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Tryptophan Metabolites, Cytokines, and Fatty Acid Binding Protein 2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
肌痛性腦脊髓炎/慢性疲勞綜合征中的色氨酸代謝物、細胞因子和脂肪酸結(jié)合蛋白 

Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) differ for triggers, mode of start, associated symptoms, evolution, and biochemical traits. Therefore, serious attempts are underway to partition them into subgroups useful for a personalized medicine approach to the disease. Here, we investigated clinical and biochemical traits in 40 ME/CFS patients and 40 sex- and age-matched healthy controls. Particularly, we analyzed serum levels of some cytokines, Fatty Acid Binding Protein 2 (FAPB-2), tryptophan, and some of its metabolites via serotonin and kynurenine. ME/CFS patients were heterogeneous for genetic background, trigger, start mode, symptoms, and evolution. ME/CFS patients had higher levels of IL-17A (p = 0.018), FABP-2 (p = 0.002), and 3-hydroxykynurenine (p = 0.037) and lower levels of kynurenine (p = 0.012) and serotonin (p = 0.045) than controls. Changes in kynurenine and 3-hydroxykynurenine were associated with increased kynurenic acid/kynurenine and 3-hydroxykynurenine/kynurenine ratios, indirect measures of kynurenine aminotransferases and kynurenine 3-monooxygenase enzymatic activities, respectively. No correlation was found among cytokines, FABP-2, and tryptophan metabolites, suggesting that inflammation, anomalies of the intestinal barrier, and changes of tryptophan metabolism may be independently associated with the pathogenesis of the disease. Interestingly, patients with the start of the disease after infection showed lower levels of kynurenine (p = 0.034) than those not starting after an infection. Changes in tryptophan metabolites and increased IL-17A levels in ME/CFS could both be compatible with anomalies in the sphere of energy metabolism. Overall, clinical traits together with serum biomarkers related to inflammation, intestine function, and tryptophan metabolism deserve to be further considered for the development of personalized medicine strategies for ME/CFS.

高效搖瓶5L

肌痛性腦脊髓炎/慢性疲勞綜合征 (ME/CFS) 患者的觸發(fā)因素、開始方式、相關(guān)癥狀、演變和生化特征各不相同。因此，正在認真嘗試將它們劃分為對疾病的個性化醫(yī)學方法有用的亞組。在這里，我們調(diào)查了 40 名 ME/CFS 患者和 40 名性別和年齡匹配的健康對照的臨床和生化特征。特別是，我們通過血清素和犬尿氨酸分析了一些細胞因子、脂肪酸結(jié)合蛋白 2 (FAPB-2)、色氨酸及其一些代謝物的血清水平。ME/CFS 患者在遺傳背景、觸發(fā)因素、開始模式、癥狀和進化方面具有異質(zhì)性。ME/CFS 患者的 IL-17A ( p = 0.018)、FABP-2 ( p= 0.002) 和 3-羥基犬尿氨酸 ( p = 0.037)，犬尿氨酸 ( p = 0.012) 和血清素 ( p = 0.045) 水平低于對照組。犬尿氨酸和 3-羥基犬尿氨酸的變化分別與犬尿氨酸/犬尿氨酸和 3-羥基犬尿氨酸/犬尿氨酸比率的增加、犬尿氨酸氨基轉(zhuǎn)移酶和犬尿氨酸 3-單加氧酶酶活性的間接測量相關(guān)。細胞因子、FABP-2和色氨酸代謝產(chǎn)物之間沒有發(fā)現(xiàn)相關(guān)性，表明炎癥、腸道屏障異常和色氨酸代謝變化可能與該疾病的發(fā)病機制獨立相關(guān)。有趣的是，感染后發(fā)病的患者表現(xiàn)出較低水平的犬尿氨酸（p= 0.034）比感染后沒有開始的那些。ME/CFS 中色氨酸代謝物的變化和 IL-17A 水平的增加都可能與能量代謝領(lǐng)域的異常相容。總體而言，臨床特征以及與炎癥、腸道功能和色氨酸代謝相關(guān)的血清生物標志物值得進一步考慮，以開發(fā) ME/CFS 的個性化醫(yī)療策略。

We found substantial heterogeneity among patients with ME/CFS; however, in spite of many differences, patients shared traits of possible significance for the explanation of their symptoms. Our data suggest that clinical aspects and serum biomarkers related to inflammation, intestinal function, and tryptophan metabolism deserve to be further investigated, both for the identification of ME/CFS subtypes and as a way towards a personalized patient care approach. This implies, on one side, the use of larger patient samples and, on the other side, the use of all modern medical tools for the diagnosis and treatment of individual cases.

細胞轉(zhuǎn)瓶2L

我們發(fā)現(xiàn) ME/CFS 患者之間存在很大的異質(zhì)性；然而，盡管存在許多差異，但患者的共同特征對于解釋他們的癥狀可能具有重要意義。我們的數(shù)據(jù)表明，與炎癥、腸道功能和色氨酸代謝相關(guān)的臨床方面和血清生物標志物值得進一步研究，以識別 ME/CFS 亞型，并作為實現(xiàn)個性化患者護理方法的一種方式。這意味著，一方面，使用更大的患者樣本，另一方面，使用所有現(xiàn)代醫(yī)療工具來診斷和治療個別病例。

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關(guān)鍵詞：ME/CFS heterogeneity,cytokines,intestinal permeability,tryptophan metabolism,kynurenine pathway,3-hydroxykynurenine,kynurenine,serotonin,biomarkers,personalized medicine,
                       ME/CFS 異質(zhì)性,細胞因子,腸道通透性,色氨酸代謝,犬尿氨酸途徑,3-羥基犬尿氨酸,犬尿氨酸,血清素,生物標志物,個性化醫(yī)療