Conserved spinal cord bioenergetics in experimental autoimmune encephalomyelitis in C57BL6 mice, measured using phosphorescence oxygen analyzer.

Background: We have previously reported that spinal cord respiration (cellular mitochondrial oxygen consumption) and ATP content are conserved in the studied model of experimental autoimmune encephalomyelitis (EAE), foreseeing a recovery of the diseased rats. This exemplary lesion of multiple sclerosis is used here to measure spinal cord bioenergetics in C57BL6 mice. Our hypothesis is that, despite the well-known focal axonal mitochondrial pathology, bioenergetics of the CNS is reasonably preserved in this disease.

The use of phosphorescence oxygen analyzer to measure the effects of rotenone and 1-methyl-4-phenylpyridinium on striatal cellular respiration in C57BL6 mice.

Background: We have previously reported on the use of the phosphorescence oxygen analyzer for measuring spinal cord cellular respiration. This analytical tool is used here to investigate the effects of two inhibitors of NADH:ubiquinone oxidoreductase, rotenone and 1-methyl-4-phenylpyridinium, on cellular respiration in striatal tissue. Both neurotoxins can induce Parkinson's disease-like symptoms, and have been used to study this disease in animals.

Bioenergetics of the spinal cord in experimental autoimmune encephalitis of rats.

Background: Mitochondrial dysregulation is important in axonal damage and demyelination in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). There is however, no evidence in the literature of any study that has examined cellular bioenergetics of the central nervous system (CNS) during the early development and clinical course of EAE. EAE, a rodent model of relapsing/remitting MS, is a CD4(+) T cell-mediated disease of the CNS.

Interaction of amorphous silica nanoparticles with erythrocytes in vitro: role of oxidative stress.

Background/aims: The use of engineered nanomaterials in the form of nanoparticles (NP) for various biomedical applications, as well as in consumer products, has raised concerns about their safety for human health. These NP are intended to be administered directly into the circulation following intravenous injection, or they may reach the circulation following other routes of administration such as oral or inhalation, and interact with circulating cells such as erythrocytes. However, little is known about the interaction of amorphous SiNP with erythrocytes.

The cytotoxicity of aflatoxin b1 in human lymphocytes.

Objectives: Aflatoxin B1 (AFB1) is a naturally occurring carcinogenic and immunosuppressive compound. This study was designed to measure its toxic effects on human peripheral blood mononuclear cells (PBMC).

Methods: The study recruited 7 healthy volunteers.

Pam3CSK(4) enhanced beta cell loss and diabetogenesis: the roles of IFN-gamma and IL-17.

Toll like receptors are primary sensors of both innate and adaptive immune systems. They activate APCs and influence T-cell function in inflammatory autoimmune response. Studies have shown that TLR manipulation may lead to either tolerance or trigger autoimmunity.

Derangements of liver tissue bioenergetics in concanavalin A-induced hepatitis.

Background: A novel in vitro system was employed to investigate liver tissue respiration (mitochondrial O2 consumption) in mice treated with concanavalin A (Con A). This study aimed to investigate hepatocyte bioenergetics in this well-studied hepatitis model.

Methods: C57Bl/6 and C57Bl/6 IFN-γ-/- mice were injected intravenously with 12 mg ConA/kg.

IFN-γ deficiency exacerbates experimental autoimmune neuritis in mice despite a mitigated systemic Th1 immune response.

Previous studies have shown that interferon-gamma (IFN-γ) is a proinflammatory cytokine that contributes to the pathogenesis of Guillain-Barré syndrome and its animal model, experimental autoimmune neuritis (EAN). Treatments with anti-IFN-γ antibodies improve clinical outcome in GBS patients and EAN animals and administration of IFN-γ markedly worsens EAN. Paradoxically, the mice deficient in IFN-γ remain susceptible to experimental autoimmune encephalomyelitis, an analogous disease in the central nervous system.

Protein phosphatase 1-dependent dephosphorylation of Akt is the prime signaling event in sphingosine-induced apoptosis in Jurkat cells.

Sphingosine (SPH) is an important bioactive lipid involved in mediating a variety of cell functions including apoptosis. However, the signaling mechanism of SPH-induced apoptosis remains unclear. We have investigated whether SPH inhibits survival signaling in cells by inhibiting Akt kinase activity.

Early influx of macrophages determines susceptibility to experimental allergic encephalomyelitis in Dark Agouti (DA) rats.

