Mast cell activation in the skin of Plasmodium falciparum malaria patients.

Background: Mast cells (MCs) play an important role in the immune response and inflammatory processes. Generally, MCs can be stimulated to degranulate and release histamine upon binding to immunoglobulin E (IgE). In malaria, MCs have been linked to immunoglobulin (Ig) E-anti-malarial antibodies.

Anti-IL-17A treatment reduces clinical score and VCAM-1 expression detected by in vivo magnetic resonance imaging in chronic relapsing EAE ABH mice.

IL-17 is argued to play an important role in the multiple sclerosis-like disease experimental autoimmune encephalitis (EAE). We investigated the therapeutic effects of anti-IL-17A in a chronic relapsing EAE ABH mouse model using conventional scoring, quantitative behavioral outcomes, and a novel vascular cell adhesion molecule 1 (VCAM-1)-targeted magnetic resonance imaging (MRI) contrast agent [anti-VCAM-microparticles of iron oxide (MPIO)] to identify conventionally undetectable neuropathology. Mice were administered prophylactic or treatment regimens of anti-IL-17A or IgG and two injections of anti-VCAM-MPIO before undergoing T2*-weighted three-dimensional and gadolinium-diethylenetriamine pentaacetic acid T1-weighted MRI.

A contrast agent recognizing activated platelets reveals murine cerebral malaria pathology undetectable by conventional MRI.

Human and murine cerebral malaria are associated with elevated levels of cytokines in the brain and adherence of platelets to the microvasculature. Here we demonstrated that the accumulation of platelets in the brain microvasculature can be detected with MRI, using what we believe to be a novel contrast agent, at a time when the pathology is undetectable by conventional MRI. Ligand-induced binding sites (LIBS) on activated platelet glycoprotein IIb/IIIa receptors were detected in the brains of malaria-infected mice 6 days after inoculation with Plasmodium berghei using microparticles of iron oxide (MPIOs) conjugated to a single-chain antibody specific for the LIBS (LIBS-MPIO).

Post-conditioning with lipopolysaccharide reduces the inflammatory infiltrate to the injured brain and spinal cord: a potential neuroprotective treatment.

Systemic infection often accompanies or precedes acute brain injury, but it remains unclear how the systemic response contributes to outcome. To examine this problem we have microinjected recombinant interleukin-1beta (IL-1beta), a cytokine associated with acute brain injury, into the rat brain parenchyma and either preceded or followed this challenge with the intravenous injection of lipopolysaccharide (LPS), which mimics systemic inflammatory response syndrome. The microinjection of IL-1beta alone into the brain parenchyma gives rise to leukocyte mobilization in the blood, and to the delayed recruitment of neutrophils and monocytes to the brain with no evidence of blood-brain barrier breakdown or overt neuronal cell death.

Cryptococcal meningitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients.

This study compared clinical manifestations, blood biochemistry and cerebrospinal fluid (CSF) results of HIV-positive and HIV-negative patients with cryptococcal meningitis. We collected 57 cases of cryptococcal meningitis from cytological specimens submitted to the Department of Tropical Pathology, Faculty of Tropical Medicine. Pertinent clinical data were analyzed retrospectively in 47 cases for clinical manifestations, laboratory features and outcomes of 38 HIV-positive and 9 HIV-negative patients.