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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 16918

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Special Issue Editor

Dr. Wonhwa Lee

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Guest Editor

Department of Chemistry, Sungkyunkwan University, 2066 Seobu-ro, Jangan-gu, Suwon 16419, Republic of Korea
Interests: vascular inflammation; infectious disease; respiratory disease; drug delivery

Special Issue Information

Dear Colleagues,

We are pleased to request a special issue of the International Journal of Molecular Sciences(IJMS) on the subject of Molecular Research on sepsis. Since 2011, we have studied the mechanism that regulates the hyper-activation of NF-kB and the epigenetic research of the systemic mechanism that regulates the stability of NK-kB p65 in the nucleus (kim D, Et al. (2018) Mol. cell). Many research papers on sepsis have been published, but there is no drug currently approved by the FDA. We are very interested in endotoxin molecule and signal transduction mechanism related to sepsis. We encourage you to submit research articles and review papers related to septic multiple organ failure and severe vascular inflammatory responses in vitro and in vivo. All articles submitted are subject to peer review.

Dr. Wonhwa Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

inflammation
Chip Sequencing
Epigentic regulation
NF-kB
sepsis

Published Papers (6 papers)

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Research

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14 pages, 4615 KiB

Open AccessArticle

Linagliptin Protects against Endotoxin-Induced Acute Kidney Injury in Rats by Decreasing Inflammatory Cytokines and Reactive Oxygen Species

by Tsung-Jui Wu, Yi-Jen Hsieh, Chia-Wen Lu, Chung-Jen Lee and Bang-Gee Hsu

Int. J. Mol. Sci. 2021, 22(20), 11190; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011190 - 17 Oct 2021

Cited by 14 | Viewed by 2029

Abstract

Septic shock can increase pro-inflammatory cytokines, reactive oxygen species (ROS), and multiple organ dysfunction syndrome (MODs) and even lead to death. Dipeptidyl peptidase-4 (DPP-4) inhibitors have been proven to exert potential antioxidant and anti-inflammatory effects. We investigated the effects of linagliptin on endotoxic shock and acute kidney injury (AKI) in animal and cell models. In the cell model, linagliptin attenuated ROS by activating the AMP-activated protein kinase (AMPK) pathway, restoring nuclear-factor-erythroid-2-related factor (Nrf2) and heme oxygenase 1 (HO-1) protein, and decreasing pro-inflammatory cytokines (tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β)). In the animal model, 14-week-old conscious Wistar–Kyoto rats were randomly divided into three groups (n = 8 in each group). Endotoxin shock with MODs was induced by the intravenous injection of Klebsiella pneumoniae lipopolysaccharide (LPS, 20 mg/kg). Linagliptin improved animal survival without affecting hemodynamic profiles. In the histopathology and immunohistochemistry examinations of the rat kidneys, linagliptin (10 mg/kg) suppressed nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and inducible nitric oxide synthase (iNOS), decreased injury scores, and preserved E-cadherin expression from LPS damage. In conclusion, linagliptin ameliorated endotoxin-shock-induced AKI by reducing ROS via AMPK pathway activation and suppressing the release of TNF-α and IL-1β in conscious rats. Full article

(This article belongs to the Special Issue Molecular Research on Sepsis)

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13 pages, 3646 KiB

Open AccessArticle

Topical Neck Cooling Prolongs Survival of Rats with Intra-Abdominal Feculent Sepsis by Activation of the Vagus Nerve

by Aimee Y. Zhang, Katherine M. Marsh, Radhika Rastogi, Di Wu, Eric J. Charles, Irving L. Kron, Robert G. Sawyer and Zequan Yang

Int. J. Mol. Sci. 2021, 22(18), 9828; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189828 - 11 Sep 2021

