Profiling the full-length transcriptome of plasma cell mastitis via nanopore sequencing.

IF 1.9 Q3 GENETICS & HEREDITY
Su Li, Hongyue Chen, Yan Fan, Can Wang, Lijing An, Qifeng Xu, Wenming Cai, Suzhen Zhao, Tian Tian, Baoyong Zhang, Mengmeng Yang, Lulu Zhang
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Abstract

Introduction: In this study, we aimed to determine the transcriptomic profile of plasma cell mastitis (PCM) and elucidate its underlying mechanisms using nanopore sequencing technology (ONT).

Methods and results: Through comparisons and analyses of redundantly removed transcripts with known reference genome annotations, we identified 39,408 novel transcripts and 20,980 genes. By exploring full-length transcriptome data, we characterized selective splicing, selective polyadenylation events, and simple sequence repeat (SSR) site information, which enhanced our understanding of genome annotation and gene structure in plasma cell mastitis. Additionally, we investigated predicted transcription factors and LncRNAs, screening those with differences for further investigations. The GO and KEGG enrichment analysis of differentially expressed genes (DEGs) and differentially expressed transcripts (DETs) revealed subtle distinctions between them, with primary enrichments being in immune response and intercellular interactions. Our protein-protein interaction (PPI) analysis of hub proteins from DETs indicated up-regulated genes' involvement in immune response and down-regulated genes' role in cell adhesion. Furthermore, we assessed immune cell infiltration in plasma cell mastitis, observing various immune cells, such as B cells, T cells, and DC cells.

Conclusion: These preliminary findings offer novel insights into the pathogenesis of plasma cell mastitis and present promising ideas for optimizing personalized treatment approaches, warranting further exploration and follow-up studies.

通过纳米孔测序分析浆细胞性乳腺炎的全长转录组。
在这项研究中,我们旨在利用纳米孔测序技术(ONT)确定浆细胞性乳腺炎(PCM)的转录组学特征,并阐明其潜在机制。方法与结果:通过与已知参考基因组注释的冗余删除转录本进行比较和分析,我们鉴定出39,408个新转录本和20,980个基因。通过探索全长转录组数据,我们表征了选择性剪接、选择性聚腺苷酸化事件和简单序列重复(SSR)位点信息,从而增强了我们对浆细胞乳腺炎基因组注释和基因结构的理解。此外,我们研究了预测转录因子和lncrna,筛选差异进行进一步研究。差异表达基因(DEGs)和差异表达转录物(DETs)的GO和KEGG富集分析揭示了它们之间的微妙区别,主要富集在免疫反应和细胞间相互作用中。我们对DETs中枢蛋白的蛋白-蛋白相互作用(PPI)分析表明,上调基因参与免疫应答,下调基因参与细胞粘附。此外,我们评估了免疫细胞在浆细胞性乳腺炎中的浸润,观察了各种免疫细胞,如B细胞、T细胞和DC细胞。结论:这些初步发现为浆细胞性乳腺炎的发病机制提供了新的见解,为优化个性化治疗方法提供了有希望的思路,值得进一步探索和后续研究。
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