Abstract
Inflammation is a biological response of the immune system to defend the body from negative stimulation. However, the excessive inflammatory response can damage host tissues and pose serious threats. Exopolysaccharide (EPS), one of the postbiotics, is secreted from lactic acid bacteria. Although many studies have described the beneficial effects of EPS, such as its anti-inflammatory and anti-oxidant effects, its underlying mechanisms have remained to be poorly understood. Thus, we identified that EPS obtained from Lactobacillus plantarum L-14 was a homogeneous polysaccharide primarily comprised of glucose. To examine these anti-inflammatory effects, an inflammatory response was induced by lipopolysaccharide (LPS) administration to mouse macrophage RAW 264.7 cells that were pretreated with EPS. The anti-inflammatory effects of EPS were identified by analyzing the changes within inflammatory markers at the molecular level. We demonstrate here that EPS suppressed proinflammatory mediators, such as cyclooxygenase-2, interleukin-6, tumor necrosis factor-α, and interleukin-1β, and downregulated the expression of an inducible nitric oxide synthase known to lead to oxidative stress. It was also confirmed that EPS had anti-inflammatory effects by blocking the interaction of LPS with Toll-like receptor 4 (TLR4), as demonstrated by using the known TLR4 inhibitor TAK-242. In addition, we found that EPS itself could suppress the expression of TLR4. Consequently, our data suggest that EPS can be a potential target for the development of natural product-derived medicine for treating inflammatory diseases related to TLR4.
Highlights
Inflammation has been identified as an essential defense reaction to protect the body from various harmful stimuli, such as infection, toxic compounds, or injury [1]
When gram-negative bacterial cells are lysed and LPS binds to Toll-like receptor 4 (TLR4) on host cells, the inflammatory response is triggered upon activation of the innate immune system
These results indicate that EPS purified from L-14 exhibited suppression upon the LPS-stimulated inflammatory response
Summary
Inflammation has been identified as an essential defense reaction to protect the body from various harmful stimuli, such as infection, toxic compounds, or injury [1]. A number of drugs for regulating inflammatory reactions have been studied and developed, a multitude of issues remain in terms of their usage, such as non-targeting effects and high prices [5]. When gram-negative bacterial cells are lysed and LPS binds to TLR4 on host cells, the inflammatory response is triggered upon activation of the innate immune system. The studies for postbiotic effects have shown that their compounds directly interact with the host and can have positive reactions [16]. A recent study has shown that EPS can prevent viral infections by modulating an antiviral immune response within intestinal epithelial cells [24]. To confirm any potential anti-inflammatory effects, EPS was pretreated in RAW 264.7 cells, and stimulation of the inflammatory response was induced by LPS.
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