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Bacterial translocation in dianhydrodulcitol-treated mice
1Institute of Microbiology, Semmelweis University Medical School, Budapest, Hungary.
Acta Microbiologica Hungarica
|January 1, 1988
Summary
Dianhydrodulcitol (DAD) causes bacterial translocation from the gut to organs like the spleen and liver in mice. This translocation correlates with drug dosage and spleen atrophy, indicating a compromised intestinal barrier.
Area of Science:
- Microbiology
- Immunology
- Toxicology
Background:
- Intestinal bacteria are normally confined to the gastrointestinal tract.
- Certain chemical agents can disrupt the intestinal barrier, leading to bacterial translocation.
- Understanding the mechanisms of bacterial translocation is crucial for assessing drug safety.
Purpose of the Study:
- To investigate the effect of dianhydrodulcitol (DAD) on bacterial translocation in mice.
- To determine the relationship between DAD dosage, spleen atrophy, and bacterial translocation.
Main Methods:
- Conventional mice were treated with varying doses of dianhydrodulcitol (DAD).
- Mesenteric lymph nodes, spleens, and livers were analyzed for the presence of bacteria.
- Spleen size and weight were assessed to evaluate atrophy.
Main Results:
- Escherichia, Proteus, Klebsiella, and Streptococcus strains were isolated from the mesenteric lymph nodes, spleens, and livers of DAD-treated mice.
- Bacterial translocation occurred in organs not typically harboring bacteria.
- The frequency of bacterial translocation directly correlated with the DAD dose administered.
- Bacterial translocation appeared concurrently with DAD-induced spleen atrophy.
Conclusions:
- Dianhydrodulcitol (DAD) induces bacterial translocation from the intestine to systemic organs in mice.
- DAD compromises the intestinal barrier function in a dose-dependent manner.
- Spleen atrophy is a potential indicator of DAD-induced intestinal barrier damage and subsequent bacterial translocation.