The extent of lymphocytic infiltration between the metastatic nodule and hepatic parenchyma may reflect host defensive activity in the liver and is closely related to prognosis in patients who underwent hepatic resection for liver metastases from colorectal cancer.

When we previously examined the participation of local expression of interleukin-10 (IL-10) and tumor necrosis factor-α (TNFα) in wound healing of an intestinal anastomosis under septic conditions in mice, we found that IL-10 and TNFα expressions were markedly enhanced around the anastomosis and that wound healing was impaired in this animal model. The purpose of the present study was to investigate the combined effect of IL-10 on proliferation and remodeling of the extracellular matrix (ECM) of cultured human skin fibroblasts. Human skin fibroblasts were cultured for 48 h with IL-10 and/or TNFα at various concentrations, then the proliferation rates were determined using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. The concentration of transforming growth factor-β1 (TGFβ1) in cell culture supernatants was measured by enzyme-linked immunosorbent assay, and type I collagen protein and matrix metalloproteinase-I (MMP-I) were detected by indirect immunofluorescence in cultured cells incubated for 48 h with 10 ng/ml of IL-10 and/or 10 ng/ml of TNFα. IL-10 itself had no effect on fibroblast proliferation, but reduced TNFα-induced fibroblast proliferation. The concentration of TGFβ1 in cell culture supernatants was significantly lower in the presence of TNFα and IL-10 than in the presence of TNFα alone. Immunolabeling of fibroblasts for type I collagen protein was decreased in cells incubated with IL-10 and/or TNFα compared to controls. MMP-I immunolabeling was increased in cells incubated with IL-10, IL-10 and TNFα compared to control and cells incubated with TNFα. It is suggested that IL-10 is an inhibitory factor for the remodeling of the ECM during wound healing.

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