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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...

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Updated: May 24, 2026

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
11:08

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

Hydroxyurea makes inflammation "just right"?

Lewis L Hsu1

  • 1University of Illinois, USA.

Blood
|February 25, 2012
PubMed
Summary
This summary is machine-generated.

Hydroxyurea treatment improved survival in sickle cell mice with pneumococcal pneumonia. This therapy reduced bacterial spread and inflammation by downregulating E-selectin.

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Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice
08:32

Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice

Published on: March 10, 2017

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Last Updated: May 24, 2026

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
11:08

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice
08:32

Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice

Published on: March 10, 2017

Area of Science:

  • Hematology
  • Immunology
  • Infectious Diseases

Background:

  • Sickle cell disease (SCD) is associated with increased susceptibility to infections, particularly bacterial pneumonia.
  • Pneumococcal pneumonia poses a significant threat to individuals with SCD, often leading to severe complications and mortality.
  • The inflammatory response in SCD can exacerbate infection outcomes.

Purpose of the Study:

  • To investigate the therapeutic effect of hydroxyurea on pneumococcal pneumonia in a sickle cell disease mouse model.
  • To elucidate the mechanisms by which hydroxyurea influences the host's response to bacterial infection in SCD.

Main Methods:

  • Sickle cell disease was induced in mice.
  • Mice were infected with Streptococcus pneumoniae.
  • Hydroxyurea treatment was administered to a subset of infected mice.
  • Survival rates, bacterial load in the bloodstream, and inflammatory markers, including E-selectin expression, were assessed.

Main Results:

  • Hydroxyurea treatment significantly improved survival rates in sickle cell mice challenged with pneumococcal pneumonia.
  • Treatment with hydroxyurea led to a reduction in the invasion of bacteria into the bloodstream.
  • Hydroxyurea administration counteracted the abnormally elevated inflammatory response observed in the sickle cell model.
  • Downregulation of E-selectin was observed in hydroxyurea-treated mice, suggesting a key role in the therapeutic effect.

Conclusions:

  • Hydroxyurea demonstrates a protective effect against pneumococcal pneumonia in a sickle cell disease mouse model.
  • The therapeutic benefits of hydroxyurea involve mitigating excessive inflammation and reducing bacterial dissemination.
  • Downregulation of E-selectin is a critical mechanism contributing to hydroxyurea's efficacy in this context.