Neuroinflammation is associated with reduced SOCS2 and SOCS3 expression during intracranial HSV-1 infection.

Herpes simplex virus type 1 (HSV-1) is the main etiological agent of acute and sporadic encephalitis. Proteins of the suppressor of cytokine signaling (SOCS) family have shown to regulate the inflammation during HSV-1 infection in the brain. However, the effects of SOCS2 and SOCS3 in viral encephalitis remain unclear.

Role of SOCS2 in the Regulation of Immune Response and Development of the Experimental Autoimmune Encephalomyelitis.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS). Experimental Autoimmune Encephalomyelitis (EAE) is the most widely used animal model for the study of MS. The Suppressor of Cytokine Signaling (SOCS) 2 protein plays a critical role in regulating the immune responses.

IL-1β Is Involved with the Generation of Pain in Experimental Autoimmune Encephalomyelitis.

Pain is one of the main symptoms of multiple sclerosis, a demyelinating disease of the central nervous system that affects millions of people worldwide. The experimental autoimmune encephalomyelitis (EAE) is considered an experimental model of multiple sclerosis, and besides motor weakness, hypernociception is one of the clinical signs of animals with EAE. In this study, we investigated the influence of some cytokines in the generation of the hypernociceptive response in a mouse model of EAE using MOG.

Suppressor of cytokine signaling 2 (SOCS2) contributes to encephalitis in a model of Herpes infection in mice.

The most severe manifestation of Herpes Simplex Type 1 virus (HSV-1) infection is encephalitis characterized by arousal impairment and seizures that can evolve to coma and death. Previous studies reported the involvement of suppressor of cytokine signaling (SOCS) proteins, specifically SOCS1 and SOCS3, in HSV-1 infection, suggesting that other members of this family could be involved in the immune response against HSV-1. No previous study has reported the role of SOCS2 in HSV-1 infection.

Platelet Activating Factor (PAF) Receptor Deletion or Antagonism Attenuates Severe HSV-1 Meningoencephalitis.

Herpes simplex virus type 1 (HSV-1) is a human pathogen that may cause severe encephalitis. The exacerbated immune response against the virus contributes to the disease severity and death. Platelet activating factor (PAF) is a mediator capable of inducing increase in vascular permeability, production of cytokines on endothelial cells and leukocytes.

[Frequency of overweight and obesity in children and adolescents with autism and attention deficit/hyperactivity disorder].

Objective:: To assess the frequency of overweight and obesity in children and adolescents with autism spectrum disorder (ASD) and with attention deficit/hyperactivity disorder (ADHD) and their parents, in comparison with children and adolescents without developmental disorders.

Methods:: Anthropometric measures were obtained in 69 outpatients with ASD (8.4±4.

Phosphatidylinositol 3-Kinase γ is required for the development of experimental cerebral malaria.

Experimental cerebral malaria (ECM) is characterized by a strong immune response, with leukocyte recruitment, blood-brain barrier breakdown and hemorrhage in the central nervous system. Phosphatidylinositol 3-kinase γ (PI3Kγ) is central in signaling diverse cellular functions. Using PI3Kγ-deficient mice (PI3Kγ-/-) and a specific PI3Kγ inhibitor, we investigated the relevance of PI3Kγ for the outcome and the neuroinflammatory process triggered by Plasmodium berghei ANKA (PbA) infection.

Plasma levels of alarmin IL-33 are unchanged in autism spectrum disorder: a preliminary study.

The pathogenesis of autism spectrum disorder (ASD) is unknown, and the immune system has been appointed to play an important role. The interleukin 33 (IL-33), a member of the IL-1, may act as an alarmin. This study aimed to evaluate plasma levels of IL-33, sST2, and IL-1β in 30 patients with ASD in comparison with 18 controls matched by gender, age and maternal age at childbirth.

Circulating levels of neurotrophic factors in autism spectrum disorders.

Objectives: Evaluate the levels of a neurotrophic factor and some neurotrophins in the plasma of patients with Autism Spectrum Disorders (ASD).

Design: This study enrolled 30 children with ASD and 19 healthy children. Plasma levels of the neurotrophins BDNF, NGF, NT3, NT4 and of the neurotrophic factor GDNF were measured by Enzyme-Linked Immunosorbent Assay.

Protection of blood brain barrier integrity and modulation of inflammatory mediators during treatment of pneumococcal meningitis with daptomycin or ceftriaxone.

Pneumococcal meningitis is associated with neurologic sequelae, such as learning and memory impairment. Most recently, a nonbacteriolytic antibiotic has been investigated to minimise the inflammatory host response and prevent cognitive damage. In this study, we compared daptomycin (DPTO) or ceftriaxone (CFX) treatment on the inflammatory parameters and on the blood-brain barrier (BBB) integrity in experimental pneumococcal meningitis.

Role of the aryl hydrocarbon receptor in the immune response profile and development of pathology during Plasmodium berghei Anka infection.

Infection with Plasmodium falciparum may result in severe disease affecting various organs, including liver, spleen, and brain, resulting in high morbidity and mortality. Plasmodium berghei Anka infection of mice recapitulates many features of severe human malaria. The aryl hydrocarbon receptor (AhR) is an intracellular receptor activated by ligands important in the modulation of the inflammatory response.

