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Calprotectin (CLP) is a calcium-binding protein produced by neutrophils and monocytes in the course of inflammation. Today, the role of faecal CLP in chronic IBD is well known, but in recent years attention has shifted towards circulating CLP. In fact, this molecule can be measured in different biological fluids: blood, saliva and urine, using different analytic methods that are described in this review. Furthermore, different data confirm the relevant role of serum CLP in autoimmune diseases. In this review we will highlight the correlation between high levels of circulating CLP and specific autoantibodies of major autoimmune pathologies paving the way to the employment of CLP measurement as useful biomarker for monitoring outcome in different pathologies.
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http://dx.doi.org/10.1093/rheumatology/kead405 | DOI Listing |
Int Immunopharmacol
September 2025
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil; Center for Research in Inflammatory Diseases, CRID, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil. Electronic address:
Sepsis, a life-threatening organ dysfunction caused by a dysregulated host response to infection, is associated with impaired neutrophil migration to the infectious focus owing to G protein-coupled receptor kinase (GRK2)-dependent CXCR2 internalization. In the present study, we investigated whether paroxetine, an antidepressant that belongs to the selective serotonin reuptake inhibitor (SSRI) class of drugs and that is also identified as a GRK2 inhibitor, can improve neutrophil recruitment in the cecal ligation and puncture (CLP)-induced sepsis model. Moderate (mCLP) and severe (sCLP) polymicrobial peritonitis were induced in C57BL/6 mice.
View Article and Find Full Text PDFIntensive Care Med Exp
September 2025
Department of Pathology and Medical Biology, Medical Biology section, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Introduction: Endothelial cells play a central role in the pathophysiology of sepsis-associated acute kidney injury (SA-AKI), yet we have limited understanding of the markers of microvascular-specific response. We therefore employed a translational approach integrating spatially resolved transcriptomics in a mouse SA-AKI model with validation in human kidney tissues and plasma, aiming to define the molecular signature of the endothelial response to SA-AKI in mice and in human patients.
Methods: In this post hoc analysis of prospectively collected data, we identified sepsis-associated target mRNAs and validated their expression via RT-qPCR in distinct renal microvascular compartments isolated by laser microdissection (LMD) from both cecal ligation and puncture (CLP) mice and post-mortem kidney biopsies of SA-AKI patients.
Pflugers Arch
August 2025
Laboratório de Farmacologia Cardiovascular, Departamento de Ciências BioMoleculares, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, Ribeirão Preto, São Paulo, Brazil.
Sepsis enhances the anticontractile effect of perivascular adipose tissue (PVAT), which contributes to a reduced response to vasoconstrictor agents. In the early stages of sepsis, the renin-angiotensin-aldosterone system (RAAS) is activated, and this response can lead to poorer clinical outcomes. We hypothesized that AT receptors (ATR) contribute to vascular hyporesponsiveness during sepsis by increasing the expression of inducible nitric oxide synthase (iNOS) in the periaortic PVAT, resulting in elevated nitric oxide (NO) production.
View Article and Find Full Text PDFInt Immunol
July 2025
Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
The aim of this study was to elucidate the effect of IL-35 on T cell differentiation and its mechanism. We evaluated the therapeutic effect of IL-35 on acute respiratory distress syndrome (ARDS) using clinical samples and mouse cecum ligation and puncture (CLP) model. The effects of IL-35 on Regulatory T cells (Treg) were verified by flow cytometry, immunohistochemistry (IHC) and qRT-PCR.
View Article and Find Full Text PDFInt J Surg
June 2025
Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China.
Background: Sepsis-induced acute skeletal muscle wasting would impede critical patients' recovery. The underlying mechanism for this metabolic disorder has not been fully elucidated. Here, we tested the hypothesis that circulating hormone ghrelin could regulate sepsis-induced acute skeletal muscle wasting via hypothalamic janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3) and agouti-related protein (AgRP) pathway.
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