Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.
J Exp Med
March 2025
Division of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.
Lysosomal stress due to the accumulation of nucleic acids (NAs) activates endosomal TLRs in macrophages. Here, we show that lysosomal RNA stress, caused by the lack of RNase T2, induces macrophage accumulation in multiple organs such as the spleen and liver through TLR13 activation by microbiota-derived ribosomal RNAs. TLR13 triggered emergency myelopoiesis, increasing the number of myeloid progenitors in the bone marrow and spleen.
View Article and Find Full Text PDFA post-injury immune challenge with lipopolysaccharide following adult traumatic brain injury alters neuroinflammation and the gut microbiome acutely, but has little effect on chronic outcomes.
Exp Neurol
January 2025
Department of Neuroscience, The School of Translational Medicine, Monash University, Melbourne, VIC, Australia. Electronic address:
Patients with a traumatic brain injury (TBI) are susceptible to hospital-acquired infections, presenting a significant challenge to an already-compromised immune system. The consequences and mechanisms by which this dual insult worsens outcomes are poorly understood. This study aimed to explore how a systemic immune stimulus (lipopolysaccharide, LPS) influences outcomes following experimental TBI in young adult mice.
View Article and Find Full Text PDFBone fracture ruptures blood vessels and disrupts the bone marrow, the site of new red blood cell production (erythropoiesis). Current dogma holds that bone fracture causes severe hypoxia at the fracture site, due to vascular rupture, and that this hypoxia must be overcome for regeneration. Here, we show that the early fracture site is not hypoxic, but instead exhibits high oxygen tension (> 55 mmHg, or 8%), similar to the red blood cell reservoir, the spleen.
View Article and Find Full Text PDFThe immunological perspective of major depressive disorder: unveiling the interactions between central and peripheral immune mechanisms.
J Neuroinflammation
January 2025
School of Nursing, Jinan University, No.601, West Huangpu Avenue, Guangzhou, 510632, Guangdong, China.
Major depressive disorder is a prevalent mental disorder, yet its pathogenesis remains poorly understood. Accumulating evidence implicates dysregulated immune mechanisms as key contributors to depressive disorders. This review elucidates the complex interplay between peripheral and central immune components underlying depressive disorder pathology.
View Article and Find Full Text PDFEsmolol upregulates the α7 nAChR/STAT3/NF-κB pathway by decreasing the ubiquitin and increasing the ChATCD4 T lymphocyte to alleviate inflammation in septic cardiomyopathy.
Int Immunopharmacol
January 2025
Department of Critical Care Medicine, the Affiliated Hospital of Qingdao University, Qingdao 266000 Shandong, China. Electronic address:
Esmolol has been demonstrated to mitigate inflammation damage and T lymphocyte apoptosis in septic cardiomyopathy. It has been established that the activation of α7 nicotinic acetylcholine receptor (nAChR) by cluster of differentiation 4(CD4) T lymphocytes expressing choline acetyltransferase (ChAT) can prevent excessive inflammation and reduce splenocyte apoptosis in septic cardiomyopathy. Given the similar anti-inflammatory effects, we hypothesized that esmolol might be associated with α7 nAChR and thereby exert its cardioprotective functions.
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!