Caspase ‐1‐dependent mechanism mediating the harmful impacts of the quorum‐sensing molecule N‐(3‐oxo‐dodecanoyl)‐l‐homoserine lactone on the intestinal cells

In this study, we emphasized on the caspases signal pathway and sterile inflammation to reveal the harmful effects of 3‐oxo‐C12‐HSL on LS174T goblet cells. Our data showed that 3‐oxo‐C12‐HSL is a major inducer of oxidative stress indicated by a high level of intracellular reactive oxygen species (ROS). However, TQ416, an inhibitor of paraoxonase 2, can effectively block oxidative stress. A higher ROS level is the trigger for activating the caspase‐1 and 3 cascade signal pathways. Blockade of ROS synthesis and caspase‐1 and 3 cascades can obviously rescue the viability of LS174T cells after 3‐oxo‐C12‐HSL treatment. We also found that paralleled with a higher level of ROS and caspases a ctivation, an abnormal expression of proinflammatory cytokines was induced by 3‐oxo‐C12‐HSL treatment; however, the blockage of TLRs‐NF‐κB pathway cannot restore cell viability and secretary function. These data collectively indicate that 3‐oxo‐C12‐HSL exposure induces damages to ce ll viability and secretary function of LS174T goblet cells, which is mediated by oxidative stress, cell apoptosis, and sterile inflammation. Overall, the data in this study will provide a better understanding of the harmful impacts of some QS molecules on host cells and their underlying mechanism.
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: ORIGINAL RESEARCH ARTICLE Source Type: research