Coding and Noncoding RNA Expression Profiles of Spleen CD4+ T Lymphocytes in Mice with Echinococcosis

Abstract

Cystic echinococcosis (CE) is a severe and neglected zoonotic disease that poses health and socioeconomic hazards. So far, the prevention and treatment of CE are far from meeting people's ideal expectations. Therefore, to gain insight into the prevention and diagnosis of CE, we explored the changes in RNA molecules and the biological processes and pathways involved in these RNA molecules as E. granulosus infects the host. Interferon (IFN)-γ, interleukin (IL)-2, IL-4, IL-6, IL-10, IL-17A, and tumor necrosis factor (TNF)-α levels in peripheral blood serum of E. granulosus infected and uninfected female BALB/c mice were measured using the cytometric bead array mouse Th1/Th2/Th17 cytokine kit. mRNA, microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA) profiles of spleen CD4+ T cells from the two groups of mice were analyzed using high-throughput sequencing and bioinformatics. The levels of IFN-γ, IL-2, IL-4, IL-6, IL-10, IL-17A, and TNF-α were significantly higher in the serum of the CE mice than in control mice (P < 0.01). In total, 1,758 known mRNAs, 37 miRNAs, 175 lncRNAs, and 22 circRNAs were differentially expressed between infected and uninfected mice (|fold change| ≥ 0.585, P < 0.05). These differentially expressed molecules are involved in chromosome composition, DNA/RNA metabolism, and gene expression in cell composition, biological function, and cell function. Moreover, closely related to the JAK/STAT signaling pathways, mitogen-activated protein kinase signaling pathways, P53 signaling pathways, PI3K/AKT signaling pathways, cell cycle, and metabolic pathways. E. granulosus infection significantly increased the levels of IFN-γ, IL-2, IL-4, IL-6, IL-10, IL-17A, and TNF-α in mouse peripheral blood of mice and significantly changed expression levels of various coding and noncoding RNAs. Further study of these trends and pathways may help clarify the pathogenesis of CE and provide new insights into the prevention and treatment of this disease.

Bioinformatics and systems biology approaches to identify the effects of COVID-19 on neurodegenerative diseases: A review

“…To identify DEGs in the dataset, after converting some counts data into fpkm data via SangerBox [24–26] (http://vip.sangerbox.com/), a difference-in-difference analysis using limma R and combined with the Benjamini-Hochberg false discovery rate method was used to screen for statistically significant genes and limit false positives. [27,28] Genes with a screening-adjusted P ≤ .05 and log 2 FC ≥ 0.585 (fold change = 1.5) [29–31] were identified as DEGs. Genes common to both datasets of the same tissue for the same disease were selected for ND as DEGs for that disease to improve precision.…”

Ghrelin regulating liver activity and its potential effects on liver fibrosis and Echinococcosis

“…Previous studies have suggested that innate immune pathways such as inflammatory vesicles and Toll-like receptor activation, and hepatocyte apoptosis are the host’s primary line of defense against the progression of liver Echinococcosis infection ( Vuitton, 2003 ; Inclan-Rico and Siracusa, 2018 ; Bakhtiar et al., 2020 ). Recently, more and more studies have found that growth metabolic pathways are activated during the process of liver Echinococcosis infection and interact with the immune-inflammation and fibrosis pathways to jointly regulate the outcome of the disease ( Seoane et al., 2016 ; Cheng et al., 2017 ; Liu et al., 2017 ; Yin et al., 2018 ; Wang et al., 2019 ; Lin et al., 2021 ; Yang et al., 2022 ). However, to date, few studies have addressed the various outcomes following interventions in growth metabolic pathways during the progression of liver Echinococcosis .…”

“…Studies have found that Ghrelin has anti-inflammatory effects that inhibit Th1 and Th17 immune responses and promote Th2 and Tregs T cell immunity ( Dixit et al., 2004 ; Symonds et al., 2009 ; Stevanovic et al., 2012 ; Paoluzi et al., 2013 ; Xu et al., 2015 ). Current studies show that in the early and progressive stages of echinococcal infection, the JAK/STAT ( Liu et al., 2017 ; Yang et al., 2022 ), MEK/ERK1/2 ( Cheng et al., 2017 ; Lin et al., 2021 ) and PI3K/Akt/mTOR ( Covarrubias et al., 2015 ; Seoane et al., 2016 ; Yin et al., 2018 ; Wang et al., 2019 ; Yang et al., 2022 ) signaling pathways are upregulated and may be involved in regulating the parasitism and survival of Echinococcosis . High expression of Ghrelin could significantly upregulate the MEK/ERK1/2 ( Moreno et al., 2010 ; Kotta et al., 2022 ) and PI3K/Akt/mTOR ( Zhu et al., 2018 ; Petrescu et al., 2020 ; Zhang and Xie, 2020 ) signaling pathways, and inhibit NF-κB ( Zhou and Xue, 2009 ; Barazzoni et al., 2014 ; Mao et al., 2015b ; Mao et al., 2015a ) and TGF-β1/Smad3 ( Mao et al., 2015b ; Ezquerro et al., 2023 ) signaling pathways through interaction, significantly reducing the proinflammatory factors secreted by Th1-type cellular immunity, inhibiting the proliferation and activation of HSCs to restore the dynamic balance of MMP2 and TIMP1 and decrease the secretion of fibrotic cytokines α-SMA, collagen I and III, playing a role in reducing chronic inflammation and fibrosis formation in the liver.…”

Retracted: Coding and Noncoding RNA Expression Profiles of Spleen CD4+ T Lymphocytes in Mice with Echinococcosis

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”