Cited by 1 | Viewed by 1481

Abstract

Global hypothermia prolongs survival in rats with intraabdominal feculent sepsis by inhibiting inflammatory responses. We hypothesized that topical neck cooling (TNC) has similar benefits. Septic shock was induced by cecal ligation and incision (CLI) in Sprague Dawley rats. Rats were randomized to sham laparotomy, control with CLI, CLI with TNC, or vagotomy at the gastroesophageal junction before CLI and TNC. Two more groups underwent peritoneal washout with and without TNC two hours after CLI. TNC significantly lowered neck skin temperature (16.7 ± 1.4 vs. 30.5 ± 0.6 °C, p < 0.05) while maintaining core body normothermia. TNC rats recovered from anesthesia 70 min earlier than the control (p < 0.05). Three hours following CLI, the control and vagotomy with TNC groups had significantly more splenic contraction, fewer circulating leukocytes and higher plasma IL-1β, IL-10 and TNF-α levels than TNC rats (p < 0.05). TNC prolonged survival duration after CLI by a median of four hours vs. control (p < 0.05), but no benefit was seen if vagotomy preceded TNC. Peritoneal washout alone increased survival by 3 h (9.2 (7.8–10.5) h). Survival duration increased dramatically with TNC preceding washout, to a 56% survival rate (>10 days). TNC significantly prolonged the survival of rats with severe intraabdominal sepsis by inhibiting systemic proinflammatory responses by activating vagal anti-inflammatory pathways. Full article

(This article belongs to the Special Issue Molecular Research on Sepsis)

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13 pages, 1232 KiB

Open AccessArticle

Myeloid-Derived Suppressor Cells Gain Suppressive Function during Neonatal Bacterial Sepsis

by Jordan K. Vance, Travis W. Rawson, Jessica M. Povroznik, Kathleen M. Brundage and Cory M. Robinson

Int. J. Mol. Sci. 2021, 22(13), 7047; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22137047 - 30 Jun 2021

Cited by 6 | Viewed by 2317

Abstract

Neonates are at an increased risk of an infectious disease. This is consistent with an increased abundance of myeloid-derived suppressor cells (MDSCs) compared with older children and adults. Using a murine model of neonatal bacterial sepsis, we demonstrate that MDSCs modulate their activity during an infection to enhance immune suppressive functions. A gene expression analysis shows that MDSCs increased NOS2, Arg-1 and IL-27p28 expression in vitro and in vivo in response to Escherichia coli O1:K1:H7 and this is regulated at the level of the gene expression. Changes in the effector gene expression are consistent with increased enzymatic activity and cytokine secretion. The neonatal MDSCs express toll-like receptor (TLR) 2, 4 and 5 capable of recognizing pathogen-associated molecular patterns (PAMPS) on E. coli. However, a variable level of effector expression was achieved in response to LPS, peptidoglycan or flagellin. Individual bacterial PAMPs did not stimulate the expression of Arg-l and IL-27p28 equivalently to E. coli. However, the upregulation of NOS2 was achieved in response to LPS, peptidoglycan and flagella. The increased immune suppressive profile translated to an enhanced suppression of CD4+ T cell proliferation. Collectively, these findings increase our understanding of the dynamic nature of MDSC activity and suggest that these cells abundant in early life can acquire activity during an infection that suppresses protective immunity. Full article

(This article belongs to the Special Issue Molecular Research on Sepsis)

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12 pages, 2677 KiB

Open AccessArticle

Chromatin Regulator SRG3 Overexpression Protects against LPS/D-GalN-Induced Sepsis by Increasing IL10-Producing Macrophages and Decreasing IFNγ-Producing NK Cells in the Liver

by Sung Won Lee, Hyun Jung Park, Jungmin Jeon, Yun Hoo Park, Tae-Cheol Kim, Sung Ho Jeon, Rho Hyun Seong, Luc Van Kaer and Seokmann Hong

Int. J. Mol. Sci. 2021, 22(6), 3043; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063043 - 16 Mar 2021

