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Biomedicines
Special Issues
Sepsis and Septic Shock: From Molecular Mechanism to Novel Therapies
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Sepsis and Septic Shock: From Molecular Mechanism to Novel Therapies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 1708

Special Issue Editor

Dr. Fuhong Su

E-Mail Website
Guest Editor
Laboratoire Experimental des Soins Intensifs, Department of Intensive Care, Hôpital Erasme, Université Libre de Bruxelles (ULB), 1070 Brussels, Belgium
Interests: sepsis; cellular regulation

Special Issue Information

Dear Colleagues,

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection (either suspected or confirmed) and is a serious health issue with high morbidity and mortality despite years of research. There is still a lack of effective therapies apart from antibiotics and fluid resuscitation.

A better understanding of molecular mechanisms involved in sepsis can help identify new and specific biomarkers and targets for the diagnosis and treatment of sepsis. For example, histone, a DAMP released by NETosis and other cell death processes such as apoptosis, necroptosis, and pyroptosis, has been identified as having harmful effects in sepsis, including inducing endothelial dysfunction, coagulopathy, and barrier damage. New therapies are thus being developed to block histone signalling pathways or histone release and to neutralize its effects. A histone neutralization compound, mCBS, has been recently shown to have beneficial effects including decreased vasopressor use, reduced inflammation, and improved tissue perfusion in translational studies and ongoing clinical phase II efficacy trials.

This is a perfect example to show the link between molecular mechanisms and the development of novel therapies for sepsis. To shed more light on this field, we are launching a Special Issue "Sepsis and Septic Shock: From Molecular Mechanism to Novel Therapies". All studies and reviews related to sepsis mechanisms and therapeutic strategies are welcome.

Dr. Fuhong Su
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • sepsis
  • septic shock
  • molecular mechanisms
  • specific biomarkers
  • histone

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Published Papers (3 papers)

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Research

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11 pages, 1808 KiB  
Article
Reduced Plasma Bone Morphogenetic Protein 6 Levels in Sepsis and Septic Shock Patients
by Niklas Schmidtner, Alexander Utrata, Patricia Mester, Stephan Schmid, Martina Müller, Vlad Pavel and Christa Buechler
Biomedicines 2024, 12(8), 1682; https://doi.org/10.3390/biomedicines12081682 - 28 Jul 2024
Viewed by 423
Abstract
Infectious diseases are associated with low iron levels and the induction of hepcidin, the primary protein regulating cellular iron export. Bone morphogenetic protein 6 (BMP6), a key regulator of hepcidin expression, has not yet been analyzed in the plasma of patients with systemic [...] Read more.
Infectious diseases are associated with low iron levels and the induction of hepcidin, the primary protein regulating cellular iron export. Bone morphogenetic protein 6 (BMP6), a key regulator of hepcidin expression, has not yet been analyzed in the plasma of patients with systemic inflammatory response syndrome (SIRS) or sepsis. An analysis of 38 SIRS, 39 sepsis, and 78 septic shock patients revealed similar levels of BMP6 in sepsis and septic shock, which were lower compared to patients with SIRS and healthy controls. Plasma BMP6 levels did not correlate with procalcitonin and C-reactive protein levels in patients with SIRS or sepsis/septic shock. Neither bacterial nor SARS-CoV-2 infections affected plasma BMP6 levels. There was no difference in BMP6 levels between ventilated and non-ventilated patients, or between patients with and without dialysis. Vasopressor therapy did not alter BMP6 levels. Survivors had plasma BMP6 levels similar to non-survivors. Due to the high variability of plasma BMP6 levels, these analyses have limited clinical relevance. Iron, ferritin, and transferrin levels were known in at least 50% of patients but did not correlate with plasma BMP6 levels. In conclusion, this study showed normal BMP6 plasma levels in SIRS, which are reduced in patients with sepsis and septic shock. This suggests that the commonly observed increase in hepcidin levels and the decline in iron levels in SIRS, sepsis, and septic shock are not due to higher BMP6. Full article
(This article belongs to the Special Issue Sepsis and Septic Shock: From Molecular Mechanism to Novel Therapies)
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15 pages, 5814 KiB  
Article
Cerebral Endothelial CXCR2 Promotes Neutrophil Transmigration into Central Nervous System in LPS-Induced Septic Encephalopathy
by Fengjiao Wu, Yuhong Han, Qianqian Xiong, Haitao Tang, Jing Shi, Qingqing Yang, Xuemeng Li, Haoxuan Jia, Jun Qian, Yishu Dong, Tuantuan Li, Yong Gao, Zhongqing Qian, Hongtao Wang and Ting Wang
Biomedicines 2024, 12(7), 1536; https://doi.org/10.3390/biomedicines12071536 - 11 Jul 2024
Viewed by 508
Abstract
Septic encephalopathy (SE) represents a severe inflammatory syndrome linked to elevated septic mortality rates, lacking specific therapeutic interventions, and often resulting in enduring neurological sequelae. The present investigation endeavors to elucidate the involvement of C-X-C Motif Chemokine Receptor 2 (CXCR2) in the pathogenesis [...] Read more.
Septic encephalopathy (SE) represents a severe inflammatory syndrome linked to elevated septic mortality rates, lacking specific therapeutic interventions, and often resulting in enduring neurological sequelae. The present investigation endeavors to elucidate the involvement of C-X-C Motif Chemokine Receptor 2 (CXCR2) in the pathogenesis of SE and to explore the potential of CXCR2 modulation as a therapeutic avenue for SE. Employing a murine SE model induced by lipopolysaccharide (LPS) administration, CXCR2 knockout mice and the CXCR2 inhibitor SB225002 were utilized to assess neutrophil recruitment, endothelial integrity, and transendothelial migration. Our findings substantiate that either CXCR2 deficiency or its inhibition curtails neutrophil recruitment without impacting their adhesion to cerebral endothelial cells. This phenomenon is contingent upon endothelial CXCR2 expression rather than CXCR2’s presence on neutrophils. Furthermore, the CXCR2 blockade preserves the integrity of tight junction protein ZO-1 and mitigates F-actin stress fiber formation in cerebral endothelial cells following septic challenge. Mechanistically, CXCL1-mediated CXCR2 activation triggers cerebral endothelial actin contraction via Rho signaling, thereby facilitating neutrophil transmigration in SE. These observations advocate for the potential therapeutic efficacy of CXCR2 inhibition in managing SE. Full article
(This article belongs to the Special Issue Sepsis and Septic Shock: From Molecular Mechanism to Novel Therapies)
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Review

