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Molecular Mechanisms and Pathophysiology of Sepsis
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Molecular Mechanisms and Pathophysiology of Sepsis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 April 2025 | Viewed by 2971

Special Issue Editor

Dr. Vlad Pădureanu

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania
Interests: genetic polymorphisms; inflammation; oxidative stress; sepsis; internal medicine; acute pancreatitis; diabetes mellitus; liver diseases; rheumatic disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Considering that antibiosis, eradication of the focus, and intensive care supply are the only treatment regimens for patients suffering from sepsis, it is obvious that new therapies are mandatory. Because the anamneses of sepsis patients are very heterogeneous, characterizing mechanistic details associated with sepsis initiation or progression will help to establish new therapeutic approaches. Therefore, manuscripts elucidating the molecular mechanisms in vitro or in vivo in preclinical models as well as patient studies providing insights into new therapeutic concepts to prevent or treat sepsis progression are welcome. Based on this research topic, this Special Issue aims to collate original research manuscripts and review articles in the field of the origin of sepsis and related therapies.

Submissions of review articles and original research papers that cover topics including, but not limited to, the following are welcome:

  1. Cell culture studies characterizing and/or identifying new factors involved in sepsis development.
  2. The role of immune cell subpopulations in sepsis progression.
  3. Animal models providing mechanistic insights into the underlying principles leading to sepsis.
  4. Therapeutic approaches to prevent or cure sepsis and future perspectives.
  5. The definition of new sepsis biomarkers.
  6. The characterization of putative subgroups of sepsis patients with a similar origin of sepsis.

Dr. Vlad Pădureanu
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • animal models
  • therapeutic concepts
  • biomarkers
  • sepsis
  • immune suppression
  • epigenetics

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Published Papers (3 papers)

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Research

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20 pages, 1646 KiB  
Article
Comparative Analysis of Hepatic Gene Expression Profiles in Murine and Porcine Sepsis Models
by Fëllanza Halimi, Tineke Vanderhaeghen, Steven Timmermans, Siska Croubels, Claude Libert and Jolien Vandewalle
Int. J. Mol. Sci. 2024, 25(20), 11079; https://doi.org/10.3390/ijms252011079 - 15 Oct 2024
Viewed by 750
Abstract
Sepsis remains a huge unmet medical need for which no approved drugs, besides antibiotics, are on the market. Despite the clinical impact of sepsis, its molecular mechanism remains inadequately understood. Recent insights have shown that profound hepatic transcriptional reprogramming, leading to fatal metabolic [...] Read more.
Sepsis remains a huge unmet medical need for which no approved drugs, besides antibiotics, are on the market. Despite the clinical impact of sepsis, its molecular mechanism remains inadequately understood. Recent insights have shown that profound hepatic transcriptional reprogramming, leading to fatal metabolic abnormalities, might open a new avenue to treat sepsis. Translation of experimental results from rodents to larger animal models of higher relevance for human physiology, such as pigs, is critical and needs exploration. We performed a comparative analysis of the transcriptome profiles in murine and porcine livers using the following sepsis models: cecal ligation and puncture (CLP) in mice and fecal instillation (FI) in pigs, both of which induce polymicrobial septic peritonitis, and lipopolysaccharide (LPS)-induced endotoxemia in pigs, inducing sterile inflammation. Using bulk RNA sequencing, Metascape pathway analysis, and HOMER transcription factor motif analysis, we were able to identify key genes and pathways affected in septic livers. Conserved upregulated pathways in murine CLP and porcine LPS and FI generally comprise typical inflammatory pathways, except for ER stress, which was only found in the murine CLP model. Conserved pathways downregulated in sepsis comprise almost exclusively metabolic pathways such as monocarboxylic acid, steroid, biological oxidation, and small-molecule catabolism. Even though the upregulated inflammatory pathways were equally induced in the two porcine models, the porcine FI model more closely resembles the metabolic dysfunction observed in the CLP liver compared to the porcine LPS model. This comprehensive comparison focusing on the hepatic responses in mouse CLP versus LPS or FI in pigs shows that the two porcine sepsis models generally resemble quite well the mouse CLP model, with a typical inflammatory signature amongst the upregulated genes and metabolic dysfunction amongst the downregulated genes. The hepatic ER stress observed in the murine model could not be replicated in the porcine models. When studying metabolic dysfunction in the liver upon sepsis, the porcine FI model more closely resembles the mouse CLP model compared to the porcine LPS model. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Sepsis)
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18 pages, 3487 KiB  
Article
C5a Induces Inflammatory Signaling and Apoptosis in PC12 Cells through C5aR-Dependent Signaling: A Potential Mechanism for Adrenal Damage in Sepsis
by Lucas Mrozewski, Sujeenthar Tharmalingam, Paul Michael, Aseem Kumar and T. C. Tai
Int. J. Mol. Sci. 2024, 25(19), 10673; https://doi.org/10.3390/ijms251910673 - 3 Oct 2024
Viewed by 853
Abstract
The complement system is critically involved in the pathogenesis of sepsis. In particular, complement anaphylatoxin C5a is generated in excess during sepsis, leading to cellular dysfunction. Recent studies have shown that excessive C5a impairs adrenomedullary catecholamine production release and induces apoptosis in adrenomedullary [...] Read more.
The complement system is critically involved in the pathogenesis of sepsis. In particular, complement anaphylatoxin C5a is generated in excess during sepsis, leading to cellular dysfunction. Recent studies have shown that excessive C5a impairs adrenomedullary catecholamine production release and induces apoptosis in adrenomedullary cells. Currently, the mechanisms by which C5a impacts adrenal cell function are poorly understood. The PC12 cell model was used to examine the cellular effects following treatment with recombinant rat C5a. The levels of caspase activation and cell death, protein kinase signaling pathway activation, and changes in inflammatory protein expression were examined following treatment with C5a. There was an increase in apoptosis of PC12 cells following treatment with high-dose C5a. Ten inflammatory proteins, primarily involved in apoptosis, cell survival, and cell proliferation, were upregulated following treatment with high-dose C5a. Five inflammatory proteins, involved primarily in chemotaxis and anti-inflammatory functions, were downregulated. The ERK/MAPK, p38/MAPK, JNK/MAPK, and AKT protein kinase signaling pathways were upregulated in a C5aR-dependent manner. These results demonstrate an apoptotic effect and cellular signaling effect of high-dose C5a. Taken together, the overall data suggest that high levels of C5a may play a role in C5aR-dependent apoptosis of adrenal medullary cells in sepsis. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Sepsis)
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Review