Cited by 6 | Viewed by 2292

Abstract

We previously showed that ubiquitous overexpression of the chromatin remodeling factor SWItch3-related gene (SRG3) promotes M2 macrophage differentiation, resulting in anti-inflammatory responses in the experimental autoimmune encephalomyelitis model of multiple sclerosis. Since hepatic macrophages are responsible for sepsis-induced liver injury, we investigated herein the capacity of transgenic SRG3 overexpression (SRG3^β-actin mice) to modulate sepsis in mice exposed to lipopolysaccharide (LPS) plus d-galactosamine (d-GalN). Our results demonstrated that ubiquitous SRG3 overexpression significantly protects mice from LPS/d-GalN-induced lethality mediated by hepatic M1 macrophages. These protective effects of SRG3 overexpression correlated with the phenotypic conversion of hepatic macrophages from an M1 toward an M2 phenotype. Furthermore, SRG3^β-actin mice had decreased numbers and activation of natural killer (NK) cells but not natural killer T (NKT) cells in the liver during sepsis, indicating that SRG3 overexpression might contribute to cross-talk between NK cells and macrophages in the liver. Finally, we demonstrated that NKT cell-deficient CD1d KO/SRG3^β-actin mice are protected from LPS/d-GalN-induced sepsis, indicating that NKT cells are dispensable for SRG3-mediated sepsis suppression. Taken together, our findings provide strong evidence that SRG3 overexpression may serve as a therapeutic approach to control overwhelming inflammatory diseases such as sepsis. Full article

(This article belongs to the Special Issue Molecular Research on Sepsis)

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Review

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19 pages, 1733 KiB

Open AccessReview

The Endothelial Glycocalyx and Neonatal Sepsis

by Ahlam Fatmi, Wiam Saadi, Jesús Beltrán-García, José Luis García-Giménez and Federico V. Pallardó

Int. J. Mol. Sci. 2023, 24(1), 364; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010364 - 26 Dec 2022

Cited by 5 | Viewed by 2651

Abstract

Sepsis carries a substantial risk of morbidity and mortality in newborns, especially preterm-born neonates. Endothelial glycocalyx (eGC) is a carbohydrate-rich layer lining the vascular endothelium, with important vascular barrier function and cell adhesion properties, serving also as a mechano-sensor for blood flow. eGC shedding is recognized as a fundamental pathophysiological process generating microvascular dysfunction, which in turn contributes to multiple organ failure and death in sepsis. Although the disruption of eGC and its consequences have been investigated intensively in the adult population, its composition, development, and potential mechanisms of action are still poorly studied during the neonatal period, and more specifically, in neonatal sepsis. Further knowledge on this topic may provide a better understanding of the molecular mechanisms that guide the sepsis pathology during the neonatal period, and would increase the usefulness of endothelial glycocalyx dysfunction as a diagnostic and prognostic biomarker. We reviewed several components of the eGC that help to deeply understand the mechanisms involved in the eGC disruption during the neonatal period. In addition, we evaluated the potential of eGC components as biomarkers and future targets to develop therapeutic strategies for neonatal sepsis. Full article

(This article belongs to the Special Issue Molecular Research on Sepsis)

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17 pages, 1352 KiB

Open AccessReview

Cellular and Exosomal Regulations of Sepsis-Induced Metabolic Alterations

by Michael G. Appiah, Eun Jeong Park, Yuichi Akama, Yuki Nakamori, Eiji Kawamoto, Arong Gaowa and Motomu Shimaoka

Int. J. Mol. Sci. 2021, 22(15), 8295; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158295 - 02 Aug 2021

Cited by 9 | Viewed by 5111

Abstract

Sepsis is a sustained systemic inflammatory condition involving multiple organ failures caused by dysregulated immune response to infections. Sepsis induces substantial changes in energy demands at the cellular level leading to metabolic reprogramming in immune cells and stromal cells. Although sepsis-associated organ dysfunction and mortality have been partly attributed to the initial acute hyperinflammation and immunosuppression precipitated by a dysfunction in innate and adaptive immune responses, the late mortality due to metabolic dysfunction and immune paralysis currently represent the major problem in clinics. It is becoming increasingly recognized that intertissue and/or intercellular metabolic crosstalk via endocrine factors modulates maintenance of homeostasis, and pathological events in sepsis and other inflammatory diseases. Exosomes have emerged as a novel means of intercellular communication in the regulation of cellular metabolism, owing to their capacity to transfer bioactive payloads such as proteins, lipids, and nucleic acids to their target cells. Recent evidence demonstrates transfer of intact metabolic intermediates from cancer-associated fibroblasts via exosomes to modify metabolic signaling in recipient cells and promote cancer progression. Here, we review the metabolic regulation of endothelial cells and immune cells in sepsis and highlight the role of exosomes as mediators of cellular metabolic signaling in sepsis. Full article

(This article belongs to the Special Issue Molecular Research on Sepsis)

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