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11 pages, 1914 KiB  
Review
The Possible Pathophysiological Role of Pancreatic Stone Protein in Sepsis and Its Potential Therapeutic Implication
by François Ventura and Pierre Tissières
Biomedicines 2024, 12(8), 1790; https://doi.org/10.3390/biomedicines12081790 - 7 Aug 2024
Viewed by 336
Abstract
According to the current understanding of the pathophysiology of sepsis, key host dysregulated responses leading to organ failure are mediated by innate immunity, through interactions between pathogen-associated molecular patterns (PAMPs) and damaged-associated molecular patterns (DAMPs) binding to four types of pattern recognition receptors [...] Read more.
According to the current understanding of the pathophysiology of sepsis, key host dysregulated responses leading to organ failure are mediated by innate immunity, through interactions between pathogen-associated molecular patterns (PAMPs) and damaged-associated molecular patterns (DAMPs) binding to four types of pattern recognition receptors (PRRs). PRRs activation triggers the protein kinase cascade, initiating the cellular response seen during sepsis. Pancreatic stone protein (PSP), a C-type lectin protein, is a well-defined biomarker of sepsis. Studies have shown that stressed and immune-activated pancreatic β-cells secrete PSP. Animal studies have shown that PSP injection aggravates sepsis, and that the disease severity score and mortality were directly correlated with the doses of PSP injected. In humans, studies have shown that PSP activates polymorphonuclear neutrophils (PMNs) and aggravates multiple organ dysfunction syndrome. Clinical studies have shown that PSP levels are correlated with disease severity, vasopressor support, progression to organ failure, mechanical ventilation, renal replacement therapy, length of stay, and mortality. As PSP is a C-type lectin protein, it may have a role in activating innate immunity through the C-type lectin receptors (CLRs), which is one of the four PRRs. Herein, we review the literature on PSP and its possible role in the pathophysiology of sepsis, and we discuss its potential therapeutic role. Full article
(This article belongs to the Special Issue Sepsis and Septic Shock: From Molecular Mechanism to Novel Therapies)
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