P1229 马拉色菌在溃疡性结肠炎患者中的作用和特定环境适应性

S Shin Shin, Y J Cho, J Yang, H K Kim, P Rintarhat, M Park, K Lagree, D M Underhill, C S Yang, J M Moon, J Seo, K Kim, W H Jung, C H Choi
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DNA was extracted from these lavage samples, and fungal isolation was conducted using PCR amplification with ITS4 and ITS5 primers. Comprehensive analysis and comparison of the genomes, transcriptomes, and virulence between M. globosa gut isolates and those of M. globosa strains isolated from the skin were performed. To determine the contribution of M. globosa gut isolates to exacerbating inflammation, 1107 fungal cells were orally gavaged to DSS-induced colitis mouse model for three days. Results Total 56 and 11 intestinal water-lavage samples from 29 UC patients and 11 HT were obtained respectively. The α- and b-diversities of mycobiota showed no significant differences between the groups, patients with UC vs. HT or the sites with inflammation vs. non-inflammation of the patient with UC. 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引用次数: 0

摘要

背景 越来越多的证据表明,肠道真菌微生物群(mycobiota)在炎症性肠病的发病过程中发挥着重要作用。我们的目的是直接从溃疡性结肠炎(UC)患者的肠道粘膜表面分离出马拉色菌菌株,并将其基因组和毒力与从人体皮肤中分离出的同种真菌进行比较研究。方法 分别从溃疡性结肠炎患者有炎症和无炎症的结肠部位采集粘膜灌洗样本。健康人(HT)的样本采集方式与 UC 患者的乙状结肠或降结肠样本相同。在我们之前的工作中,我们从 HT 身上采集了皮肤样本。从这些灌洗样本中提取 DNA,并使用 ITS4 和 ITS5 引物进行 PCR 扩增,分离真菌。我们对肠道分离出的球孢霉和从皮肤分离出的球孢霉菌株的基因组、转录组和毒力进行了综合分析和比较。为了确定球孢霉肠道分离株对加剧炎症的作用,对DSS诱导的结肠炎小鼠模型进行了为期三天的口服灌胃,共灌胃1107个真菌细胞。结果 从 29 名 UC 患者和 11 名 HT 患者中分别获得了 56 份和 11 份肠道水-粪便样本。在 UC 患者与 HT 患者、UC 患者的炎症部位与非炎症部位之间,霉菌生物群的 α 和 b 多样性无显著差异。马拉色菌是所有样本中第五个最常发现的真菌属,从 UC 和 HT 患者身上分离出的活真菌菌株分别属于 28 个和 7 个不同的菌种。在有炎症的肠道粘膜表面,UC 患者的球孢子菌和限制型球孢子菌的频率往往高于 HT 患者。全基因组测序显示,肠道分离的球孢子菌和皮肤分离的球孢子菌没有特定的基因组特征。然而,在不同的氧气浓度下,肠道分离的球孢霉菌比皮肤分离的球孢霉菌更容易受到高浓度氧气的影响。在小鼠模型中,肠道分离的球孢霉菌表现出更明显的DSS诱导的结肠炎恶化和炎性细胞因子(包括TNF-a、IL-6、IL-12p40、IL-1b和IL-18)产生的升高,而皮肤分离的球孢霉菌与阴性对照相比没有差异(图)。结论 我们的数据揭示了球孢霉菌在 UC 发病机制中的关键作用,强调了生态位特异性适应对该真菌毒力的潜在影响。这些发现为了解肠道真菌生物群成员与宿主健康之间复杂的相互作用提供了重要见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
P1229 The Role and Niche-Specific Adaptation of Malassezia in patients with Ulcerative colitis
Background Accumulating evidence has underscored the role of gut fungal microbiota (mycobiota) in the development of inflammatory bowel disease. We aimed to isolate a Malassezia strain directly from the human intestine mucosal surface from the patients with ulcerative colitis (UC) and investigated its genome and virulence in comparison with the same fungal species isolated from the human skin. Methods Mucosal lavage samples were collected separately from colonic areas with and without inflammation in patients with UC. Samples from healthy individuals (HT) were obtained in the same manner as from patients with UC at sigmoid or descending colon. Skin samples were taken from HT in our previous work. DNA was extracted from these lavage samples, and fungal isolation was conducted using PCR amplification with ITS4 and ITS5 primers. Comprehensive analysis and comparison of the genomes, transcriptomes, and virulence between M. globosa gut isolates and those of M. globosa strains isolated from the skin were performed. To determine the contribution of M. globosa gut isolates to exacerbating inflammation, 1107 fungal cells were orally gavaged to DSS-induced colitis mouse model for three days. Results Total 56 and 11 intestinal water-lavage samples from 29 UC patients and 11 HT were obtained respectively. The α- and b-diversities of mycobiota showed no significant differences between the groups, patients with UC vs. HT or the sites with inflammation vs. non-inflammation of the patient with UC. Malassezia was the fifth most frequently found fungal genus throughout the samples, and live fungal strains belong to 28 and 7 different species were isolated from the patients with UC and HT, respectively. The patients with UC tend to have higher frequency of M. globosa and M. restricta than HT in their gut mucosal surface with inflammation. Whole genome sequencing showed no specific genomic characteristics between gut-isolated M. globosa and skin-isolated M. globosa. However, gut-isolated M. globosa were suffered more from the higher oxygen levels than the skin isolates in different oxygen concentrations. In a mouse model, gut-isolated M. globosa exhibited a more pronounced exacerbation of DSS-induced colitis and elevated production of inflammatory cytokines, including TNF-a, IL-6, IL-12p40, IL-1b, and IL-18, while the skin isolates showed no difference compared to the negative control (Figure). Conclusion Our data shed new light on the pivotal role of M. globosa in the pathogenesis of UC, highlighting the potential influence of niche-specific adaptations on the virulence of this fungus. These findings provide critical insights into the complex interplay between the member of the gut mycobiota and host health.
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