Kochevar I E, Moran M, Granstein R D
Wellman Laboratories of Photomedicine, Department of Dermatology, Massachusetts General Hospital, Boston 02114.
J Invest Dermatol. 1994 Dec;103(6):797-800. doi: 10.1111/1523-1747.ep12413286.
Chronic exposure of human or murine skin to ultraviolet B (UVB) radiation alters dermal extracellular matrix composition and increases the number of mast cells and inflammatory cells. Experiments were designed to test the possible role of UVB-induced tumor necrosis factor-alpha in these photoaging changes based on reports that C3H/HeN, but not C3H/HeJ or Balb/c mice, produce excess TNF-alpha in response to UVB exposure. Pigmented C3H/HeN and C3H/HeJ strains were exposed to a total of 75 J/cm2 of UVB radiation, and unpigmented Balb/c mice were exposed to 19 J/cm2. The UVB-induced increases in collagen, glycosaminoglycans, and neutrophil number were similar or the same in all three strains. The elastin increase was greater in C3H/HeJ than in C3H/HeN mice. The most striking difference between the strains was a 7.7-fold UVB-induced increase in mast cells in C3H/HeN mice compared to no increase in irradiated C3H/HeJ mice and a 2.3-fold increase in Balb/c mice. These results suggest that excess TNF-alpha (or other mediator) produced in C3H/HeN skin (but not C3H/HeJ skin) in response to UVB exposure is involved in the mast cell increase and partial inhibition of elastin increase, but that neither these mediators nor mast cell products are important mediators for the chronic UVB-induced increases in neutrophils, glycosaminoglycans, and collagen. When a possible source of the excess TNF-alpha was investigated, it was found that isolated epidermal cells from all three strains produced increases in TNF-alpha in response to UVB radiation. These results, as well as the previous results showing differences between these strains in UVB-induced effects on cutaneous immune function, are consistent with a model in which UVB-induced mediators from the epidermis stimulate another cell type to produce excess TNF-alpha (and other mediators) in the C3H/HeN but not C3H/HeJ or Balb/c mice.
人体或鼠类皮肤长期暴露于紫外线B（UVB）辐射会改变真皮细胞外基质的组成，并增加肥大细胞和炎症细胞的数量。有报道称，C3H/HeN小鼠而非C3H/HeJ或Balb/c小鼠在暴露于UVB后会产生过量的肿瘤坏死因子-α（TNF-α），基于此，设计了实验来测试UVB诱导的TNF-α在这些光老化变化中可能发挥的作用。将有色素的C3H/HeN和C3H/HeJ品系暴露于总量为75 J/cm²的UVB辐射下，将无色素的Balb/c小鼠暴露于19 J/cm²的UVB辐射下。在所有三个品系中，UVB诱导的胶原蛋白、糖胺聚糖和中性粒细胞数量的增加相似或相同。C3H/HeJ小鼠中弹性蛋白的增加幅度大于C3H/HeN小鼠。品系之间最显著的差异是，与未受辐射的C3H/HeJ小鼠中肥大细胞无增加以及Balb/c小鼠中肥大细胞增加2.3倍相比，C3H/HeN小鼠中肥大细胞在UVB诱导下增加了7.7倍。这些结果表明，C3H/HeN皮肤（而非C3H/HeJ皮肤）在暴露于UVB后产生的过量TNF-α（或其他介质）与肥大细胞增加以及弹性蛋白增加的部分抑制有关，但这些介质和肥大细胞产物都不是慢性UVB诱导的中性粒细胞、糖胺聚糖和胶原蛋白增加的重要介质。当对过量TNF-α的可能来源进行研究时，发现来自所有三个品系的分离表皮细胞在暴露于UVB辐射后TNF-α均增加。这些结果，以及之前显示这些品系在UVB诱导的皮肤免疫功能影响方面存在差异的结果，与一个模型一致，即UVB诱导的来自表皮的介质刺激另一种细胞类型在C3H/HeN小鼠而非C3H/HeJ或Balb/c小鼠中产生过量的TNF-α（和其他介质）。
