کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2064592 | 1544138 | 2015 | 9 صفحه PDF | دانلود رایگان |
• Cellular endotoxin contents of various bacteria/cyanobacteria were determined.
• Indigenous bacteria in river and BAC effluent showed moderate endotoxin contents.
• Inflammatory potencies caused by purified LPSs were compared using human monocytes.
• Acinetobacter and indigenous bacterial LPSs induced strong cytokines in monocytes.
• Bacteria in water supply systems can lead an increase in inflammatory potency.
Inflammatory substances derived from indigenous bacteria in aquatic environments or water systems are of great concern. Lipopolysaccharides (LPSs), one of the major inflammatory substances in water, are usually identified using Limurus amoebocyte lysate (LAL) assay on the basis of their endotoxic activity, but endotoxin levels do not accurately represent their inflammatory potency in humans. In this investigation, the cellular endotoxin contents of pure-cultured bacteria/cyanobacteria, which are frequently detected in water sources and distribution systems, and of indigenous bacteria in a river and in biologically activated carbon (BAC) effluent, were investigated. The indigenous bacteria showed the highest endotoxin contents exceeding 10−3 EU/cell. The LPSs were then purified from those samples, and their inflammatory potencies were examined using a human monocytic cell line. The LPSs from Acinetobacter lwoffii culture, the river water, and the BAC effluent sample revealed a unique cytokine secretion pattern; they induced both IL-8 and TNF-α more strongly than the other tested bacterial LPSs. These results suggest that natural bacterial/cyanobacterial flora in aquatic environments and water distribution systems have the potential to induce relatively strong inflammatory responses in humans; therefore, further accumulation of data on water quality from the perspective of not just endotoxins but inflammatory potency is needed.
Journal: Toxicon - Volume 97, April 2015, Pages 23–31