Related Experiment Video

Updated: Jul 19, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Increased regional interleukin-4 during the acute stage of severe intracranial disorders

Makoto Katsuno1, Hiroyuki Yokota, Yasuhiro Yamamoto

  • 1Department of Emergency and Critical Care, Nippon Medical School, Tokyo, Japan. mkatsuno@nms.ac.jp

Neurologia Medico-Chirurgica
|October 26, 2006
PubMed

Interleukin (IL)-4 levels in the internal jugular vein were measured during the acute stage in patients with head injuries, subarachnoid hemorrhage, or intracerebral hemorrhage to investigate the prognostic value. Levels of IL-4, interferon (IFN)-gamma, glucose, and lactate, and oxygen saturation were measured in the internal jugular vein to investigate cerebral local reactions and in the radial artery as a control at admission and 4 hours after onset. The subjects were divided into a survival group and a deceased group. IL-4 levels were high in the internal jugular veins and arterio-jugular venous differences in oxygen content (AjDO(2)) were low at 4 hours after onset in the deceased group. Increased glucose and lactate levels were found at 4 hours after onset in the deceased group. No significant difference was found for IFN-gamma. The severity of cerebral disorders evaluated using AjDO(2) showed a negative correlation with intracerebral IL-4 level. This finding suggests that secretion of IL-4, which has a neuroprotective effect, may increase with the severity of neuropathy and may be useful as a prognostic index.

Related Concept Videos

Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...