Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Defense Against Bacterial Pathogens

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...

Other Stress Responses in Bacteria

Other Stress Responses in Bacteria

Bacteria have global regulatory systems that control several types of stress mechanisms. These include Pho regulon and the heat shock response, which are essential systems for environmental adaptation, such as nutrient limitation and proteotoxic stress. The Pho regulon and the heat shock response exemplify bacterial resilience, enabling rapid adaptation to fluctuating environmental conditions.Pho RegulonBacteria require phosphorus for essential cellular processes, including nucleic acid...

Bacterial Toxins

Bacterial Toxins

Bacterial toxins are sophisticated virulence factors that enable pathogenic bacteria to interact with, invade, and damage host tissues. These toxins fall broadly into two types: protein exotoxins, which are secreted into the environment and target specific host receptors, and lipopolysaccharide endotoxins, which are structural components of the bacterial outer membrane released primarily during bacterial lysis or membrane shedding. Exotoxins generally act more selectively, binding to cell...

Bacterial Meningitis II: Pathophysiology

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Inclusive Search for Anomalous Single-Photon Production in MicroBooNE.

Physical review letters·2026

Same author

First Search for Dark Sector e^{+}e^{-} Explanations of the MiniBooNE Anomaly at MicroBooNE.

Physical review letters·2026

Same author

First Measurement of Charged-Current Muon-Neutrino-Induced K^{+} Production on Argon Using the MicroBooNE Detector.

Physical review letters·2026

Same author

Correction: TRAF2 is a biologically important necroptosis suppressor.

Cell death and differentiation·2025

Same author

Search for an Anomalous Production of Charged-Current ν_{e} Interactions without Visible Pions across Multiple Kinematic Observables in MicroBooNE.

Physical review letters·2025

Same author

First Measurement of ν_{e} and ν[over ¯]_{e} Charged-Current Single Charged-Pion Production Differential Cross Sections on Argon Using the MicroBooNE Detector.

Physical review letters·2025

Search research articles

Related Experiment Video

Updated: Jun 27, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat

Published on: October 29, 2014

Protection against endotoxic shock by bactericidal/permeability-increasing protein in rats

H Jin¹, R Yang, S Marsters

¹Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

The Journal of Clinical Investigation

|April 1, 1995

Summary

Bactericidal/permeability-increasing protein (BPI) administration shortly after LPS injection significantly reduced mortality and improved hemodynamics in endotoxic shock rats. BPI effectively lowered endotoxin and IL-6 levels, suggesting a protective mechanism independent of TNF.

More Related Videos

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

Published on: February 20, 2021

Lipopolysaccharide Infusion as a Porcine Endotoxemic Shock Model

Lipopolysaccharide Infusion as a Porcine Endotoxemic Shock Model

Published on: December 8, 2023

Related Experiment Videos

Last Updated: Jun 27, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat

Published on: October 29, 2014

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

Published on: February 20, 2021

Lipopolysaccharide Infusion as a Porcine Endotoxemic Shock Model

Lipopolysaccharide Infusion as a Porcine Endotoxemic Shock Model

Published on: December 8, 2023

Area of Science:

Immunology
Pharmacology

Background:

Bactericidal/permeability-increasing protein (BPI) is a neutrophil protein known to inhibit lipopolysaccharide (LPS) effects in vitro.
Endotoxic shock, induced by LPS, causes significant hemodynamic changes, increased mortality, and dysregulated cytokine production.

Purpose of the Study:

To investigate the therapeutic potential of BPI in a rat model of endotoxic shock.
To evaluate the effects of BPI on hemodynamics, mortality, and circulating endotoxin and cytokine levels.

Main Methods:

Conscious rats were subjected to intravenous LPS injection.
Human recombinant BPI or vehicle was administered intravenously at different time points (immediately, 30 min, or 2 h) after LPS.
Mean arterial pressure (MAP), heart rate, and circulating endotoxin and cytokine levels (IL-6, TNF) were monitored.

Main Results:

BPI administration immediately or 30 minutes after LPS prevented LPS-induced MAP reduction and significantly reduced mortality.
BPI administration 2 hours after LPS showed no protective effect.
Early BPI treatment reduced circulating endotoxin and IL-6 levels but increased TNF levels.

Conclusions:

BPI demonstrates significant protective effects against endotoxic shock when administered promptly after LPS exposure.
The protective mechanism of BPI appears to be TNF-independent, primarily through the inhibition of endotoxin-stimulated IL-6 production.