The Division of Clinical Cancer Epidemiology, Department of Oncology at the Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, 413 90 Gothenburg, Sweden.
Department of Infectious Diseases at the Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, 413 90 Gothenburg, Sweden.
Int J Mol Sci. 2021 Dec 31;23(1):439. doi: 10.3390/ijms23010439.
Dietary fiber is considered a strong intestinal protector, but we do not know whether dietary fiber protects against the long-lasting mucosal damage caused by ionizing radiation. To evaluate whether a fiber-rich diet can ameliorate the long-lasting pathophysiological hallmarks of the irradiated mucosa, C57BL/6J mice on a fiber-rich bioprocessed oat bran diet or a fiber-free diet received 32 Gray in four fractions to the distal colorectum using a linear accelerator and continued on the diets for one, six or 18 weeks. We quantified degenerating crypts, crypt fission, cell proliferation, crypt survival, macrophage density and bacterial infiltration. Crypt loss through crypt degeneration only occurred in the irradiated mice. Initially, it was most frequent in the fiber-deprived group but declined to levels similar to the fiber-consuming group by 18 weeks. The fiber-consuming group had a fast response to irradiation, with crypt fission for growth or healing peaking already at one week post-irradiation, while crypt fission in the fiber-deprived group peaked at six weeks. A fiber-rich diet allowed for a more intense crypt cell proliferation, but the recovery of crypts was eventually lost by 18 weeks. Bacterial infiltration was a late phenomenon, evident in the fiber-deprived animals and intensified manyfold after irradiation. Bacterial infiltration also coincided with a specific pro-inflammatory serum cytokine profile. In contrast, mice on a fiber-rich diet were completely protected from irradiation-induced bacterial infiltration and exhibited a similar serum cytokine profile as sham-irradiated mice on a fiber-rich diet. Our findings provide ample evidence that dietary fiber consumption modifies the onset, timing and intensity of radiation-induced pathophysiological processes in the intestinal mucosa. However, we need more knowledge, not least from clinical studies, before this finding can be introduced to a new and refined clinical practice.
膳食纤维被认为是一种强有力的肠道保护剂，但我们并不知道膳食纤维是否能预防电离辐射引起的持久黏膜损伤。为了评估富含膳食纤维的饮食是否能改善辐射后肠黏膜的持久病理生理特征，我们用线性加速器将富含生物加工燕麦麸膳食纤维的饮食或无膳食纤维饮食的 C57BL/6J 小鼠分为四组，对其远端结肠进行 32 Gray 的照射，然后继续喂食上述两种饮食 1、6 或 18 周。我们对退化隐窝、隐窝分裂、细胞增殖、隐窝存活、巨噬细胞密度和细菌渗透进行了量化分析。只有接受辐射的小鼠才会出现隐窝退化导致的隐窝丢失。最初，这种情况在无膳食纤维组中最为常见，但到 18 周时，其频率已降至与膳食纤维组相似的水平。膳食纤维组对辐射的反应较快，在辐射后 1 周时，用于生长或修复的隐窝分裂达到峰值，而无膳食纤维组在 6 周时达到峰值。富含膳食纤维的饮食可促进隐窝细胞的强烈增殖，但到 18 周时，隐窝的恢复最终丢失。细菌渗透是一个迟发现象，在无膳食纤维组动物中明显，且在辐射后呈多倍增加。细菌渗透也与特定的促炎血清细胞因子谱相关。相比之下，富含膳食纤维的饮食可使小鼠完全免受辐射引起的细菌渗透的影响，且其血清细胞因子谱与接受富含膳食纤维饮食的假照射小鼠相似。我们的研究结果充分证明，膳食纤维的摄入可改变辐射诱导的肠黏膜病理生理过程的发生、时间和强度。然而，在这一发现能够被引入到新的、更精细的临床实践之前，我们还需要更多的知识，尤其是来自临床研究的知识。
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