Maresin 1 protects against lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting macrophage pyroptosis and inflammatory response.

Maresin 1 protects against lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting macrophage pyroptosis and inflammatory response

Lactobacillus plantarum (LP) has been shown to exhibit protective effects on intestinal barrier function in septic rats, although the regulatory mechanism has not been established. We determined whether LP imparts such protective effects in a lipopolysaccharide (LPS)-induced Caco2 cell monolayer model and whether cAMP-PKA signaling is the underlying mechanism of action. The cyclic adenosine monophosphate (cAMP) agonist, forskolin (FSK), and the protein kinase A (PKA) inhibitor, HT89, were used to study the protective effect of LP on the destruction of the tight junction (TJ) structure of cells treated with LPS and the corresponding changes in cAMP-PKA signaling. Our experimental results demonstrated that LP promoted the expression of TJ proteins between Caco2 cells after LPS treatment, and increased the electrical barrier detection (TEER) between Caco2 cells. Moreover, transmission electron microscopy (TEM) revealed that the TJ structural integrity of cells treated with LPS + LP was improved compared to cells treated with LPS alone. In addition, our findings were consistent between the FSK and LP intervention group, while HT89 inhibited LP influence. Taken together, our results indicate that LP has an improved protective effect on LPS-induced damage to the monolayer membrane barrier function of Caco2 cells and is regulated by the cAMP-PKA pathway.

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Lactobacillus plantarum improves LPS-induced Caco2 cell line intestinal barrier damage via cyclic AMP-PKA signaling

Inflammation plays an important role in the pathogenesis of metabolic syndrome, which increases the risk of heart disease, stroke, type 2 diabetes, atherosclerosis, non-alcoholic fatty liver disease (NAFLD), and obesity. Here, we produced potent anti-inflammatory probiotic lysates, termed MSF (miracle synergistic material made using Filipendula glaberrima), using fermentation with F. glaberrima extracts. MSF inhibited lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production through down-regulation of c-Jun N-terminal kinase (JNK) signaling. MSF-induced tolerance for TNF-α was mediated by induction of TNF alpha-induced protein 3 (TNFAIP3 or A20). On the other hand, MSF showed a synergistic effect on interleukin (IL)-1β production in LPS-stimulated human monocytic leukemia cell line (THP-1 cells). This synergistic effect of the combination of MSF and LPS might be mediated by nuclear factor kappa B (NF-kB) signaling. The inhibitory effect of TNF-α and synergistic effect of IL-1β due to combining MSF and LPS were significantly higher than those of a combination of L. plantarum K8 lysates and LPS. The MSF and LPS combination showed reduced mouse mortality compared to a combination of L. plantarum K8 lysates and LPS, which correlated with decreased levels of cytokines, hepatic alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in the blood and liver. These results show that probiotic lysates fermented with natural extracts such as F. glaberrima have higher anti-inflammatory efficacy than conventional probiotic lysates or natural extracts.

/pdf/anti-inflammatory-properties-of-msf-a-lactiplantibacillus-3js4u915.pdf

Anti-Inflammatory Properties of MSF, a Lactiplantibacillus plantarum K8 Lysate Fermented with Filipendula glaberrima Extract

http://www.cell.com/article/S2405844023001330/pdf

Anti-obesity potential of heat-killed Lactiplantibacillus plantarum K8 in 3T3-L1 cells and high-fat diet mice

We previously showed that Lactiplantibacillus plantarum K8 and its cell wall components have immunoregulatory effects. In this study, we demonstrate that pre-treatment of L. plantarum K8 lysates reduced LPS-induced TNF-α production in THP-1 cells by down-regulating the early signals of mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB). The down-regulation of signals may be caused by the induction of negative regulators involved in toll-like receptor (TLR)-mediated signaling. However, co-treatment with high concentrations of L. plantarum K8 lysates and lipopolysaccharide (LPS) activated the late signaling of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and NF-κB pathways and resulted in the induction of absent in melanoma 2 (AIM2) inflammasome-mediated interleukin (IL)-1β secretion. Intraperitoneal injection of L. plantarum K8 lysates in LPS-induced endotoxin shock mice alleviated mortality and reduced serum tumor-necrosis factor (TNF)-α, IL-1β, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. In addition, the mRNA levels of TNF-α, IL-1β, and IL-6 decreased in livers from mice injected with L. plantarum K8 followed by LPS. Hematoxylin and eosin (H&E) staining of the liver showed that the cell size was enlarged by LPS injection and slightly reduced by L. plantarum K8 lysate pre-injection followed by LPS injection. Macrophage infiltration of the liver also decreased in response to the combination injection compared with mice injected with only LPS. Taken together, our results show that although L. plantarum K8 lysates differentially regulated the production of LPS-induced inflammatory cytokines in THP-1 cells, the lysates inhibited overall inflammation in mice. Thus, this study suggests that L. plantarum K8 lysates could be developed as a substance that modulates immune homeostasis by regulating inflammation.

https://www.mdpi.com/1422-0067/22/11/5921/pdf

Hangeun Kim

Papers

Alleviation of lps-induced inflammation and septic shock by lactiplantibacillus plantarum k8 lysates