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Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
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Published on: July 12, 2018

The endogenous bacteria alter gut epithelial apoptosis and decrease mortality following Pseudomonas aeruginosa

Amy C Fox1, Kevin W McConnell, Benyam P Yoseph

  • 1Department of Surgery, Washington University School of Medicine, St Louis, MO, USA.

Shock (Augusta, Ga.)
|October 9, 2012
PubMed
Summary
This summary is machine-generated.

Endogenous bacteria protect against pneumonia-induced sepsis mortality. Germ-free mice lacking these microbes experienced higher mortality, suggesting a crucial role for gut microbiota in host defense during critical illness.

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07:24

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Area of Science:

  • Microbiology
  • Immunology
  • Critical Care Medicine

Background:

  • The role of endogenous bacteria in critical illness pathophysiology, particularly sepsis, remains unclear.
  • Understanding how commensal bacteria influence host responses to sepsis is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the impact of commensal bacteria on host response and mortality in a mouse model of sepsis.
  • To elucidate the mechanisms by which endogenous bacteria modulate the host's reaction to pneumonia-induced sepsis.

Main Methods:

  • Comparison of survival rates between conventional and germ-free (GF) mice subjected to Pseudomonas aeruginosa pneumonia.
  • Assessment of intestinal integrity, including apoptosis, proliferation, and permeability, in septic mice.
  • Analysis of local and systemic cytokine levels (e.g., TNF-α, IL-1β) in bronchoalveolar lavage fluid and serum.

Main Results:

  • Germ-free mice exhibited significantly higher mortality rates compared to conventional mice following pneumonia-induced sepsis.
  • Reduced bacterial inoculum in GF mice improved survival, indicating a dose-dependent protective effect.
  • GF mice showed altered intestinal apoptosis and reduced local inflammatory responses (lower TNF-α and IL-1β) but similar systemic cytokine levels and intestinal permeability.

Conclusions:

  • Endogenous bacteria play a protective role in mortality associated with pneumonia-induced sepsis.
  • The protective effect may involve modulation of intestinal epithelial apoptosis and local inflammatory responses.
  • Sepsis-induced lymphocyte-dependent increases in gut epithelial apoptosis are mediated by endogenous bacteria.