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Related Experiment Videos

Cells that trigger fever.

Andrej A Romanovsky1, Alexandre A Steiner, Kiyoshi Matsumura

  • 1Systemic Inflammation Laboratory, Trauma Research, St. Joseph's Hospital and Medical Center, Phoenix, Arizona 85013, USA. aromano@chw.edu

Cell Cycle (Georgetown, Tex.)
|September 14, 2006
PubMed
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Bacterial lipopolysaccharide (LPS) triggers fever through toll-like receptor 4 (TLR4) on immune cells. Macrophages in the lungs and liver rapidly produce prostaglandin E(2), initiating the early fever response.

Area of Science:

  • Immunology
  • Physiology
  • Cell Biology

Background:

  • Bacterial lipopolysaccharide (LPS) is a potent immune activator recognized by toll-like receptor 4 (TLR4).
  • Fever, a rise in body temperature, is a common response to LPS, often mediated by prostaglandin E(2) (PGE(2)).
  • The specific cellular and receptor mechanisms linking LPS to fever onset remain unclear.

Purpose of the Study:

  • To identify the specific cells and receptors responsible for initiating LPS-induced fever.
  • To determine the source of prostaglandin E(2) that triggers the earliest phase of fever.

Main Methods:

  • Used mouse chimeras lacking TLR4 in hematopoietic or nonhematopoietic cells to study LPS fever.
  • Investigated LPS fever in rats, quantifying cells expressing cyclooxygenase-2 (COX-2), a PGE(2)-synthesizing enzyme.

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Main Results:

  • The first phase of LPS-induced fever is mediated by TLR4 expressed on hematopoietic cells.
  • In rats, COX-2 expressing cells, primarily macrophages, surged in the lungs and liver at fever onset.
  • LPS-induced PGE(2) production in macrophages is dependent on TLR4.

Conclusions:

  • Hematopoietic cells expressing TLR4 are critical for initiating LPS fever.
  • Pulmonary and hepatic macrophages are key cellular players, producing PGE(2) to trigger fever.
  • These findings elucidate the cellular mechanisms underlying LPS-induced fever.