Genetic characteristics play an important role in alien species for achieving high adaptation and rapid evolution in a new environment. The American mink (Neovison vison) is one of the best-known and most widespread invasive species that has successfully invaded the Eurasian mainland over quite a short period, including most parts of northeastern China. However, genetic information on farmed and feral American mink populations introduced in China is completely lacking. In this study, we combined mitochondrial DNA sequences and polymorphic microsatellites to examine the genetic divergence and genetic diversity of farmed and feral American mink populations. Our results suggest that there is admixture of individuals of different genetic characteristics between farmed and feral populations of mink. Furthermore, the genetic diversity of both farmed and feral American mink populations was high, and no bottleneck or population expansion was detected in most of the populations. These findings not only highlight the genetic characteristics of American mink in northeastern China but also contribute to the general understanding of the invasiveness of farmed species.

The rise in multidrug resistant (MDR) organisms portends a serious global threat to the healthcare system with nearly untreatable infectious diseases, including pneumonia and its often fatal sequelae, acute respiratory distress syndrome (ARDS) and sepsis. Gram-negative bacteria (GNB) including Acinetobacter baumannii, Pseudomonas aeruginosa , and carbapenemase-producing Klebsiella pneumoniae (CPKP), are among the World Health Organization and National Institutes of Health’s high priority MDR pathogens for targeted development of new therapies. Here we show that stabilizing the host’s vasculature by genetic deletion or pharmacological inhibition of the small GTPase ADP-ribosylation factor 6 (ARF6) increases survival rates of mice infected with A. baumannii , P. aeruginosa , CPKP pneumonia. We show that pharmacological inhibition of ARF6-GTP phenocopies endothelial-specific Arf6 disruption in enhancing survival of mice with A. baumannii pneumonia, suggesting that inhibition is on target. Finally, we show that the mechanism of protection elicited by these small molecule inhibitors is by restoration of vascular integrity disrupted by GNB lipopolysaccharide (LPS) activation of TLR4/MyD88/ARNO/ARF6 pathway. By targeting the host’s vasculature with small molecule inhibitors of ARF6 activation, we circumvent microbial drug resistance and provide a potential alternative/adjunctive treatment for emerging and re-emerging pathogens.