Soluble CD163, soluble CD14 and cellular HIV-1-DNA levels reflect two different aspects of HIV infection: immune activation and the reservoir of infected cells. The aim of this study was to describe their relationships in a cohort of HIV-HCV co-infected patients successfully treated for both HCV and HIV infections. Fifty-five patients were recruited and studied prior to the start of direct-acting antivirals (DAAs) (T0), at week 12 of DAA treatment (T1) and 24 weeks after T0 (T2). The subjects were classified as having undetectable plasma HIV viraemia (UV) or low-level viraemia (LLV) in the 18 months before T2. Plasma levels of sCD163 and of sCD14 were comparable in patients with UV and in subjects with LVL at T0, T1 and T2. The HIV DNA level was positively correlated with LLV but not with sCD163 and sCD14 levels; these two markers of inflammation were positively correlated (p = 0.017). Soluble CD163 and sCD14 decreased over time from T0 to T2 (p = 0.000 and p = 0.034, respectively). In conclusion, the significant decrease in sCD163 and sCD14 levels in patients cured of HCV infection, regardless of the presence of LLV, suggests a main role for HCV in immune activation in HIV-HCV co-infected patients.
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http://dx.doi.org/10.1007/s00430-018-0538-1 | DOI Listing |
Clin Exp Hepatol
March 2024
General Surgery Department, Hepatobiliary Surgery Unit, Faculty of Medicine, Alexandria University, Egypt.
Aim Of The Study: Metabolic associated steatotic liver disease (MASLD) is one of the most frequent chronic liver diseases in the world; macrophage activation is reflected by increased expression of CD163, which sheds as serum soluble CD163 that is linked to hepatic steatosis, inflammation, and fibrosis. Aim of the study was assessment of liver macrophage activation and hepatic histopathological changes in patients with MASLD.
Material And Methods: A total of 30 patients with MASLD and equal numbers of age- and sex-matched healthy controls were enrolled in the study.
Am J Cancer Res
December 2024
Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health Bethesda, MD 20892, USA.
Anaplastic thyroid cancer (ATC) is a lethal endocrine malignancy. It has been shown that tumor-associated macrophages (TAMs) contribute to the aggressiveness of ATC. However, stimulatory factors that could facilitate the induction and infiltration of TAMs in the ATC tumor microenvironment (TME) are not fully elucidated.
View Article and Find Full Text PDFJ Agric Food Chem
January 2025
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Yuanmingyuan West Road, Beijing 100193, China.
In clinical mastitis of dairy cows, the abnormal accumulation of apoptotic cells (ACs) and subsequent secondary necrosis and inflammation pose significant concerns, with macrophage-mediated efferocytosis, crucial for ACs clearance, remaining unexplored in this context. In nonruminants, MER proto-oncogene tyrosine kinase (MERTK) receptors are essential for efferocytosis and A Disintegrin and Metalloproteinase 17 (ADAM17) is thought to play a role in regulating MERTK integrity. This study aimed to delineate the in situ role of efferocytosis in clinical mastitis, with a particular focus on the interaction between MERTK and ADAM17 in bovine macrophages.
View Article and Find Full Text PDFPancreas
December 2024
Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford, California.
Objectives: Activation of type M2 macrophages has been implicated in the pathogenesis of chronic pancreatitis (CP). In a clinical pilot study, we investigated blood-based markers of macrophage activation at different stages of CP.
Methods: We performed a cross-sectional analysis of prospectively collected plasma samples from healthy controls and patients with suspected or definitive CP according to the M-ANNHEIM criteria.
J Hepatol
October 2024
Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:
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