AI Article Synopsis
Article Abstract
CD14 is a glycoprotein that binds bacterial LPS in MØ. It is an essential component of the phagocytic system and is increased in septic shock. Critical injury and sepsis result in elevated endogenous CA levels. CAs have a significant impact on MØ inflammatory functions. We tested the hypothesis that β-adrenergic stimulation regulates CD14 expression and bacterial phagocytosis in BMØ. Murine BMØ stimulated with isoproterenol (>8 h) induced a dose-dependent increase in cell surface CD14 expression. Specific PKA inhibitor (H-89) and gene-silencing (siRNA) studies demonstrated the role of cAMP-dependent PKA in mediating this response. In addition, we observed a correlation between an isoproterenol-mediated increase in CD14 expression and live Escherichia coli uptake in BMØ. Further, the essential role of CD14 in an isoproterenol-mediated increase in E. coli uptake was highlighted from experiments using CD14(-/-) mice. Moreover, the dose response of isoproterenol stimulation to CD14 expression and E. coli phagocytosis overlapped with similar EC50. Additionally, isoproterenol-mediated E. coli phagocytosis was prevented by H-89, suggesting that β-adrenergic stimulus in BMØ increases CD14 expression and live E. coli phagocytosis through a common signaling pathway. Our studies indicate the potential impact of β-adrenergic agents on important innate immune functions.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974431 | PMC |
| http://dx.doi.org/10.1189/jlb.0410186 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Esophageal microbial dysbiosis impairs mucosal barrier integrity via toll-like receptor 2 pathway in patients with gastroesophageal reflux symptoms.
J Transl Med
December 2024
Department of Gastroenterology, The First Affiliated Hospital of Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou, Guangdong, 510080, China.
Background: Previous research on the lower gastrointestinal tract has proved that microbial dysbiosis can lead to intestinal barrier dysfunction and enhanced visceral sensitivity, thus triggering bowel symptoms. Whether esophageal microbial dysbiosis also contributes to the development of gastroesophageal reflux (GER) symptoms, which are known to be associated with impaired esophageal barrier integrity, remains to be explored.
Methods: Patients with GER symptoms (gastroesophageal reflux disease [GERD] and functional esophageal disorders [FED]), duodenal ulcer patients and healthy controls were prospectively included for esophageal microbial analysis.
Short Communication: Profiling of activated monocyte populations in autism and associations with increased severity and comorbid behaviors.
Brain Behav Immun
December 2024
Department of Medical Microbiology and Immunology, University of California, Davis, CA, USA; MIND Institute, University of California, Sacramento, CA, USA. Electronic address:
Immune dysfunction in autism spectrum disorder (ASD) has been widely reported and is associated with increased impairments in social interactions, communication, repetitive behaviors, anxiety and gastrointestinal problems. Several lines of evidence point towards increased activation of the innate immune system including activation of microglia, increases in innate inflammatory cytokines/chemokines in blood, brain tissue and CSF, activated dendritic cells and macrophages, and abnormal peripheral monocyte cell function. Monocytes are major players in innate immunity and have important functions in the phagocytosis of pathogens or debris, immune defense and cytokine/chemokine production.
View Article and Find Full Text PDFExploratory Research for HIF-1α Overexpression Tumor Antigen in the Activation of Dendritic Cells and the Potent Anti-Tumor Immune Response.
Cancer Manag Res
December 2024
Clinical Laboratory, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, People's Republic of China.
Background: Tumor-specific antigens play an important role in dendritic cell (DC)-based immunotherapy. The acquisition of tumor-specific antigens, which are essential for DC-based immunotherapy, poses a significant challenge. This study aimed to explore the efficacy of hypoxia inducible factor-1α (HIF-1α) overexpression tumor antigens in DC-based immunotherapy.
View Article and Find Full Text PDFMuramyl dipeptide potentiates lipoteichoic acid-induced nitric oxide production via TLR2/NOD2/PAFR signaling pathways.
Front Immunol
December 2024
Department of Oral Microbiology and Immunology, and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Republic of Korea.
Lipoteichoic acid (LTA) and peptidoglycan (PGN) are considered as key virulence factors of , which is a representative sepsis-causing Gram-positive pathogen. However, cooperative effect of LTA and PGN on nitric oxide (NO) production is still unclear despite the pivotal roles of NO in initiation and progression of sepsis. We here evaluated the cooperative effects of LTA (SaLTA) and muramyl dipeptide (MDP), the minimal structure of PGN, on NO production in both a mouse macrophage-like cell line, RAW 264.
View Article and Find Full Text PDFRemodeling of the chromatin landscape in peripheral blood cells in patients with severe Delta COVID-19.
Front Immunol
December 2024
The Federal Medical Biological Agency (FMBA of Russia), Moscow, Russia.
COVID-19 is characterized by systemic pro-inflammatory shifts with the development of serious alterations in the functioning of the immune system. Investigations of the gene expression changes accompanying the infection state provide insight into the molecular and cellular processes depending on the sickness severity and virus variants. Severe Delta COVID-19 has been characterized by the appearance of a monocyte subset enriched for proinflammatory gene expression signatures and a shift in ligand-receptor interactions.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!