An imbalance in apoptosis or survival of immune cells plays an essential role in the pathophysiology of sepsis. Phagocytosis-induced cell death (PICD) is a common result of the pathogen-host cell interaction mediated by reactive oxygen species (ROS). Neonatal sepsis is frequently characterized by hyperinflammation. Cord blood monocytes (CBMO) are equivalent to monocytes of adults [peripheral blood monocytes (PBMO)], both in terms of phagocytosis and killing of Escherichia coli. We investigated whether CBMO are less sensitive toward PICD compared with PBMO. Monocytes were infected with green fluorescent protein (GFP)-labeled E. coli. Phagocytic activity, cell-count, Annexin V staining, hypoploid DNA content, CD95 and CD95L expression, and caspase-8 and -9 activities were analyzed by flow cytometry, ROS production by chemiluminescence, and CD95L mRNA expression by reverse-transcriptase polymerase chain reaction. With equal phagocytic activity and ROS production, PBMO cell count was decreased by 82 +/- 6% versus 28 +/- 8% for CBMO after infection. Annexin V binding was enhanced fivefold on PBMO; 56 +/- 15% of PBMO showed a hypodiploid DNA content compared with 9 +/- 6% of CBMO. Caspases CD95L and CD95L mRNA were up-regulated in PBMO. Our results indicate that CBMO are less sensitive toward E. coli-mediated PICD than PBMO. Modifying monocyte apoptosis may be a target for future interventions in sepsis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1203/PDR.0b013e31815b8e9f | DOI Listing |
Biomedicines
December 2024
Department of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy.
Background: Anaplastic lymphoma kinase (ALK) plays a role in the development of lymphoma, lung cancer and neuroblastoma. While tyrosine kinase inhibitors (TKIs) have improved treatment outcomes, relapse remains a challenge due to on-target mutations and off-target resistance mechanisms. ALK-positive (ALK+) tumors can evade the immune system, partly through tumor-associated macrophages (TAMs) that facilitate immune escape.
View Article and Find Full Text PDFPhytomedicine
December 2024
Department of Neurology, Center for Cognitive Neurology, Fujian Medical University Union Hospital, 29 Xinquan Road, Fuzhou 350001, China; Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, 29 Xinquan Road, Fuzhou 350001, China; Institute of Clinical Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou 350001, China; Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, 88 Jiaotong Road, Fuzhou 350001, China; Clinical Research Center for Precision Diagnosis and Treatment of Neurological Diseases of Fujian Province, Fuzhou 350001, China. Electronic address:
Cells
July 2024
Center of Excellence in Hip, Scottish Rite for Children, Dallas, TX 75219, USA.
Cancer Res
October 2024
State Key Laboratory of Oral Disease & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Developing effective treatments for patients with head and neck squamous cell carcinoma (HNSCC) is a significant challenge. Cetuximab, a first-line targeted therapy for HNSCC, exhibits limited efficacy. Here, we used pooled CRISPR screening to find targets that can synergize with cetuximab and identified CD47 as the leading candidate.
View Article and Find Full Text PDFToxicon
August 2024
Laboratório de Farmacologia - Instituto Butantan, São Paulo, Brazil. Electronic address:
Phagocytosis, an essential process for host defense, requires the coordination of a variety of signaling reactions. MT-II, an enzymatically inactive Lys49 phospholipase A (PLA) homolog, and MT-III, a catalytically-active Asp49 PLA, are known to activate phagocytosis in macrophages. In this study, the signaling pathways mediating phagocytosis, focusing on protein kinases, were investigated.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!