Department of Biomedical Sciences, Rochester Institute of Technology, 153 Lomb Memorial Drive, Rochester, NY, 14623, USA.
Division of Biological and Health Sciences, University of Pittsburgh Bradford, Bradford, PA, USA.
Sci Rep. 2024 Jul 23;14(1):16901. doi: 10.1038/s41598-024-67663-w.
Malaria transmission and endemicity in Africa remains hugely disproportionate compared to the rest of the world. The complex life cycle of P. falciparum (Pf) between the vertebrate human host and the anopheline vector results in differential expression of genes within and between hosts. An in-depth understanding of Pf interaction with various human genes through regulatory elements will pave way for identification of newer tools in the arsenal for malaria control. Therefore, the regulatory elements (REs) involved in the over- or under-expression of various host immune genes hold the key to elucidating alternative control measures that can be applied for disease surveillance, prompt diagnosis and treatment. We carried out an RNAseq analysis to identify differentially expressed genes and network elucidation of non-coding RNAs and target genes associated with immune response in individuals with different clinical outcomes. Raw RNAseq datasets, retrieved for analyses include individuals with severe (Gambia-20), symptomatic (Burkina Faso-15), asymptomatic (Mali-16) malaria as well as uninfected controls (Tanzania-20; Mali-36). Of the total 107 datasets retrieved, we identified 5534 differentially expressed genes (DEGs) among disease and control groups. A peculiar pattern of DEGs was observed, with individuals presenting with severe/symptomatic malaria having the highest and most diverse upregulated genes, while a reverse phenomenon was recorded among asymptomatic and uninfected individuals. In addition, we identified 141 differentially expressed micro RNA (miRNA), of which 78 and 63 were upregulated and downregulated respectively. Interactome analysis revealed a moderate interaction between DEGs and miRNAs. Of all identified miRNA, five were unique (hsa-mir-32, hsa-mir-25, hsa-mir-221, hsa-mir-29 and hsa-mir-148) because of their connectivity to several genes, including hsa-mir-221 connected to 16 genes. Six-hundred and eight differentially expressed long non coding RNA (lncRNA) were also identified, including SLC7A11, LINC01524 among the upregulated ones. Our study provides important insight into host immune genes undergoing differential expression under different malaria conditions. It also identified unique miRNAs and lncRNAs that modify and/or regulate the expression of various immune genes. These regulatory elements we surmise, have the potential to serve a diagnostic purpose in discriminating between individuals with severe/symptomatic malaria and those with asymptomatic infection or uninfected, following further clinical validation from field isolates.
与世界其他地区相比,非洲的疟疾传播和流行仍然极不均衡。恶性疟原虫(Pf)在脊椎动物人类宿主和按蚊媒介之间的复杂生命周期导致宿主内和宿主间基因的差异表达。深入了解 Pf 与各种人类基因的相互作用通过调节元件,将为疟疾控制的新工具的识别铺平道路。因此,参与各种宿主免疫基因过度或低表达的调节元件(REs)是阐明替代控制措施的关键,这些措施可用于疾病监测、及时诊断和治疗。我们进行了 RNAseq 分析,以鉴定不同临床结局个体中与免疫反应相关的差异表达基因和非编码 RNA 及靶基因的网络阐明。用于分析的原始 RNAseq 数据集包括来自严重(冈比亚-20)、有症状(布基纳法索-15)、无症状(马里-16)疟疾以及未感染对照(坦桑尼亚-20;马里-36)个体。在总共检索到的 107 个数据集,我们在疾病和对照组之间鉴定了 5534 个差异表达基因(DEGs)。观察到一个特殊的 DEGs 模式,表现为患有严重/有症状疟疾的个体具有最高和最多样化的上调基因,而无症状和未感染个体则出现相反的现象。此外,我们鉴定了 141 个差异表达 micro RNA(miRNA),其中 78 个和 63 个分别上调和下调。互作分析显示 DEGs 和 miRNA 之间存在中度相互作用。在所鉴定的所有 miRNA 中,有五个是独特的(hsa-mir-32、hsa-mir-25、hsa-mir-221、hsa-mir-29 和 hsa-mir-148),因为它们与包括 hsa-mir-221 在内的多个基因连接,hsa-mir-221 与 16 个基因连接。还鉴定了 608 个差异表达的长非编码 RNA(lncRNA),包括上调的 SLC7A11 和 LINC01524。我们的研究为不同疟疾条件下宿主免疫基因差异表达提供了重要的见解。它还鉴定了独特的 miRNA 和 lncRNA,它们修饰和/或调节各种免疫基因的表达。我们推测,这些调节元件有可能在进一步的临床验证后,从现场分离株中用于区分患有严重/有症状疟疾和无症状感染或未感染的个体的诊断目的。