Background/aims: Upregulated CD64 expression on neutrophils is the most useful marker for acute bacterial infections and systemic inflammation. However, it is unknown whether CD64 is involved in the pathogenesis of acute pancreatitis (AP). This study was designed to determine whether CD64 is implicated in severe acute pancreatitis (SAP), and thus, is a suitable marker for SAP.
Methods: SAP was induced in rats with an intraperitoneal injection of L-arginine. CD64 expression in the rat pancreas was determined by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry. Additionally, the CD64 mRNA expression in peripheral blood leukocytes from 21 patients with mild acute pancreatitis (MAP) and 10 patients with SAP was investigated at the time of admission and during remission by qRT-PCR.
Results: CD64 mRNA and protein expression in the pancreas was significantly higher in rats with SAP, compared to the controls. The CD64 expression was higher in the patients with SAP than in the patients with MAP. During remission, CD64 mRNA decreased in both the MAP and SAP patients. The area under the curve of CD64 expression for the detection of SAP was superior to both the Ranson and the Acute Physiology and Chronic Health Evaluation II scores.
Conclusions: The CD64 level was significantly increased in correlation with the disease severity in SAP and may act as a useful marker for predicting the development of SAP.
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http://dx.doi.org/10.5009/gnl.2014.8.4.445 | DOI Listing |
J Immunol Methods
December 2024
Institute for Animal Health, Henan Academy of Agricultural Sciences, Zhengzhou, China; College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, China; Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoon-Ose, Yangzhou University, Yangzhou, China. Electronic address:
Background: Bovine IgG1 Fc receptor (boFcγRI) is a homologue to human FcγRI (CD64) that has three extracellular Ig-like domains and can bind bovine IgG1 with high affinity. Identification of the linear epitope for Fc-binding on boFcγRI provides new insights for the IgG-Fcγ interaction and FcγR-targeting drugs development.
Methods: The boFcγRI molecules were expressed on cell surface of the boFcγRI -transfected COS-7 cells.
Am J Physiol Regul Integr Comp Physiol
January 2025
College of Sport and Health, Shandong Sport University, Jinan, Shandong, 250102, China.
Obesity can change the immune microenvironment of adipose tissue and induce inflammation. This study is dedicated to exploring the internal mechanism by which different intensities of exercise reprogram the immune microenvironment of epididymal adipose tissue in nutritionally obese mice. C57BL/6J male obese mouse models were constructed by high-fat diet, which were respectively obese control group (OC), moderate intensity continuous exercise group (HF-M), high intensity continuous exercise group (HF-H) and high intensity intermittent exercise group (HF-T).
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China. Electronic address:
Inflammatory response plays an essential role in the pathogenesis of cholestatic liver injury. PPARα agonists have been shown to regulate bile acid homeostasis and hepatic inflammation. However, the immunoregulatory mechanisms through which PPARα agonists ameliorate cholestatic liver injury remain unclear.
View Article and Find Full Text PDFSci Immunol
December 2024
Department of Immunobiology, Université de Lausanne, Epalinges, Switzerland.
The molecular mechanisms by which worm parasites evade host immunity are incompletely understood. In a mouse model of intestinal helminth infection using (), we show that helminthic glutamate dehydrogenase (heGDH) drives parasite chronicity by suppressing macrophage-mediated host defense. Combining RNA-seq, ChIP-seq, and targeted lipidomics, we identify prostaglandin E (PGE) as a major immune regulatory mechanism of heGDH.
View Article and Find Full Text PDFPLoS Negl Trop Dis
November 2024
Dept. of Pharmacology, Institute of Post Graduate Medical Education and Research (IPGME&R), Kolkata, India.
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