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Updated: Oct 3, 2025

Bone Marrow-derived Macrophage Production
Published on: November 22, 2013
Blood Bacteria-Free DNA in Septic Mice Enhances LPS-Induced Inflammation in Mice through Macrophage Response
Warerat Kaewduangduen1,2, Peerapat Visitchanakun1,2, Wilasinee Saisorn1,2
1Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Abstract:
Although bacteria-free DNA in blood during systemic infection is mainly derived from bacterial death, translocation of the DNA from the gut into the blood circulation (gut translocation) is also possible. Hence, several mouse models with experiments on macrophages were conducted to explore the sources, influences, and impacts of bacteria-free DNA in sepsis. First, bacteria-free DNA and bacteriome in blood were demonstrated in cecal ligation and puncture (CLP) sepsis mice. Second, administration of bacterial lysate (a source of bacterial DNA) in dextran sulfate solution (DSS)-induced mucositis mice elevated blood bacteria-free DNA without bacteremia supported gut translocation of free DNA. The absence of blood bacteria-free DNA in DSS mice without bacterial lysate implies an impact of the abundance of bacterial DNA in intestinal contents on the translocation of free DNA. Third, higher serum cytokines in mice after injection of combined bacterial DNA with lipopolysaccharide (LPS), when compared to LPS injection alone, supported an influence of blood bacteria-free DNA on systemic inflammation. The synergistic effects of free DNA and LPS on macrophage pro-inflammatory responses, as indicated by supernatant cytokines (TNF-α, IL-6, and IL-10), pro-inflammatory genes (NFκB, iNOS, and IL-1β), and profound energy alteration (enhanced glycolysis with reduced mitochondrial functions), which was neutralized by TLR-9 inhibition (chloroquine), were demonstrated. In conclusion, the presence of bacteria-free DNA in sepsis mice is partly due to gut translocation of bacteria-free DNA into the systemic circulation, which would enhance sepsis severity. Inhibition of the responses against bacterial DNA by TLR-9 inhibition could attenuate LPS-DNA synergy in macrophages and might help improve sepsis hyper-inflammation in some situations.
Insights
Bacteria-free DNA in sepsis blood can originate from gut translocation, worsening inflammation. TLR-9 inhibition may reduce this inflammatory response and improve sepsis outcomes.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Systemic infections like sepsis involve bacteria-free DNA in the blood.
- This DNA can originate from bacterial death or translocation from the gut.
Purpose of the Study:
- To investigate the sources, influences, and impacts of bacteria-free DNA in sepsis.
- To explore the role of gut translocation in sepsis-associated bacteria-free DNA.
Main Methods:
- Used cecal ligation and puncture (CLP) and dextran sulfate solution (DSS)-induced mucositis mouse models.
- Administered bacterial lysate and lipopolysaccharide (LPS) to induce inflammation.
- Analyzed blood bacteria-free DNA, serum cytokines, and macrophage responses.
- Investigated the effect of TLR-9 inhibition (chloroquine).
Main Results:
- Demonstrated bacteria-free DNA and bacteriome in CLP sepsis mice.
- Showed gut translocation of free DNA in DSS mice treated with bacterial lysate.
- Confirmed that bacteria-free DNA enhances systemic inflammation and synergistic effects with LPS on macrophages.
- Observed that TLR-9 inhibition neutralized these synergistic effects.
Conclusions:
- Gut translocation contributes to bacteria-free DNA in sepsis, exacerbating severity.
- TLR-9 inhibition can attenuate LPS-DNA synergy in macrophages, potentially improving sepsis hyper-inflammation.

