Dexmedetomidine attenuates sepsis-associated acute lung injury by regulating macrophage efferocytosis through the ROS/ADAM10/AXL pathway.

Background: The lungs are highly susceptible to damage during sepsis, with severe lung injury potentially progressing to acute respiratory distress syndrome and even fatal sepsis. Effective efferocytosis of apoptotic cells is crucial in alleviating inflammation and tissue injury.

Methods: We established a septic lung injury mouse model via intraperitoneal injection of lipopolysaccharide.

Macrophage STING signaling promotes NK cell to suppress colorectal cancer liver metastasis via 4-1BBL/4-1BB co-stimulation.

Background And Aims: Macrophage innate immune response plays an important role in tumorigenesis. However, the role and mechanism of macrophage STING signaling in modulating tumor microenvironment to suppress tumor growth at secondary sites remains largely unclear.

Methods: STING expression was assessed in liver samples from patients with colorectal cancer (CRC) liver metastasis.

Defective mitophagy in aged macrophages promotes mitochondrial DNA cytosolic leakage to activate STING signaling during liver sterile inflammation.

Macrophage-stimulator of interferon genes (STING) signaling mediated sterile inflammation has been implicated in various age-related diseases. However, whether and how macrophage mitochondrial DNA (mtDNA) regulates STING signaling in aged macrophages remains largely unknown. We found that hypoxia-reoxygenation (HR) induced STING activation in macrophages by triggering the release of macrophage mtDNA into the cytosol.

MGP promotes CD8 T cell exhaustion by activating the NF-κB pathway leading to liver metastasis of colorectal cancer.

Matrix Gla protein (MGP) was originally reported as a physiological suppressor of ectopia calcification and has also been reported to be associated with cancer. However, the relation between the biological functions of MGP and the immune response in colorectal cancer (CRC) remains unclear. Here, we investigated the regulatory role of MGP in the immune microenvironment of CRC.

m6A modification of circHPS5 and hepatocellular carcinoma progression through HMGA2 expression.

N6-methyladenosine (m6A) is capable of mediating circRNA generation in carcinoma biology. Nevertheless, the posttranscriptional systems of m6A and circRNA in hepatocellular carcinoma (HCC) development are still unclear. The present study identified a circRNA with m6A modification, circHPS5, which was increased in neoplasm HCC tissues and indicated poor patient survival.

Obstructive jaundice secondary to fungal infection: a rare case report.

Obstructive jaundice is characterized by an obstruction of the intrahepatic or extrahepatic biliary system, and the most common causes include pancreatic and duodenal periampullary cancer. There have been some cases reporting obstructive jaundice caused by infection. Deep tissue infection usually develops in the individuals who are immunologically compromised or chronically ill, while a few cases reported in the immunocompetent patients.

Aging aggravated liver ischemia and reperfusion injury by promoting hepatocyte necroptosis in an endoplasmic reticulum stress-dependent manner.

Background: Aggravated liver ischemia and reperfusion (IR) injury has been reported in aged mice. Although necroptosis inhibition showed no crucial effect on hepatic IR injury in young mice, whether and how necroptosis affects liver IR injury in aged mice remains unclear.

Methods: Young and aged mice were subjected to liver IR modeling.

Aging aggravated liver ischemia and reperfusion injury by promoting STING-mediated NLRP3 activation in macrophages.

Although aggravated liver injury has been reported in aged livers post-ischemia and reperfusion (IR), the underlying mechanism of innate immune activation of aged macrophages is not well understood. Here, we investigated whether and how Stimulator of interferon genes (STING) signaling regulated macrophage proinflammatory activation and liver IR injury. Mice were subjected to hepatic IR in vivo.

N-acetylcysteine alleviates liver injury by suppressing macrophage-mediated inflammatory response post microwave ablation.

Object: To investigate N-acetyl-cysteine (NAC) would able to alleviate liver injury and systemic inflammatory response caused by microwave ablation (MWA) in rats.

Materials And Methods: Male Sprague-Dawley rats weighing 150-200 g were randomly divided into sham group (only anesthesia and laparotomy except MWA but with intraperitoneal PBS or NAC solution injection according to different situations), control group (intraperitoneal PBS injection for comparation 2 h prior to MWA), and NAC-treated group (intraperitoneal N-acetyl-cysteine (300 mg/kg) injection 2 h prior to MWA). Experimental rats were sacrificed at 4 h following operation in line with the liver injury severity curve.

Dexmedetomidine preconditioning alleviated murine liver ischemia and reperfusion injury by promoting macrophage M2 activation via PPARγ/STAT3 signaling.

Background: Although a protective role of dexmedetomidine in liver ischemia and reperfusion (IR) injury has been reported, the underlying mechanism remains to be determined. The aim of this study is to analyze the effects of dexmedetomidine on the regulation of macrophage innate immune activation during liver IR.

Methods: Mice were randomly divided into dexmedetomidine preconditioning (DEX) and phosphate buffered saline vehicle control (VEH) groups.

Combined ischemic and rapamycin preconditioning alleviated liver ischemia and reperfusion injury by restoring autophagy in aged mice.

Old livers are more damaged by hepatic ischemia and reperfusion (IR) injury than young livers. The aim of this study was to investigate the effects of ischemic and rapamycin preconditioning on IR injury in old livers. Young (8-week-old) and aged (60-week-old) mice were subjected to IR or a sham control procedure.