Assembly structures and dynamics of active colloidal cells.

Many types of active matter are deformable, such as epithelial cells and bacteria. To mimic the feature of deformability, we built a model called an active colloidal cell (ACC), i.e. a vesicle enclosed with self-propelled particles (SPPs), which as a whole can move actively. Based on the model, we then study the role of deformability in the assembly structures and dynamics of ACCs by Langevin dynamics simulation. We find that deformability weakens the self-trapping effect and hence suppresses the clustering and phase separation of the deformable soft ACCs (sACCs). Instead of forming a large compact cluster like ordinary SPPs, sACCs pack into a loose network or porous structure in the phase-separation region. The condensed phase is liquid-like, in which sACCs are strongly compressed and deformed but still keep high motility. The interface between the gas and the condensed phases is blurry and unstable, and the effective interfacial energy is very low. Our work gives new insights into the role of deformability in the assembly of active matter and also provides a reference for further studies on different types of deformable active matter.

The efficacy of chimeric vaccines constructed with PEP-1 and Ii-Key linking to a hybrid epitope from heterologous viruses.

The heterologous epitope-peptide from different viruses may represent an attractive candidate vaccine. In order to evaluate the role of cell-permeable peptide (PEP-1) and Ii-Key moiety from the invariant chain (Ii) of MHC on the heterologous peptide chimeras, we linked the two vehicles to hybrid epitopes on the VP2 protein (aa197-209) of the infectious bursal disease virus and HN protein (aa345-353) of the Newcastle disease virus. The chimeric vaccines were prepared and injected into mice. The immune effects were measured by indirect ELISA. The results showed that the vehicle(s) could significantly boost immune effects against the heterologous epitope peptide. The Ii-Key-only carrier induced more effective immunological responses, compared with the PEP-1 and Ii-Key hybrid vehicle. The carrier-peptide hybrids all showed strong colocalization with major histocompatibility complex (MHC) class II molecules compared with the epitope-peptide (weakly-binding) after co-transfection into 293T cells. Together, our results lay the groundwork for designing new hybrid vaccines based on Ii-Key and/or PEP-1 peptides.

Avian leukosis virus subgroup J triggers caspase-1-mediated inflammatory response in chick livers.

Many pathogens trigger caspase-1-mediated innate immune responses. Avian leukosis virus subgroup J (ALV-J) causes serious immunosuppression and diverse tumors in chicks. The caspase-1 inflammasome mechanism of response to ALV-J invading remains unclear. Here we investigated the expression of caspase-1, the inflammasome adaptor NLRP3, IL-1ß and IL-18 in response to ALV-J infection in the liver of chick. We found caspase-1 mRNA expression was elevated at 5 dpi and peaked at 7 dpi in ALV-J infected animals. Corresponding to this, the expressions of NLRP3 and proinflammatory cytokines IL-1ß and IL-18 were significantly increased at 5 or 7 dpi. In addition, caspase-1 protein expression and inflammatory cell infiltration were induced after virus infection. These results indicated that ALV-J infection could trigger the caspase-1- mediated inflammatory response in chicks. Thus, an understanding of the inflammatory responses can provide a better insight into the pathogenicity of ALV-J and a possible anti-virus target for ALV-J infection.