Quorum-sensing (QS) system is a rapidly developing field in which we are gradually expanding our understanding about how bacteria communicate with each other and regulate their activities in bacterial sociality. In addition to collectively modifying bacterial behavior, QS-related autoinducers may also be embedded in the crosstalk between host and parasitic microbes. In this review, we summarize current studies on QS in the intestinal microbiome field and its potential role in maintaining homeostasis under physiological conditions. Additionally, we outline the canonical autoinducers and their related QS signal-response systems by which several pathogens interact with the host under pathological conditions, with the goal of better understanding intestinal bacterial sociality and facilitating novel antimicrobial therapeutic strategies.

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The tapping of municipal wastewater for potable reuse significantly enhances drinking water supply in drought-stricken regions worldwide. Membrane-based potable reuse treatment trains commonly employ ultraviolet-based advanced oxidation processes (UV-AOPs) to degrade trace organic contaminants in water to produce high-quality recycled water. Hydrogen peroxide (H 2 O 2 ) is used as the default photo-oxidant. Meanwhile, chloramines, which are added to prevent biofouling, pass through the membranes and impact the treatment efficiency of UV-AOP. Water reuse facilities therefore face the dilemma of optimizing H 2 O 2 (an added photo-oxidant) and chloramines (a carry-over photooxidant) doses. Utilizing a uniquely designed pilot-scale reactor and real-time recycled water, we evaluated treatment efficiencies of UV-AOP on six important indicator contaminants, with monochloramine (NH 2 Cl) and H 2 O 2 as photo-oxidants. Hydroxyl radical (HO • ) and reactive chlorine species, such as the chlorine atom (Cl • ) and chlorine dimer (Cl 2•− ), were the major reactive species. Overall, radicals generated from photolysis of NH 2 Cl alone achieved removal of indicator compounds, which can be further improved by optimizing UV fluence, i.e., the UV dose. Furthermore, the addition of H 2 O 2 enhanced HO • formation and improved contaminant removal. However, the addition of H 2 O 2 , when the background NH 2 Cl level was above 2 mg L −1 (as Cl 2 ), provided limited improvement in treatment efficiency. These trade-offs between chloramine and H 2 O 2 as oxidants, and the recommended optimization of the associated effective UV fluence, are critical for energy-efficient and costeffective potable reuse to address the challenges of global water scarcity.

Patients being treated for pulmonary tuberculosis often suffer liver injury due to the effects of anti-TB drugs, and the underlying mechanisms for those injuries need to be clarified. In this study, rats and hepatic cells were administrated isoniazid (INH) and rifampin (RIF) and then treated with NLRP3-inflammasome inhibitors (INF39 and CP-456773) or NLRP3 siRNA. Histopathological changes that occurred in liver tissue were examined by H&E staining. Additionally, the levels IL-33, IL-18, IL-1β, NLRP3, ASC, and cleaved-caspase 1 expression in the liver tissues were also determined. NAT2 and CYP2E1 expression were identified by QRT-PCR analysis. Finally, in vitro assays were performed to examine the effects of siRNA targeting NLRP3. Treatment with the antituberculosis drugs caused significant liver injuries, induced inflammatory responses and oxidative stress (OS), activated NLRP3 inflammasomes, reduced the activity of drug-metabolizing enzymes, and altered the antioxidant defense system in rats and hepatic cells. The NLRP3 inflammasome was required for INH- and RIF-induced liver injuries that were produced by inflammatory responses, OS, the antioxidant defense system, and drug-metabolizing enzymes. This study indicated that the NLRP3 inflammasome is involved in antituberculosis drug-induced liver injuries (ATLIs) and suggests NLRP3 as a potential target for attenuating the inflammation response in ATLIs.