Current progress in antimicrobial peptides against bacterial biofilms / 生物工程学报

Microbial biofilm, a consortium of microbial cells protected by a self-produced polymer matrix, is considered as one main cause of current bacterial drug resistance. As a new type of antimicrobial agents, antimicrobial peptides provide a new strategy for the treatment of antibiotic resistant bacteria biofilm infections. Antimicrobial peptides have shown unique advantages in preventing microbial colonization of surfaces, killing bacteria in biofilms or disrupting the mature biofilm structure. This review systemically analyzes published data in the recent 30 years to summarize the possible anti-biofilm mechanisms of antimicrobial peptides. We hope that this review can provide reference for the treatment of infectious diseases by pathogenic microbial biofilm.

Apoptosis repressor with caspase recruitment domain deficiency accelerates ischemia/reperfusion (I/R)-induced acute kidney injury by suppressing inflammation and apoptosis: The role of AKT/mTOR signaling.

Acute kidney injury (AKI) is a significant medical problem worldwide. Ischemia-reperfusion (I/R) injury of the kidney is a major cause of AKI. However, the pathogenesis that contributes to renal I/R injury is still unclear. Apoptosis repressor with caspase recruitment domain (ARC) is abundantly expressed in various tissues, and has been reported to play a strong protective role during pathological processes. Our results indicated that ARC expression was decreased in the reperfused kidneys. ARC deficiency markedly accelerated renal dysfunction, promoted reperfusion-regulated tubular epithelial cell apoptosis, and enhanced the vulnerability of kidney to I/R damage. Furthermore, in the kidney samples of mice underwent renal I/R injury, ARC knockout significantly accelerated the expression levels of inflammatory factors, including interleukin (IL)-1ß, IL-6, tumor necrosis factor a (TNF-α), monocyte chemoattractant protein-1 (MCP-1) and IL-2. In addition, renal I/R injury-induced apoptosis was further exacerbated in ARC-deficient mice through promoting the expression of cleaved Caspase-3 and poly (ADP-ribose) polymerase (PARP). From the molecular level, ARC deletion obviously accelerated mitochondrial injury, as evidenced by the further decreased adenosine triphosphate (ATP) levels and mitochondrial potential in hypoxia-reoxygenation (H/R)-treated cells. Moreover, ARC knockout exacerbated AKI through activating phosphorylated protein kinase B (AKT), mammalian target of Rapamycin (mTOR) and p53, whereas reducing phosphorylated glycogen synthase kinase 3ß (GSK3ß). Of note, blocking AKT/mTOR signaling markedly attenuated inflammation, mitochondrial damage and apoptosis stimulated by H/R in ARC knockdown cells. In summary, our results suggested that ARC played a pivotal role in the pathogenesis of AKI induced by renal I/R operation through regulating AKT/mTOR signaling.