Department of Biology, São Paulo State University (UNESP), São José do Rio Preto, São Paulo 15054-000, Brazil.
Graduate Program in Animal Biology, Universidade Estadual Paulista (UNESP), São José do Rio Preto, São Paulo 15054-000, Brazil.
J Photochem Photobiol B. 2018 Mar;180:109-117. doi: 10.1016/j.jphotobiol.2018.01.022. Epub 2018 Jan 31.
Ultra-Violet (UV) radiation is a stressor of the immune system and causes DNA damage. Leukocytes can change in response to environmental changes in anurans, making them an important biomarker of stressful situations. The initial barrier against UV in ectothermic animals is melanin-containing cells in skin and in their internal organs. Here, we tested the effects of UV exposure on immune cells and DNA integrity in pigmented and non-pigmented tadpoles of Lithobates catesbeianus. We used an inflammation model with lipopolysaccharide (LPS) of Escherichia coli to test synergic effects of UV and LPS. We tested the following hypotheses: 1) DNA damage caused by UV will be more pronounced in non-pigmented than in pigmented animals; 2) LPS increases leukocytes in both pigmented and non-pigmented animals by systemic inflammation; 3) The combined LPS and UV exposure will decrease the number of leukocytes. We found that the frequency of immune cells differed between pigmented and non-pigmented tadpoles. UV exposure increased mast cells and DNA damage in erythrocytes in both pigmented and non-pigmented tadpoles, while leukocytes decreased after UV exposure. Non-pigmented tadpoles experienced DNA damage and a lower lymphocyte count earlier than pigmented tadpoles. UV altered immune cells likely as a consequence of local and systemic inflammation. These alterations were less severe in pigmented than in non-pigmented animals. UV and LPS increased internal melanin in pigmented tadpoles, which were correlated with DNA damage and leukocytes. Here, we described for the first time the effects of UV and LPS in immune cells of pigmented and non-pigmented tadpoles. In addition, we demonstrated that internal melanin in tadpoles help in these defenses, since leukocyte responses were faster in non-pigmented animals, supporting the hypothesis that melanin is involved in the initial innate immune response.
紫外线(UV)辐射是免疫系统的应激源,会导致 DNA 损伤。白细胞可以对外界环境的变化做出反应,因此成为应激情况的重要生物标志物。在变温动物中,最初抵御 UV 的屏障是皮肤和内部器官中含有黑色素的细胞。在这里,我们测试了 UV 暴露对 Lithobates catesbeianus 色素和非色素蝌蚪免疫细胞和 DNA 完整性的影响。我们使用大肠杆菌脂多糖(LPS)的炎症模型来测试 UV 和 LPS 的协同作用。我们提出了以下假设:1)UV 引起的 DNA 损伤在非色素动物中比在色素动物中更为明显;2)LPS 通过全身炎症增加色素和非色素动物中的白细胞;3)LPS 和 UV 联合暴露会减少白细胞数量。我们发现,有色素和无色素蝌蚪之间的免疫细胞频率存在差异。UV 暴露增加了有色素和无色素蝌蚪的肥大细胞和红细胞中的 DNA 损伤,而 UV 暴露后白细胞数量减少。非色素蝌蚪比色素蝌蚪更早经历 DNA 损伤和淋巴细胞计数降低。UV 可能会改变免疫细胞,这是局部和全身炎症的结果。与非色素动物相比,色素动物的这些变化不太严重。UV 和 LPS 增加了有色素蝌蚪的内部黑色素,这与 DNA 损伤和白细胞有关。在这里,我们首次描述了 UV 和 LPS 对色素和非色素蝌蚪免疫细胞的影响。此外,我们证明了蝌蚪体内的黑色素有助于这些防御,因为非色素动物的白细胞反应更快,这支持了黑色素参与初始先天免疫反应的假设。