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Bacterial translocation, microcirculation injury and sepsis
I H J Koh1, A M A Liberatore, J L Menchaca-Diaz
1Department of Surgery of Escola Paulista de Medicina, Federal University of São Paulo, São Paulo, Brazil. ivankoh@terra.com.br
Endocrine, Metabolic & Immune Disorders Drug Targets
|June 22, 2006
Summary
Bacterial translocation (BT) contributes to sepsis by causing microcirculation injury and systemic spread. Understanding this complex bacterial-host interaction is key to developing new sepsis therapies.
Area of Science:
- Microbiology
- Immunology
- Pathophysiology
Background:
- Sepsis arises from dysregulated bacterial-host interactions.
- Bacterial translocation (BT) is increasingly implicated in sepsis induction.
- BT may also play a role in developing intestinal immunity.
Purpose of the Study:
- To examine evolving concepts of BT.
- To discuss BT's role in microcirculation injury and sepsis.
- To investigate factors predisposing to BT.
Main Methods:
- In-vivo animal model of bacterial translocation.
- Analysis of bacterial overgrowth and pathogenic determinants.
- Investigation of lymphatic and hematological routes of BT.
Main Results:
- Bacterial overgrowth and pathogenic factors predispose to BT.
- Lymphatic BT activates GALT response, causing microcirculation injury.
- Hematological BT leads to systemic bacterial spread.
- BT exacerbates sepsis in pre-existing infections.
Conclusions:
- BT is a significant factor in sepsis pathogenesis.
- Understanding BT's role in microcirculation injury and immune response is crucial.
- Targeting bacterial-host interactions and BT may lead to novel sepsis treatments.
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