The prevention and control of pathogenic bacteria, fungi, and viruses is a herculean task for all the countries since they greatly threaten global public health. Rapid detection and effective elimination of these pathogens is crucial for the treatment of related diseases. It is urgently demanded to develop new diagnostic and therapeutic strategies to combat bacteria, fungi, and viruses‐induced infections. The emergence of aggregation‐induced emission (AIE) luminogens (AIEgens) is a revolutionary breakthrough for the treatment of many diseases, including pathogenic infections. In this review, the main focus is on the applications of AIEgens for theranostic treatment of pathogenic bacteria, fungi, and viruses. Due to the AIE characteristic, AIEgens are promising fluorescent probes for the detection of bacteria, fungi, and viruses with excellent sensitivity and photostability. Moreover, AIEgen‐based theranostic platforms can be fabricated by introducing bactericidal moieties or designing AIE photosensitizers and AIE photothermal agents. The current strategies and ongoing developments of AIEgens for the treatment of pathogenic bacteria, fungi, and viruses will be discussed in detail.

Background Sorafenib is the first-line treatment for advanced-stage hepatocellular carcinoma (HCC). Several studies have shown that the up-regulation of β-catenin plays a role in sorafenib resistance in HCC; however, the mechanism associated with this phenomenon remains elusive. Methods Western blotting, flow cytometry, and an evaluation of IC 50 values were used to confirm the role of β-catenin in HCC sorafenib resistance. Immunoprecipitation and western blotting were then performed to identify regulatory interactions between β-catenin and Nek2. Further, western blotting, flow cytometry, and an in vivo xenograft model were used to evaluate the function of Nek2 in HCC sorafenib resistance, whereas rescue experiments were performed to confirm that Nek2 induces sorafenib resistance via β-catenin. Finally, western blotting and immunohistochemistry were used to evaluate the expression level of Nek2 in paired HCC and non-tumor tissues. Results We showed that β-catenin could suppress sorafenib-induced apoptosis and cell growth inhibition in HCC cell lines. By screening β-catenin-interacting proteins, we found that Nek2 could bind β-catenin in sorafenib-treated HCC cell lines. Our results also showed that Nek2 stabilizes β-catenin and promotes its translocation to the nucleus, consequently activating the transcription of downstream target genes. We further confirmed that Nek2 could induce sorafenib resistance in HCC cell lines, and that β-catenin was the key element involved in this process. Further, a xenograft tumor model showed that Nek2 knockdown could improve the anti-tumor effect of sorafenib, whereas an analysis of tumor proteins showed that Nek2 regulates β-catenin protein levels and its nuclear translocation in vivo. In addition, Nek2 was found to be up-regulated in HCC tissue, and especially in advanced-stage disease. Conclusions Our study proves that Nek2 induces HCC sorafenib resistance via β-catenin and suggests a novel therapeutic strategy to improve the anti-tumor effects of sorafenib in HCC. Electronic supplementary material The online version of this article (10.1186/s13046-019-1311-z) contains supplementary material, which is available to authorized users.

Neutrophils play important roles in innate immunity and are mainly dependent on various enzyme-containing granules to kill engulfed microorganisms. Zebrafish nephrosin (npsn) is specifically expressed in neutrophils; however, its function is largely unknown. Here, we generated an npsn mutant (npsnsmu5) via CRISPR/Cas9 to investigate the in vivo function of Npsn. The overall development and number of neutrophils remained unchanged in npsn-deficient mutants, whereas neutrophil antibacterial function was defective. Upon infection with Escherichia coli, the npsnsmu5 mutants exhibited a lower survival rate and more severe bacterial burden, as well as augmented inflammatory response to challenge with infection when compared with wild-type embryos, whereas npsn-overexpressing zebrafish exhibited enhanced host defence against E. coli infection. These findings demonstrated that zebrafish Npsn promotes host defence against bacterial infection. Furthermore, our findings suggested that npsn-deficient and -overexpressing zebrafish might serve as effective models of in vivo innate immunity.

As a species of waterfowl, ducks rely on access to water to facilitate feeding behaviors. Further, wet preening behavior in ducks relies on access to water and is a key behavior for duck welfare. Traditionally, Chinese duck farms provide not only free access to drinking water in the duck house but also an open water pool outside of the house. However, recent restrictions prohibit the use of an open water pool for raising ducks in some areas of China. Little is known about the effects of not providing an open water pool on duck welfare, in particular, the development of the preen gland and wet preening behaviors. The preen gland secretes oil which is crucial for maintaining plumage conditions. A total of one hundred twenty 1-day-old Sanshui White ducks ( SSWD ) were randomly divided into 2 groups and fed for 6 wk with access to a water pool ( WP ) or without access to a water pool and provided drinking water only ( LWP ). The live body weights of ducks from the WP group were significantly increased compared with those of ducks in the LWP group starting from 3 wks of age ( P < 0.05). Feed intake was increased in the WP group at 2 wk of age and from 4 to 6 wk of age ( P < 0.05). The feed conversion ratio ( FCR ) was significantly different only at 4 and 5 wks of age, when the FCR was increased by 5.7% and 9.5%, respectively, in the LWP group compared with the WP group ( P < 0.05). Lack of access to an open water pool significantly inhibited the growth of the preen gland based on its weight, size, and quantity of oil secretions ( P < 0.05). In addition, the proportion of ducks exhibiting wet preening behavior was significantly reduced in the LWP group compared with the WP group (5.5 ± 0.2% vs. 24.8 ± 2.1%, P < 0.05). This study indicated that a lack of access to an open water source had negative impacts on the development of the preen gland and on the preening behavior of SSWD.