Objectives: The aim of this study was to assess the cell surface expression of adhesion (CD11a, CD11b, CD11c, CD18, CD54, and CD58) and activation (CD14, HLA-DR, and CD16) molecules on the circulating monocytes in Helicobacter pylori (H. pylori)-infected and noninfected children with gastritis, with the goal of comparing the results with those obtained from the controls.
Materials And Methods: Ninety-four children were studied: 47 of them with H. pylori infection (of those 25 children after the failure of eradication therapy) and 26 children with gastritis where H. pylori infection was excluded, as well as 21 controls. H. pylori infection status was assessed based on [¹³C] urea breath test, rapid urease test, and histology. Analysis of the monocyte surface molecule expression was carried out by flow cytometry.
Results: H. pylori-infected children and children who experienced a failure of the eradication therapy differed significantly in the expression of adhesion and activation molecule on circulating monocytes. A decrease, both in the proportion of CD11c- and CD14-bearing monocytes, and the expression of CD11c and CD14 molecules on circulating monocytes, was found in children in whom the eradication therapy failed (p < .05). Low expression of CD11b (p = .04) and CD18 (p = .02) integrins on monocytes was also observed. Additionally, the percentage of HLA-DR-bearing monocytes was decreased (p = .04), while the CD16 density receptor was increased (p = .02). Compared with the controls, low percentage of CD16-positive monocytes was noted in noninfected children with gastritis (p = .01).
Conclusion: H. pylori eradication therapy in children causes inhibition of inflammatory response via a reduction in CD11b, CD11c, and CD18 beta2 integrin monocyte expression.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/j.1523-5378.2011.00932.x | DOI Listing |
Microbiol Spectr
December 2024
Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky, USA.
Unlabelled: are facultative intracellular bacterial pathogens that cause foodborne disease in humans. The bacteria can use the surface protein InlA to invade intestinal epithelial cells or transcytose across M cells in the gut, but it is not well understood how the bacteria traffic from the underlying lamina propria to the draining mesenteric lymph nodes (MLN). Previous studies indicated that associated with both monocytes and dendritic cells in the intestinal lamina propria.
View Article and Find Full Text PDFJ Inflamm Res
December 2024
Department of Neurology, Liaocheng People's Hospital, Shandong University, Jinan, Shandong, 250012, People's Republic of China.
Background: Plaque enhancement is a non-specific marker of local inflammatory response, which may offer additional insights together with circulating inflammatory markers. Few studies have analyzed the association between intracranial atherosclerotic stenosis (ICAS) plaque enhancement and circulating inflammatory markers. Given the age-related variability in the progression of ICAS, this study aims to explore the association between the two across different age groups.
View Article and Find Full Text PDFJ Reprod Immunol
December 2024
Placenta Lab, Department of Obstetrics, Jena University Hospital, Jena, Germany. Electronic address:
Released from trophoblast and other fetal cells, placental extracellular vesicles (EVs) reach the maternal peripheral blood and modulate immune responses. Increased EVs in plasma of preeclampsia (PE) patients indicate their involvement in the etiology of this condition. This study addresses the uptake of plasma EVs by peripheral blood mononuclear cells (PBMCs) and explores the underlying internalization mechanisms.
View Article and Find Full Text PDFClin Pharmacol Ther
December 2024
Incyte Corporation, Wilmington, Delaware, USA.
Axatilimab, a high-affinity humanized immunoglobulin G4 monoclonal antibody against colony-stimulating factor 1 receptor (CSF-1R), is approved for the treatment of chronic graft-versus-host disease (cGVHD), and under investigation for idiopathic pulmonary fibrosis and solid tumors. The population pharmacokinetics (PK) and pharmacodynamics (PD) of axatilimab were characterized in healthy participants and patients with solid tumors or cGVHD using data from four clinical studies with 325 participants, including 278 patients with cGVHD. The model structure reflected the mechanism of action of axatilimab: blocking CSF-1R signaling with axatilimab reduces the circulating levels of cells in the mononuclear phagocytic cell lineage (including nonclassical monocytic cells (NCMCs) and Kupffer cells), resulting in increases in circulating enzymes owing to reduced clearance by Kupffer cells.
View Article and Find Full Text PDFAdv Radiat Oncol
February 2025
University of Minnesota Medical School, Minneapolis, Minnesota.
Purpose: The immunosuppressive function of myeloid-derived suppressor cells (MDSCs) has been implicated in the regulation of immune responses against cancer and is associated with poor prognosis. Radiation treatment is known to alter immune cell populations within the tumor; however, whether this results in the recruitment of immunosuppressive MDSC populations is not well understood. Here we evaluate the response of circulating MDSC populations in patients treated per standard-of-care cisplatin chemoradiation therapy (CRT) for locally invasive cervical cancer.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!