukin 20, Cytokine, Lymphokine, Interleukin, Lipopolysaccharide, Keratinocyte, Interleukin 19, Immunology

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