Objective: To characterize the hepatic leukocyte endothelial cell interactions occurring in early sepsis and to determine whether this is influenced by fluid treatment.
Methods: Sepsis was induced by cecal ligation and perforation in C57Bl/6 mice. One of 6 iv fluid regimes was given immediately postsurgery and at 6 h. The hepatic microcirculation was examined by intravital microscopy at 6 h.
Results: All 0.9% saline-based solutions were associated with an increase in leukocyte-endothelial cell interactions as demonstrated by an increase in the rolling flux in the sham and naïve mice. In the septic mice treated with normal saline, there was a 20-fold increase in leukocyte adhesion within the postsinusoidal venules, compared to sham mice. Treatment with lactated Ringer's reduced the sepsis-mediated leukocyte recruitment by 50%. When septic mice received 6% pentastarch in a balanced solution or 3% saline, venular leukocyte adhesion was reduced by an additional 50%. When the pentastarch was prepared in normal saline there was no further reduction in venular leukocyte adhesion compared to the lactated Ringer's-treated mice. All hyperosmolar solutions improved the sepsis-induced reduction in sinusoidal perfusion but only the pentastarch in the balance solution significantly reduced the number of adherent leukocytes within the sinusoids.
Conclusions: Hepatic leukocyte recruitment occurs early in sepsis. Pentastarch in a balanced solution but not in normal saline significantly reduces hepatic leukocyte recruitment, suggesting solution composition, as well as osmolarity impact the innate immune response.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1080/10739680490517712 | DOI Listing |
Signal Transduct Target Ther
January 2025
Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Dynamic communication between hepatocytes and the environment is critical in hepatocellular carcinoma (HCC) development. Clinical immunotherapy against HCC is currently unsatisfactory and needs more systemic considerations, including the identification of new biomarkers and immune checkpoints. Transmembrane 4 L six family member 5 (TM4SF5) is known to promote HCC, but it remains unclear how cancerous hepatocytes avoid immune surveillance and whether avoidance can be blocked.
View Article and Find Full Text PDFThe immune system shapes body metabolism, while interactions between peripheral neurons and immune cells control tissue homeostasis and immunity. However, whether peripheral neuroimmune interactions orchestrate endocrine system functions remains unexplored. After fasting, mice lacking type 2 innate lymphoid cells (ILC2s) displayed disrupted glucose homeostasis, impaired pancreatic glucagon secretion, and inefficient hepatic gluconeogenesis.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Pharmacy, College of Pharmacy, Kangwon National University, Chuncheon, South Korea.
Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by severe liver inflammation and fibrosis due to an imbalanced immune response caused by enhanced bacterial components. The progression of MASH is closely linked to increased permeability of intestinal mucosal barrier facilitating enter of bacterial components into hepatic portal venous system. B cells are important immune cells for adaptive responses and enhance hepatic inflammation through cytokine production and T cell activation.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Clinical Laboratory, the Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Backgrounds And Aims: CD8+T cells are crucially associated with the fight against hepatitis B virus (HBV) infection. CD161 has been shown to express remarkably on HCV-specific CD8+T cells. However, the accurate function of CD161+CD8+T cells in HBV immunity or pathogenesis remains undetermined.
View Article and Find Full Text PDFCureus
December 2024
Pharmacy, Punjab University College of Pharmacy, Lahore, PAK.
Berardinelli-Seip congenital lipodystrophy (BSCL), also known as congenital generalized lipodystrophy (CGL), is an exceptionally rare autosomal recessive disorder marked by a significant deficiency of adipose tissue throughout the body. This lack of adipose tissue, normally found beneath the skin and between internal organs, leads to impaired adipocyte formation and fat storage, causing lipids to accumulate in atypical tissues such as muscles and the liver. The extent of adipose tissue loss directly influences the severity of symptoms, which can include a muscular appearance, increased appetite, bone cysts, marrow fat depletion, acromegalic features, severe insulin resistance, skeletal muscle hypertrophy, hypertrophic cardiomyopathy, hepatic steatosis, hepatomegaly, cirrhosis, and intellectual disability.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!