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Related Concept Videos

Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
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,...
Inflammation01:38

Inflammation

Overview
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: 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...
Acute Inflammation I: Cellular Phase01:26

Acute Inflammation I: 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...
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,...

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Related Experiment Video

Updated: May 7, 2026

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
07:36

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting

Published on: May 1, 2015

Lymphatic vascular response to acute inflammation.

Pier-Anne Lachance1, Amy Hazen, Eva M Sevick-Muraca

  • 1The Center for Molecular Imaging, The Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas, United States of America ; Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, United States of America.

Plos One
|October 3, 2013
PubMed
Summary
This summary is machine-generated.

During acute inflammation, lymphatic endothelial cells (LECs) proliferate but lymphatic vessel density remains unchanged. Remodeling leads to vessel leakiness and reduced lymph fluid ejection, suggesting factors beyond VEGF-C/D regulate lymphatic function.

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Area of Science:

  • Immunology
  • Vascular Biology
  • Dermatology

Background:

  • Functioning lymphatics are crucial for reducing edema and immune cell transport during inflammation.
  • The precise impact of dermal lymphatic remodeling on transport and its regulatory factors during acute inflammation remain unclear.

Purpose of the Study:

  • To quantify lymphatic endothelial cell (LEC) proliferation during acute cutaneous hypersensitivity (CHS).
  • To examine the expression of pro-angiogenic and lymphangiogenic factors during CHS.
  • To investigate the functional consequences of lymphatic remodeling on lymph transport.

Main Methods:

  • Quantification of LECs during acute CHS.
  • Analysis of pro-angiogenic and lymphangiogenic factor expression.
  • Assessment of lymphatic vessel density, leakiness, and lymph fluid ejection.

Main Results:

  • LECs actively proliferate during CHS, but lymphatic vessel density does not increase.
  • Lymphatic remodeling is associated with increased vessel leakiness and reduced lymph fluid ejection in proximal vessels draining the inflamed area.
  • While FGF-2, PLGF-2, HGF, EGF, and KC/CXCL17 show differential expression, VEGF-C and VEGF-D levels do not significantly change.

Conclusions:

  • VEGF-C and VEGF-D are not the sole regulators of LEC proliferation and altered lymphatic function in acute CHS.
  • Other factors likely contribute to the observed changes in lymphatic microenvironment and function during inflammation.