Biochemical and Ultrastructural Analysis of Ovaries of African Sharptooth Catfish,Clarias gariepinus (Burchell) Exposed to Pollutants from River Yamuna in Delhi Region,India

Biology Bulletin - The increasing level of pollution in River Yamuna has turned it into sewage carrying drain, thus, distressing aquatic life as the river traverses downstream from Wazirabad (entry...     

Acute Multiple Sclerosis Characterized by Extensive Mononuclear Phagocyte Infiltration

In this study, we examine the clinical, neuroradiological, and immunohistochemical findings of a 51 year old white female who died 27 months after onset of acute multiple sclerosis despite treatment with interferon-, azathioprine, corticosteroids, and cyclophosphamide. Immunohistochemical studies revealed extensive gliosis and mononuclear phagocyte infiltration with corresponding upregulation of proinflammatory cytokines (eg. IFN-, TNF-). The significance of immunohistochemical findings with respect to clinical presentation is discussed.     

Intra-peritoneal Injection of Polyclonal Anti-Interferon Alpha Antibodies Cross the Blood Brain Barrier and Neutralize Interferon Alpha

The central nervous system (CNS) is known to be an immunologically privileged organ in the body largely because the blood brain barrier (BBB) prevents the flow of large molecules, proteins, and cells from crossing into the CNS from the periphery. These restrictive properties of the BBB have made it difficult to treat CNS diseases. In this study, mice were infected intracranially (i.c.) with Sindbis virus (SV) and then treated either i.c. or intraperitoneally (i.p.) with neutralizing antibodies against interferon alpha (IFNα). SV infected control mice received i.p. saline. Antibodies against mouse IFNα were detected in the brain tissue of mice that received i.p. and i.c. injections of the antibody. ELISA analysis showed that both i.c. and i.p. antibody treated mice had significantly decreased levels of IFNα in the brain tissue. Also, mice that received IFNα neutralizing antibodies showed decreased presence of protein kinase R (PKR) measured by immunohistochemical densitometry, indicating the antibody successfully inhibited IFNα. The data shows that antibodies are capable of crossing the BBB and inhibiting IFNα, indicating that it is possible to target molecules of interest in the CNS with peripheral antibody treatment.     

Interferon-α (IFNα) neurotoxicity

Clinical studies indicate that increased central nervous system (CNS) interferon-alpha (IFNα) is associated with cognitive dysfunction in a wide variety of conditions. This has perhaps been best studied in HIV-associated neurocognitive disorders (HAND). These findings on IFNα neurotoxicity have been corroborated in animal studies. Probably the best demonstration of the neurotoxicity of IFNα was through the use of a mouse model of HAND, where it was shown that blocking IFNα with neutralizing antibodies prevented behavioral deficits and associated histopathological effects. In vitro studies have demonstrated a dose dependent, detrimental effect of IFNα on neuronal dendrites. Development of therapeutics that block IFNα may prove to be an effective treatment of HAND and other inflammatory conditions where there is increased CNS IFNα.     

Morphine Exposure During HIV Encephalitis in SCID Mice

Neurochemical Research - HIV encephalitis (HIVE) is often complicated by opiate abuse. Based on human pathological, animal and in vitro studies, opiates are thought to exacerbate HIVE. To test this...     

Long term intraparenchymal Ig secretion after acute viral encephalitis in mice.

Oligoclonal bands in the cerebrospinal fluid indicate intrathecal synthesis of Ig of restricted heterogeneity and are associated with a number of central nervous system inflammatory diseases. To gain better insight into the persistence of oligoclonal bands found in the central nervous system we studied mice infected with Sindbis virus (SV), a RNA virus that causes an acute, nonfatal encephalitis in mice. SV was inoculated intracerebrally into weanling mice and brains and spleens were harvested at various time points long after the acute encephalitis had resolved. A modified enzyme-linked immunoassay was used to study cultured B cells separated from the brain and spleen for their Ig isotype expression and specificity for SV. We used the polymerase chain reaction technique to detect SV RNA in brain. Three mo after inoculation 47% of the B cells found in brain are secreting antibody specific for SV structural proteins. By 1 yr 62% are SV specific. B cells secreting IgG2a predominate. Polymerase chain reaction data indicate that despite complete clearance of infectious virus by 7 days SV RNA is still present in brain at least 6 mo after infection. The data indicate that B cells in brain secrete antibody to SV long after the acute encephalitis has resolved. The persistence of SV RNA suggests that viral protein may continue to be made, providing the impetus for the continued presence of SV-specific B cells in the brain.