Searching for the immune basis of obsessive-compulsive disorder.

The etiopathogenesis of obsessive-compulsive disorder (OCD) remains elusive. Clinical observation of the elevated frequency of obsessive-compulsive symptoms in patients with rheumatic fever, a post-streptococcal autoimmune disease, prompted the study of immune parameters in OCD. Anti-basal ganglia antibodies have been described in a subset of OCD patients.

Changes in adipokine levels in autism spectrum disorders.

Background And Objective: The etiopathogenesis of autism spectrum disorders (ASD) is largely unknown, but it seems to involve dysfunction in several biological systems. Among many possible biological pathways, the immune system has emerged as potentially involved. Recent studies have shown association between cytokines (molecules that mediate immune cell interaction) and ASD.

Blockade of CXCR1/2 chemokine receptors protects against brain damage in ischemic stroke in mice.

Objective: Ischemic stroke may result from transient or permanent reductions of regional cerebral blood flow. Polymorphonuclear neutrophils have been described as the earliest inflammatory cells to arrive in ischemic tissue. CXCR1/2 receptors are involved in the recruitment of these cells.

Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis.

Background: The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5.

Dengue-3 encephalitis promotes anxiety-like behavior in mice.

Dengue virus is a human pathogen that may cause meningoencephalitis and other neurological syndromes. The current study investigated anxiety-like behavior and expression of proinflammatory cytokines and pro-apoptotic caspase-3 in the hippocampus of C57BL/6 mice infected with non-adapted Dengue virus 3 genotype I (DENV-3) inoculated intracranially with 4×10(3) (plaque-forming unit) PFU. Anxiety-like behavior was assessed in control and DENV-3 infected mice using the elevated plus maze.

Behavioral investigation of mice with experimental autoimmune encephalomyelitis.

Multiple sclerosis is a neuroinflammatory disease that results in serious neurological disability. Besides physical impairment, behavioral symptoms are also common in patients with multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is considered to be a model of multiple sclerosis and mimics the main features of the disease, such as demyelination and motor impairment.

Role of IL-4 in an experimental model of encephalitis induced by intracranial inoculation of herpes simplex virus-1 (HSV-1).

Herpes simplex virus-1 (HSV-1) is a pathogen that may cause severe encephalitis in humans. In this study, we aimed to investigate the role of interleukin-4 (IL-4) in a model of HSV-1 brain infection. IL-4 knockout (IL-4-/-) and wild type (WT) C57BL/6 mice were inoculated with 10(4) plaque-forming units of HSV-1 by the intracranial route.

Absence of PAF receptor alters cellular infiltrate but not rolling and adhesion of leukocytes in experimental autoimmune encephalomyelitis.

Experimental autoimmune encephalomyelitis (EAE) is a condition induced in some susceptible species to the study of multiple sclerosis (MS). The platelet activating factor (PAF) is an important mediator of immune responses and seems to be involved in MS. However, the participation of PAF in EAE and MS remains controversial.

Anxiety-like behavior and proinflammatory cytokine levels in the brain of C57BL/6 mice infected with Plasmodium berghei (strain ANKA).

Cerebral malaria (CM) is a severe complication resulting from Plasmodium falciparum infection. The underlying mechanisms of CM pathogenesis remain incompletely understood. The imbalance between the release of proinflammatory and anti-inflammatory cytokines has been associated with central nervous system dysfunction found in human and experimental CM.

A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: a behavioral and neurochemical study.

Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome resulting from liver failure. In the present study, we aimed to standardize an animal model of HE induced by thioacetamide (TAA) in C57BL/6 mice evaluating behavioral symptoms in association with liver damage and alterations in neurotransmitter release.

Method: HE was induced by an intraperitoneal single dose of TAA (200 mg/kg, 600 mg/kg or 1,200 mg/kg).

TNFR1 plays a critical role in the control of severe HSV-1 encephalitis.

Herpes simplex virus-1 (HSV-1) is a pathogen for humans that may cause severe encephalitis. Tumor necrosis factor alpha (TNF-alpha) plays a role in several viral diseases of the central nervous system (CNS). The classic proinflammatory activities of TNF-alpha are mediated mainly through activation of the receptor 1 for TNF-alpha (TNFR1).

Absence of PI3Kgamma leads to increased leukocyte apoptosis and diminished severity of experimental autoimmune encephalomyelitis.

Phosphatidylinositol-3-kinase gamma (PI3Kgamma) plays an important role in the motility of leukocytes in several models of inflammation. In this work, the role of PI3Kgamma in experimental autoimmune encephalomyelitis (EAE) was investigated. EAE was induced in wild-type and PI3Kgamma deficient mice (PI3Kgamma(-)(/)(-)).

Inflammatory changes in the central nervous system are associated with behavioral impairment in Plasmodium berghei (strain ANKA)-infected mice.

Experimental cerebral malaria is a neuroinflammatory condition that results from the host immune response to the parasite. Using intravital microscopy, we investigated leukocyte recruitment in the brain microcirculation and the temporal relationship of this process to the behavioral changes observed in Plasmodium berghei (strain ANKA)-infected C57Bl/6 mice. We found that leukocyte recruitment was increased from day 5 post-infection (p.