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Cells
Special Issues
Cellular Reprogramming during Sepsis and Potential Therapeutic Targets
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Cellular Reprogramming during Sepsis and Potential Therapeutic Targets

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 6001

Special Issue Editor

Dr. Brendon P. Scicluna

E-Mail Website
Guest Editor
Centre for Molecular Medicine and Biobanking, Department of Applied Biomedical Sciences, Faculty of Health Sciences, Mater Dei Hospital, University of Malta, Msida, Malta
Interests: Immunity; Immunobiology; Infectious diseases; sepsis; genomics; personalized medicine

Special Issue Information

Dear Colleagues, 

Sepsis is a life-threatening syndrome of organ dysfunction that is caused by an abnormal host response to infection. Despite advancement in critical care medicine and empirical antimicrobial therapy, it is expected that sepsis will remain a healthcare problem (recognized by the World Health Assembly and WHO as a global health priority in 2017). To date, no specific treatment for sepsis has been approved. For years, the pathogenesis of sepsis was focused on an abnormal inflammatory response to infection; albeit numerous clinical trials targeting features of inflammation have been ineffective. Those unsuccessful trials were ascribed, at least in part, to the inadequate selection of therapeutic targets. It has become evident that the initial “hyperinflammation” model does not capture the complexity of sepsis pathogenesis. Current knowledge on the host response during sepsis centres on concurrent features of inflammation, including the activation of the complement system, coagulation system and neutrophil reactions, concomitant with immune-suppression, which is mainly caused by the functional reprogramming of antigen-presenting cells, and either apoptosis or exhaustion of lymphocytes. While it may be argued that those changes may reflect a fundamental reorganization of cellular metabolism and epigenetic state, it remains difficult to create an overarching framework of the key “drivers” in sepsis pathobiology versus secondary changes that are less decisive to patient outcome. Improving our understanding of cellular reprogramming during sepsis is critical for the development of precise therapeutics and patient management. Therefore, this Special Issue is dedicated to improvements in our understanding of how cells are functionally reprogrammed during sepsis, and the potential therapeutic implications.

Dr. Brendon Scicluna
Guest Editor

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Published Papers (2 papers)

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17 pages, 2196 KiB  
Article
MicroRNA Profiles in Intestinal Epithelial Cells in a Mouse Model of Sepsis
by Siqingaowa Caidengbate, Yuichi Akama, Anik Banerjee, Khwanchanok Mokmued, Eiji Kawamoto, Arong Gaowa, Louise D. McCullough, Motomu Shimaoka, Juneyoung Lee and Eun Jeong Park
Cells 2023, 12(5), 726; https://doi.org/10.3390/cells12050726 - 24 Feb 2023
Cited by 2 | Viewed by 2775
Abstract
Sepsis is a systemic inflammatory disorder that leads to the dysfunction of multiple organs. In the intestine, the deregulation of the epithelial barrier contributes to the development of sepsis by triggering continuous exposure to harmful factors. However, sepsis-induced epigenetic changes in gene-regulation networks [...] Read more.
Sepsis is a systemic inflammatory disorder that leads to the dysfunction of multiple organs. In the intestine, the deregulation of the epithelial barrier contributes to the development of sepsis by triggering continuous exposure to harmful factors. However, sepsis-induced epigenetic changes in gene-regulation networks within intestinal epithelial cells (IECs) remain unexplored. In this study, we analyzed the expression profile of microRNAs (miRNAs) in IECs isolated from a mouse model of sepsis generated via cecal slurry injection. Among 239 miRNAs, 14 miRNAs were upregulated, and 9 miRNAs were downregulated in the IECs by sepsis. Upregulated miRNAs in IECs from septic mice, particularly miR-149-5p, miR-466q, miR-495, and miR-511-3p, were seen to exhibit complex and global effects on gene regulation networks. Interestingly, miR-511-3p has emerged as a diagnostic marker in this sepsis model due to its increase in blood in addition to IECs. As expected, mRNAs in the IECs were remarkably altered by sepsis; specifically, 2248 mRNAs were decreased, while 612 mRNAs were increased. This quantitative bias may be possibly derived, at least partly, from the direct effects of the sepsis-increased miRNAs on the comprehensive expression of mRNAs. Thus, current in silico data indicate that there are dynamic regulatory responses of miRNAs to sepsis in IECs. In addition, the miRNAs that were increased with sepsis had enriched downstream pathways including Wnt signaling, which is associated with wound healing, and FGF/FGFR signaling, which has been linked to chronic inflammation and fibrosis. These modifications in miRNA networks in IECs may lead to both pro- and anti-inflammatory effects in sepsis. The four miRNAs discovered above were shown to putatively target LOX, PTCH1, COL22A1, FOXO1, or HMGA2, via in silico analysis, which were associated with Wnt or inflammatory pathways and selected for further study. The expressions of these target genes were downregulated in sepsis IECs, possibly through posttranscriptional modifications of these miRNAs. Taken together, our study suggests that IECs display a distinctive miRNA profile which is capable of comprehensively and functionally reshaping the IEC-specific mRNA landscape in a sepsis model. Full article
(This article belongs to the Special Issue Cellular Reprogramming during Sepsis and Potential Therapeutic Targets)
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6 pages, 638 KiB  
Brief Report
DNA Methyltransferase 3b in Myeloid Cells Does Not Affect the Acute Immune Response in the Airways during Pseudomonas Pneumonia
by Wanhai Qin, Xanthe Brands, Cornelis van’t Veer, Alex F. de Vos, Brendon P. Scicluna and Tom van der Poll
Cells 2022, 11(5), 787; https://doi.org/10.3390/cells11050787 - 24 Feb 2022
Cited by 1 | Viewed by 2047
Abstract
DNA methyltransferase 3b (Dnmt3b) has been suggested to play a role in the host immune response during bacterial infection. Neutrophils and other myeloid cells are crucial for lung defense against Pseudomonas (P.) aeruginosa infection. This study aimed to investigate the role of Dnmt3b [...] Read more.
DNA methyltransferase 3b (Dnmt3b) has been suggested to play a role in the host immune response during bacterial infection. Neutrophils and other myeloid cells are crucial for lung defense against Pseudomonas (P.) aeruginosa infection. This study aimed to investigate the role of Dnmt3b in neutrophils and myeloid cells during acute pneumonia caused by P. aeruginosa. Neutrophil-specific (Dnmt3bfl/flMrp8Cre) or myeloid cell-specific (Dnmt3bfl/flLysMCre) Dnmt3b-deficient mice and littermate control mice were infected with P. aeruginosa PAK via the airways. Bacteria burdens, neutrophil recruitment, and activation (CD11b expression, myeloperoxidase, and elastase levels), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF) were measured in bronchoalveolar lavage fluid (BALF) at 6 and 24 h after infection. Our data showed that the bacterial loads and neutrophil recruitment and activation did not differ in BALF obtained from neutrophil-specific Dnmt3b-deficient and control mice, whilst BALF IL-6 and TNF levels were lower in the former group at 24 but not at 6 h after infection. None of the host response parameters measured differed between myeloid cell-specific Dnmt3b-deficient and control mice. In conclusion, dnmt3b deficiency in neutrophils or myeloid cells does not affect acute immune responses in the airways during Pseudomonas pneumonia. Full article
(This article belongs to the Special Issue Cellular Reprogramming during Sepsis and Potential Therapeutic Targets)
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