Update of inflammasome activation in microglia/macrophage in aging and aging-related disease.

Aging and aging-related CNS diseases are associated with inflammatory status. As an efficient amplifier of immune responses, inflammasome is activated and played detrimental role in aging and aging-related CNS diseases. Macrophage and microglia display robust inflammasome activation in infectious and sterile inflammation.

Development of a PD-L1-Expressing Orthotopic Liver Cancer Model: Implications for Immunotherapy for Hepatocellular Carcinoma.

Background: Anti-programmed cell death-1(anti-PD1) treatment has shown promising antitumor efficacy in patients with advanced hepatocellular carcinoma (HCC). This study sought to explore the functional significance of programmed death ligand-1 (PD-L1) expression in tumor cells in the tumor microenvironment.

Methods: The mouse liver cancer cell line BNL-MEA was transfected with PD-L1 plasmids and stable clones expressing PD-L1 were selected.

[Preliminary study of DTI on cerebral white matter micro-structure of patients with idiopathic olfactory loss].

Objectives: To investigate the cerebral white matter micro-structure in patients with idiopathic olfactory loss using diffusion tensor imaging (DTI).

Methods: Sixteen patients with idiopathic olfactory loss and sixteen normal subjects matched by age and sex were recruited in this study. Sniffin'Stick olfactory test was performed to evaluate the olfactory function of all subjects.

IL-23 is required for long-term control of Mycobacterium tuberculosis and B cell follicle formation in the infected lung.

IL-23 is required for the IL-17 response to infection with Mycobacterium tuberculosis, but is not required for the early control of bacterial growth. However, mice deficient for the p19 component of IL-23 (Il23a(-/-)) exhibit increased bacterial growth late in infection that is temporally associated with smaller B cell follicles in the lungs. Cxcl13 is required for B cell follicle formation and immunity during tuberculosis.

Peripheral blood mononuclear cell gene array profiles in patients with overactive bladder.

Objectives: To investigate the utility of using peripheral blood mononuclear cells (PBMC) as a marker for patients with overactive bladder (OAB). Patients with OAB may suffer from varying degrees of symptoms such as frequency, urgency, nocturia, and incontinence; however, there is no definitive test for OAB at this time. Questionnaires may provide useful tools for screening patients for OAB but often clinicians may need to rely on more invasive procedures to confirm the diagnosis.

Pancreatitis-associated protein 2 modulates inflammatory responses in macrophages.

Pancreatitis-associated proteins (PAP) are stress-induced secretory proteins that are implicated in immunoregulation. Previous studies have demonstrated that PAP is up-regulated in acute pancreatitis and that gene knockdown of PAP correlated with worsening severity of pancreatitis, suggesting a protective effect for PAP. In the present study, we investigated the effect of PAP2 in the regulation of macrophage physiology.

Small-interference RNA gene knockdown of pancreatitis-associated proteins in rat acute pancreatitis.

Objectives: Pancreatitis-associated proteins (PAPs) are induced in acute pancreatitis and antisense-mediated gene knockdown of PAP decreased PAP gene expression and worsened pancreatitis. Here, we investigated the effect of a more stable inhibition of PAP using small-interference RNA gene knockdown in vitro and in an in vivo model of experimental pancreatitis.

Methods: Pancreatitis-associated protein-specific siRNA was administered to AR42J cell cultures or rats induced with pancreatitis.

Use of gene expression profiles in cells of peripheral blood to identify new molecular markers of acute pancreatitis.

Hypothesis: Blood leukocytes play a major role in mediating local and systemic inflammation during acute pancreatitis. We hypothesize that peripheral blood mononuclear cells (PBMCs) in circulation exhibit unique changes in gene expression and could provide a "reporter" function that reflects the inflammatory response in the pancreas with acute pancreatitis.

Design: To determine specific changes in blood leukocytes during acute pancreatitis, we studied the gene transcription profile in PBMCs in a rat model of experimental pancreatitis (sodium taurocholate).

Dexamethasone mediates protection against acute pancreatitis via upregulation of pancreatitis-associated proteins.

Aim: To examine the influence of dexamethasone on pancreatitis-associated protein (PAP) gene expression using both in vitro and in vivo models of acute pancreatitis and to study how PAP gene expression correlates with severity of pancreatitis.

Methods: In vitro, IL-6 stimulated pancreas acinar AR42J cells were cultured with increasing concentrations of dexamethasone and assayed for PAP expression (RT-PCR). In vivo, pancreatitis was induced in rats by retrograde injection of 40 g/L taurocholate into the pancreatic duct.

Sophorolipids block lethal effects of septic shock in rats in a cecal ligation and puncture model of experimental sepsis.

Objective: Sophorolipids, a family of natural and easily chemoenzymatically modified microbial glycolipids, are promising modulators of the immune response. The potential of the therapeutic effect of sophorolipids was investigated in vivo in a rat model of sepsis and in vitro by analysis of nitric oxide and cytokine production.

Design: Prospective, randomized animal study.

Pancreatic elastase is proven to be a mannose-binding protein--implications for the systemic response to pancreatitis.

Background: Mannose-binding proteins (MBPs) have been isolated from serum, liver, lung, and kidney and are believed to play an important role in first-line host defense during acute phase inflammatory response. Because of the inflammatory nature of pancreatitis, we postulate that the pancreas produces endogenous MBP.

Methods: Pancreatic juice, from both human and rat, was collected by pancreatic duct cannulation and subjected to mannose-Sepharose affinity chromatography to isolate pancreatic MBP (pMBP).