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27 pages, 3319 KiB  
Review
Neonatal Fungemia by Non-Candida Rare Opportunistic Yeasts: A Systematic Review of Literature
by Alexandra Mpakosi, Vasileios Cholevas, Joseph Meletiadis, Martha Theodoraki and Rozeta Sokou
Int. J. Mol. Sci. 2024, 25(17), 9266; https://doi.org/10.3390/ijms25179266 - 27 Aug 2024
Viewed by 892
Abstract
Fungal colonization poses a significant risk for neonates, leading to invasive infections such as fungemia. While Candida species are the most commonly identified pathogens, other rare yeasts are increasingly reported, complicating diagnosis and treatment due to limited data on antifungal pharmacokinetics. These emerging [...] Read more.
Fungal colonization poses a significant risk for neonates, leading to invasive infections such as fungemia. While Candida species are the most commonly identified pathogens, other rare yeasts are increasingly reported, complicating diagnosis and treatment due to limited data on antifungal pharmacokinetics. These emerging yeasts, often opportunistic, underscore the critical need for early diagnosis and targeted therapy in neonates. This systematic review aims to comprehensively analyze all published cases of neonatal fungemia caused by rare opportunistic yeasts, examining geographical distribution, species involved, risk factors, treatment approaches, and outcomes. Searching two databases (PubMed and SCOPUS), 89 relevant studies with a total of 342 cases were identified in the 42-year period; 62% of the cases occurred in Asia. Pichia anomala (31%), Kodamaea ohmeri (16%) and Malassezia furfur (15%) dominated. Low birth weight, the use of central catheters, prematurity, and the use of antibiotics were the main risk factors (98%, 76%, 66%, and 65%, respectively). 22% of the cases had a fatal outcome (80% in Asia). The highest mortality rates were reported in Trichosporon beigelii and Trichosporon asahii cases, followed by Dirkmeia churashimamensis cases (80%, 71%, and 42% respectively). Low birth weight, the use of central catheters, the use of antibiotics, and prematurity were the main risk factors in fatal cases (84%, 74%, 70%, and 67%, respectively). 38% of the neonates received fluconazole for treatment but 46% of them, died. Moreover, the rare yeasts of this review showed high MICs to fluconazole and this should be taken into account when planning prophylactic or therapeutic strategies with this drug. In conclusion, neonatal fungemia by rare yeasts is a life-threatening and difficult-to-treat infection, often underestimated and misdiagnosed. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Sepsis)
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