Modelling the dynamic basic reproduction number of dengue based on MOI of Aedes albopictus derived from a multi-site field investigation in Guangzhou, a subtropical region.

Background: More than half of the global population lives in areas at risk of dengue (DENV) transmission. Developing an efficient risk prediction system can help curb dengue outbreaks, but multiple variables, including mosquito-based surveillance indicators, still constrain our understanding. Mosquito or oviposition positive index (MOI) has been utilized in field surveillance to monitor the wild population density of Aedes albopictus in Guangzhou since 2005.

CD24-p53 axis suppresses diethylnitrosamine-induced hepatocellular carcinogenesis by sustaining intrahepatic macrophages.

It is generally assumed that inflammation following diethylnitrosamine (DEN) treatment promotes development of hepatocellular carcinoma (HCC) through the activity of intrahepatic macrophages. However, the tumor-promoting function of macrophages in the model has not been confirmed by either macrophage depletion or selective gene depletion in macrophages. Here we show that targeted mutation of dramatically increased HCC burden while reducing intrahepatic macrophages and DEN-induced hepatocyte apoptosis.

HDAC6 Suppresses Age-Dependent Ectopic Fat Accumulation by Maintaining the Proteostasis of PLIN2 in Drosophila.

Age-dependent ectopic fat accumulation (EFA) in animals contributes to the progression of tissue aging and diseases such as obesity, diabetes, and cancer. However, the primary causes of age-dependent EFA remain largely elusive. Here, we characterize the occurrence of age-dependent EFA in Drosophila and identify HDAC6, a cytosolic histone deacetylase, as a suppressor of EFA.

Interleukin-22 restored mitochondrial damage and impaired glucose-stimulated insulin secretion through down-regulation of uncoupling protein-2 in INS-1 cells.

Defective glucose-stimulated insulin secretion (GSIS) induced by chronic exposure to fatty acids is a hallmark of type 2 diabetes (T2D). Interleukin-22 (IL-22) has been shown to exert beneficial effects on insulin secretion and to protect pancreatic β-cells from stress. Moreover, uncoupling protein-2 (UCP-2) plays a central role in the regulation of GSIS and β-cell dysfunction, whereas the role of UCP-2 in IL-22-enhanced glycemic control under conditions of lipotoxicity remains unclear.

Interleukin-22 Alleviated Palmitate-Induced Endoplasmic Reticulum Stress in INS-1 Cells through Activation of Autophagy.

Objective: Stimulation with saturated fatty acids has been shown to induce oxidative stress and endoplasmic reticulum (ER) stress in β cells and has been recognized as an important component of the pathogenesis of type 2 diabetes (T2D). Interleukin-22 (IL-22) plays a critical role in preventing β cells from oxidative and ER stress, and autophagy is associated with the survival and function of β cells. However, whether IL-22 alleviates cellular stress through activation of autophagy is unclear.

Calcineurin B subunit triggers innate immunity and acts as a novel Engerix-B HBV vaccine adjuvant.

We showed previously that calcineurin B subunit (CnB) protein activates innate immune cells including macrophages, monocytes and dendritic cells and acts as an adjuvant of a model antigen (ovalbumin) and a recombinant pneumolysin antigen, but the detailed mechanism is not clear and whether it can serve as an adjuvant of a commercial HBV vaccine is unknown. Here, we report that CnB promotes inflammatory cytokines production, splenocytes proliferation and NK lytic activity, and that CnB-induced inflammatory cytokines (IFN-γ, IL-6, TNF-α) production is dependent on integrin αM. Animal experiments demonstrate that CnB markedly increases the total anti-HBs antibodies in a dose and time dependent manner.

Calcineurin subunit B is an immunostimulatory protein and acts as a vaccine adjuvant inducing protective cellular and humoral responses against pneumococcal infection.

Protective immunity involves a dynamic balance between humoral and cellular immune responses. In the present work we demonstrated that recombinant human calcineurin subunit B (rhCnB) stimulated the expression of the surface molecules CD83, CD80, CD86, CD40, and HLA-DR. It also promoted secretion of inflammatory cytokines IL-6, TNF-α, and IL-1β by human PBMC-derived dendritic cells.

Calcineurin subunit B activates dendritic cells and acts as a cancer vaccine adjuvant.

Safe and potent adjuvants are required to establish effective vaccines. In the present work, we show that calcineurin subunit B promotes the secretion of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin-12p70 (IL-12 p70), IL-6 and the chemokine IL-8. It also up-regulates transcript levels of chemokines in bone marrow-derived dendritic cells.