Background: Current knowledge on the exact ligand causing expression of TREM-1 on neutrophils and monocytes is limited. The present study aimed at the role of underlying infection and of the causative pathogen in the expression of TREM-1 in sepsis.
Methods: Peripheral venous blood was sampled from 125 patients with sepsis and 88 with severe sepsis/septic shock. The causative pathogen was isolated in 91 patients. Patients were suffering from acute pyelonephritis, community-acquired pneumonia (CAP), intra-abdominal infections (IAIs), primary bacteremia and ventilator-associated pneumonia or hospital-acquired pneumonia (VAP/HAP). Blood monocytes and neutrophils were isolated. Flow cytometry was used to estimate the TREM-1 expression from septic patients.
Results: Within patients bearing intrabdominal infections, expression of TREM-1 was significantly lower on neutrophils and on monocytes at severe sepsis/shock than at sepsis. That was also the case for severe sepsis/shock developed in the field of VAP/HAP. Among patients who suffered infections by Gram-negative community-acquired pathogens or among patients who suffered polymicrobial infections, expression of TREM-1 on monocytes was significantly lower at the stage of severe sepsis/shock than at the stage of sepsis.
Conclusions: Decrease of the expression of TREM-1 on the membrane of monocytes and neutrophils upon transition from sepsis to severe sepsis/septic shock depends on the underlying type of infection and the causative pathogen.
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http://dx.doi.org/10.1186/1471-2334-11-309 | DOI Listing |
Cell Death Dis
January 2025
NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Xuzhou, China.
Neuroinflammation is a key factor in the pathogenesis of Parkinson's disease (PD). Activated microglia in the central nervous system (CNS) and infiltration of peripheral immune cells contribute to dopaminergic neuron loss. However, the role of peripheral immune responses, particularly triggering receptor expressed on myeloid cells-1 (TREM-1), in PD remains unclear.
View Article and Find Full Text PDFFront Immunol
December 2024
SignaBlok, Inc., Shrewsbury, MA, United States.
TREM-1 and TREM-2 as Therapeutic Targets: Clinical Challenges and Perspectives.
View Article and Find Full Text PDFMedicine (Baltimore)
December 2024
Anhui Engineering Research Center for Neural Regeneration Technology and Medical New Materials, School of Life Science, Bengbu Medical University, Bengbu City, Anhui Province, China.
This study employed Mendelian randomization (MR) analysis to explore potential causal relationships between 731 immune cell subtypes and periodontitis. Utilizing a 2-sample MR design, our study delved into the diverse landscape of immune cell interactions with periodontitis-associated factors. Multiple MR methods, including inverse variance weighting, weighted median, and MR-Egger tests, were employed to ensure reliability and mitigate potential pleiotropic effects.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Odborarske namestie 14, 811 08 Bratislava, Slovakia.
Stress responses can impact bladder cancer (BC) outcomes via immune-inflammatory pathway modulation. This study explores heart rate variability (HRV) associations with serum immune-inflammatory biomarkers, blood count inflammatory markers, and psychosocial self-report measures in patients versus healthy controls. The TREM-1 and TREM-2 expressions on peripheral blood monocytes were analysed via flow cytometry; serum inflammatory biomarkers by ELISA; HRV (5-min ECG) pre-tumour resection; blood counts by haematology analyser; and psychosocial factors by validated questionnaires.
View Article and Find Full Text PDFFront Aging Neurosci
November 2024
Department of Endocrinology, Mianzhu People's Hospital, Mianzhu, Sichuan, China.
Background And Purpose: Triggering receptor expressed on myeloid cells-1 (TREM-1) was reported to be critical for mediating the neurological function after stroke, while the impact of soluble TREM-1 (sTREM-1) on cognitive impairment after ischemic stroke is unclear. We aimed to explore the association between sTREM-1 and post-stroke cognitive impairment (PSCI).
Methods: We prospectively recruited consecutive ischemic stroke patients who admitted hospital within 7 days of onset.
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