Tularemia progression accompanied with oxidative stress and antioxidant alteration in spleen and liver of BALB/c mice
Jazyk angličtina Země Jižní Korea Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- antioxidancia analýza MeSH
- bakteriální nálož MeSH
- Francisella tularensis patogenita MeSH
- interferon gama krev MeSH
- interleukin-6 krev MeSH
- játra mikrobiologie MeSH
- krev mikrobiologie MeSH
- malondialdehyd analýza MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední BALB C MeSH
- myši MeSH
- oxidační stres * MeSH
- slezina mikrobiologie MeSH
- tularemie mikrobiologie patologie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antioxidancia MeSH
- interferon gama MeSH
- interleukin-6 MeSH
- malondialdehyd MeSH
Francisella tularensis is the causative agent of tularemia. It is an intracellular pathogen with the ability to survive within phagosomes and induce pyroptotic cell death. In this study, we attempted to prove whether oxidative imbalance plays a significant role in tularemia pathogenesis. In our experimental model, we subcutaneously infected female BALB/c mice (dose 10(5) CFU of F. tularensis LVS). Liver, spleen, and blood were collected from mice at regular intervals from days 1-15 after infection. The bacterial burden was assessed by a cultivation test. The burden was unchanging from the 2(nd) to 6(th) day after infection. The bacterial burden corresponded to the plasmatic level of IFN-γ, IL-6, and liver malondialdehyde. After the phase of acute bacteraemia and the innate immunity reaction, the levels of reduced glutathione and total low molecular weight antioxidants decreased significantly and the activity of caspase-3 increased in the liver. The level of reduced glutathione decreased to 25% of the original level, and the total level of low molecular weight antioxidants was less than 50% of the initial amount. The demonstrated effects of tularemia-induced pathology had a more extensive impact on the liver than on the spleen.
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