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As immune cells, neutrophils serve as the first line of defense against infections; however, the mechanism by which neutrophils regulate lipid metabolism is unknown. The neutrophil depletion group was treated with 100 μg InVivoMAb anti-mouse Ly6G 6 times, whereas the control group mice were intraperitoneally injected with the same quantity of InVivoMAb rat IgG2a. Body fat content, triglycerides (TGs), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) in the jejunum and ileum, as well as 9 long-chain fatty acids (LCFAs) in the intestinal contents were significantly decreased. Furthermore, genes involved in the absorption of lipids in each segment of the intestine also showed decreased expression. Neutrophil-depletion and control models were administered 25 μCi of H-cholesterol by gavage. The distribution of H cholesterol in the intestinal segment, heart, liver, serum, and feces was not altered by anti-Ly6G antibodies. Metagenomics was applied to investigate uncultured microorganisms in the intestinal contents to identify bacteria containing lipid metabolism genes. At the species level, 12 bacteria were involved in unsaturated LCFA synthesis, among which 2 increased and 10 decreased. The overall relative abundance of these bacteria decreased from 3.102% to 0.734%. Many genes involved in lipid metabolism were also reduced as a result, such as fatty acid synthase and peroxisome proliferator-activated receptor γ. In conclusion, neutrophil depletion does not affect intestinal lipid absorption in the diet but leads to a decrease in the overall relative abundance of gut bacteria involved in unsaturated LCFA synthesis. Consequently, intestinal lipid synthesis and absorption are reduced.
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http://dx.doi.org/10.1002/cbf.70060 | DOI Listing |
Infect Immun
September 2025
Institute of Medical Microbiology and Hospital Hygiene, Heinrich Heine University, Düsseldorf, Germany.
Lymphotoxin β receptor (LTβR/TNFRSF3) signaling plays a crucial role in immune defense. Notably, LTβR-deficient (LTβR) mice exhibit severe defects in innate and adaptive immunity against various pathogens and succumb to infection. Here, we investigated the bone marrow (BM) and peritoneal cavity (PerC) compartments of LTβR mice during infection, demonstrating perturbed B-cell and T-cell subpopulations in the absence of LTβR signaling.
View Article and Find Full Text PDFAlveolar macrophages (AMs) are the first immune cells to encounter Mycobacterium tuberculosis (Mtb) in the lungs, but they frequently fail to eliminate this causative agent of tuberculosis (TB), allowing Mtb to persist or replicate. Interstitial macrophages (IMs) are recruited to restrict Mtb growth and limit immune evasion. While IMs have been implicated in the control of acute Mtb infection, their role during latent tuberculosis infection (LTBI) has not yet been explored.
View Article and Find Full Text PDFJ Clin Invest
September 2025
Tianjin Key Laboratory of Inflammatory Biology, Department of Pharmacology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
VEXAS (Vacuoles, E1 enzyme, X-linked, Autoinflammatory, Somatic) syndrome is a haemato-rheumatoid disease caused by somatic UBA1 mutations in hematopoietic stem cells (HSCs). The pathogenic cell type(s) responsible for the syndrome are unknown and murine models recapitulating the disease are lacking. We report that loss of Uba1 in various mouse hematopoietic cell types resulted in pleiotropic consequences and demonstrate that murine mutants with about 70% loss of Uba1 in neutrophils induced non-lethal VEXAS-like symptoms.
View Article and Find Full Text PDFPLoS Pathog
September 2025
Department of Pediatric Pneumology, Allergology and Neonatology, Hannover Medical School, Hannover, Germany.
Many microorganisms can degrade alkanes, using them as carbon source. The first and key step in alkane utilization is its hydroxylation, which requires a catalytic membrane-bound monooxygenase, a soluble rubredoxin and a soluble rubredoxin reductase. By comparing the phenotype of Pseudomonas aeruginosa strain TBCF10839 with an isogenic mutant that carries a plasposon within the rubredoxin reductase gene rubB (PA5349) and the complemented mutant, we report multiple, yet unknown roles of rubredoxin reductase in the physiology of P.
View Article and Find Full Text PDFWorld J Methodol
December 2025
The 2 Department of Propaedeutic Surgery, Hippokration General Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki 54642, Greece.
Hepatic ischemia-reperfusion injury is an important mechanism of liver failure that occurs in many clinical conditions, including massive hemorrhage, major hepatectomy and liver transplantation, and leads to poor outcomes. The underlying cellular and molecular reactions are extremely complex and not completely understood. Anaerobic metabolism, ATP depletion, intracellular acidosis, calcium overload, mitochondrial dysfunction, oxidative stress, activation of Kupffer cells and neutrophils, platelet aggregation, nitric oxide production, activation of the complement system and overexpression of cytokines and chemokines constitute the main pathophysiological actions and pathways for possible therapeutic strategies.
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