Related Experiment Video

Updated: Aug 16, 2026

Development of an Insert Co-culture System of Two Cellular Types in the Absence of Cell-Cell Contact
11:29

Development of an Insert Co-culture System of Two Cellular Types in the Absence of Cell-Cell Contact

Published on: July 17, 2016

Lipopolysaccharide, tumor necrosis factor, and interleukin-1 interact to cause hypotension

J R Weinberg1, P Boyle, A Meager

  • 1Department of Medicine, Charing Cross & Westminster Medical School, London.

The Journal of Laboratory and Clinical Medicine
|August 1, 1992
PubMed

Insights

Low doses of lipopolysaccharide (LPS), interleukin-1 (IL-1), and tumor necrosis factor (TNF) interact to cause hypotension in septic shock models. These interactions, not just TNF alone, contribute to the drop in blood pressure during sepsis.

Area of Science:

  • Immunology
  • Pathophysiology
  • Pharmacology

Background:

  • Sepsis is a life-threatening condition characterized by a dysregulated host response to infection.
  • Septic shock, a severe form of sepsis, involves hypotension and organ dysfunction.
  • Lipopolysaccharide (LPS) from Gram-negative bacteria triggers inflammatory mediators like TNF and IL-1, implicated in septic shock pathogenesis.

Purpose of the Study:

  • To investigate the synergistic effects of low, non-hypotensive doses of LPS, IL-1, and TNF on blood pressure in a rabbit model.
  • To determine the role of TNF bioactivity in LPS-induced hypotension during endotoxic shock.

Main Methods:

  • Utilized a restrained, unanesthetized rabbit model.
  • Administered individual and combined non-hypotensive doses of LPS, IL-1, and TNF.
  • Measured blood pressure changes and TNF bioactivity.

Main Results:

  • Combinations of LPS, IL-1, and TNF at non-hypotensive doses induced significant hypotension (p < 0.05).
  • TNF bioactivity was lower in animals made hypotensive by combined agents compared to TNF alone.
  • LPS-stimulated TNF release is not the sole cause of hypotension in this endotoxic shock model.

Conclusions:

  • Interactions between LPS, IL-1, and TNF play a crucial role in the hypotension observed in this septic shock model.
  • Understanding these cytokine interactions is vital for managing hypotension during sepsis episodes.
  • Further research into the complex interplay of inflammatory mediators is warranted.

More Related Videos

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

Evaluation of the In vivo Antitumor Activity of Polyanhydride IL-1&#945; Nanoparticles09:57

Evaluation of the In vivo Antitumor Activity of Polyanhydride IL-1α Nanoparticles

Published on: June 28, 2021

Related Concept Videos

Inflammation01:38

Inflammation

Overview
NF-&#954;B-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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...
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),...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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...