https://www.selleckchem.com/ As a result of intracellular signaling analysis, Jak1-IRS2-ERK/PI3K pathway was essential for IL-4-induced DNase1L3 expression. IL-4-treated monocyte-derived dendritic cells and MDMs secreted active DNase1L3 protein that could degrade liposome-DNA complexes, which were resistant to DNase1. Our results indicate DNase1L3 is secreted by innate immune cells and may play a critical role in the tissue homeostasis and on prevention of developing autoimmunity by degrading self-DNA. Copyright © 2020 by The American Association of Immunologists, Inc.Vibrio parahaemolyticus is a Gram-negative halophilic pathogen that frequently causes acute gastroenteritis and occasional wound infection. V. parahaemolyticus contains several virulence factors, including type III secretion systems (T3SSs) and thermostable direct hemolysin (TDH). In particular, T3SS1 is a potent cytotoxic inducer, and T3SS2 is essential for causing acute gastroenteritis. Although much is known about manipulation of host signaling transductions by the V. parahaemolyticus effector, little is known about the host metabolomic changes modulated by V. parahaemolyticus To address this knowledge gap, we performed a metabolomic analysis of the epithelial cells during V. parahaemolyticus infection using capillary electrophoresis-time of flight mass spectrometry (CE-TOF/MS). Our results revealed significant metabolomic perturbations upon V. parahaemolyticus infection. Moreover, we identified that T3SS1's VopQ effector was responsible for inducing the significant metabolic changes in the infected cells. The VopQ effector dramatically altered the host cell's glycolytic, tricarboxylic acid cycle (TCA), and amino acid metabolisms. VopQ effector disrupted host cell redox homeostasis by depleting cellular glutathione and subsequently increasing the level of reactive oxygen species (ROS) production.IMPORTANCE The metabolic response of host cells upon infection is pathogen specific, and infection-induce