Experimental allergic encephalomyelitis (EAE) is characterized by inflammatory infiltrates of myelin antigen(s) specific T cells and consecutive demyelination. Injection of encephalitogen into the footpads induces disease in genetically susceptible Dark Agouti rats (DA) but not in Albino Oxford (AO) rats although mild inflammatory infiltrates are observed in both strains early after disease induction. In addition, only DA rats develop disease when cells from (AO×DA) F(1) hybrids are passively transferred into sub-lethally radiated AO and DA parent hosts.

UVC-induced apoptosis in Dubca cells is independent of JNK activation and p53(Ser-15) phosphorylation.

Ultraviolet C (UVC) irradiation in mammalian cell lines activates a complex signaling network that leads to apoptosis. By using Dubca cells as a model system, we report the presence of a UVC-induced apoptotic pathway that is independent of c-Jun N-terminal kinases (JNKs) activation and p53 phosphorylation at Ser(15). Irradiation of Dubca cells with UVC results in a rapid JNK activation and phosphorylation of its downstream target c-Jun, as well as, phosphorylation of activating transcription factor 2 (ATF2).

Regulatory T cells and ST2 signaling control diabetes induction with multiple low doses of streptozotocin.

Several peripheral mechanisms appear to be operational in limiting autoimmune damage of the islets of Langerhans and organ-specific T cell-mediated autoimmunity in general. These include cyclophosphamide sensitive T regulatory cells (Treg cells) and Th2 derived cytokine downregulation. We used the model of multiple low doses of streptozotocin (MLD-STZ) induced diabetes in susceptible C57BL/6 mice and resistant BALB/c mice to study these regulatory mechanisms.

Galectin-3 deficiency reduces the severity of experimental autoimmune encephalomyelitis.

Galectin-3 (Gal-3) is a member of the beta-galactoside-binding lectin family and plays an important role in inflammation. However, the precise role of Gal-3 in autoimmune diseases remains obscure. We have investigated the functional role of Gal-3 in experimental autoimmune encephalomyelitis (EAE) following immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide.

Induction of interferon-gamma by Taenia crassiceps glycans and Lewis sugars in naive BALB/c spleen and peritoneal exudate cells.

Helminth parasites are known to alter host immune responses and the responsible molecules are a potential source of biological immunoadjuvants. Previously, we have reported strong Th-2 type immunomodulatory properties of Taenia crassiceps glycans. In this study, we report interferon-gamma (IFN-gamma) stimulatory activity of fractionated Taenia glycans and Lewis sugars with comparable glycan composition.

IL-23 leads to diabetes induction after subdiabetogenic treatment with multiple low doses of streptozotocin.

IL-23, a proximal regulator of IL-17, may be a major driving force in the induction of autoimmune inflammation. We have used a model of subdiabetogenic treatment with multiple low doses of streptozotocin (MLD-STZ; 4 x 40 mg/kg body weight) in male C57BL/6 mice to study the effect of IL-23 on immune-mediated beta cell damage and the development of diabetes, as evaluated by blood glucose, quantitative histology, immunohistochemistry and expression of relevant cytokines in the islets. Ten daily injections of 400 ng IL-23, starting on the first day of MLD-STZ administration led to significant and sustained hyperglycemia along with weight loss compared with controls (no IL-23), and a significant increase in the number of infiltrating cells, a lower insulin content, enhanced apoptosis, expression of IFN-gamma and IL-17 (not seen in the controls) and a significant increase in the expression of TNF-alpha and IL-18 in the pancreatic islets.

Adjuvant effect of Taenia crassiceps glycans against leishmanial antigens in mice infected with Leishmania mexicana.

Complex glycans derived from lipid, nucleic acid and protein free extracts of Taenia crassiceps metacestode larvae were found to have adjuvant effect against Leishmania mexicana antigens in BALB/c mice experimentally infected with L. mexicana. A single intraperitoneal or subcutaneous injection of Taenia glycans altered the Th-1/Th-2 balance in experimentally infected mice as determined by Western blot analysis of IgG 1 and IgG 2a antibodies to L.

Taenia crassiceps carbohydrates stimulate IL-6 expression in naïve murine macrophages via Toll-like receptors (TLRs).

In murine infections of Schistosoma mansoni and Taenia crassiceps, a characteristic polarization of the immune response from a Th-1 type to a Th-2 type occurs with progression of infection. In S. mansoni, egg glycoprotein carbohydrates are said to be responsible for this immunomodulatory activity.

Induction of immunoglobulin G1, interleukin-6 and interleukin-10 by Taenia crassiceps metacestode carbohydrates.

T helper type 2 (Th2) -polarized immune responses are characteristically dominant in helminth infections. Two murine models that show a Th1 to Th2 polarization with infection progression are those of Schistosoma mansoni and Taenia crassiceps. In both, an early Th1 response is replaced by a late Th2 response.