Related Experiment Video

Updated: Jul 20, 2026

A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
07:43

A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice

Published on: September 28, 2016

Modulation of the triggering receptor expressed on myeloid cells-1 pathway during pneumonia in rats

Sébastien Gibot1, Corentine Alauzet, Frédéric Massin

  • 1Service de Réanimation Médicale, Hôpital Central, 54035 Nancy, France. s.gibot@chu-nancy.fr

The Journal of Infectious Diseases
|September 9, 2006
PubMed
Abstract

Insights

Modulating the Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) pathway with LP17 peptide improved outcomes in rats with Pseudomonas aeruginosa pneumonia, reducing inflammation and improving survival.

Area of Science:

  • Immunology
  • Microbiology
  • Pathology

Background:

  • Triggering receptor expressed on myeloid cells-1 (TREM-1) amplifies inflammatory responses during sepsis.
  • TREM-1 activation by microbial components may cause hyperresponsiveness in early sepsis.

Purpose of the Study:

  • To investigate the therapeutic potential of modulating the TREM-1 pathway in experimental pneumonia.

Main Methods:

  • Rats were infected with Pseudomonas aeruginosa.
  • Treatment involved a synthetic peptide analogue of TREM-1 (LP17).

Main Results:

  • LP17 treatment improved hemodynamic status, reduced lactic acidosis and hypoxemia in septic rats.
  • LP17 modulated lung and systemic inflammation and coagulation.
  • LP17 treatment reduced lung damage and improved survival rates.

Conclusions:

  • Modulating the TREM-1 pathway with synthetic peptides like LP17 is beneficial.
  • LP17 attenuates inflammatory responses in Pseudomonas aeruginosa-induced pneumonia.

More Related Videos

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness12:21

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

Published on: September 28, 2022

Related Concept Videos

Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:
Pneumonia I: Introduction01:29

Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
Bacterial Meningitis II: Pathophysiology01:26

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...
Atypical Pneumonia01:14

Atypical Pneumonia

Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease include...