Consumption of edible insects has been widely suggested as an environmentally sustainable substitute for meat to reduce greenhouse gas emissions. However, the novel research field for edible insects relies on the content of bioactive ingredients and on the ability to induce a functional effect in humans. The goal of this manuscript is to review the available body of evidence on the properties of edible insects in modulating oxidative and inflammatory stress, platelet aggregation, lipid and glucose metabolism and weight control. A search for literature investigating the functional role of edible insects was carried out in the PubMed database using specific keywords. A total of 55 studies, meeting inclusion criteria after screening, were divided on the basis of the experimental approach: in vitro studies, cellular models/ex vivo studies or in vivo studies. In the majority of the studies, insects demonstrated the ability to reduce oxidative stress, modulate antioxidant status, restore the impaired activity of antioxidant enzymes and reduce markers of oxidative damage. Edible insects displayed anti-inflammatory activity reducing cytokines and modulating specific transcription factors. Results from animal studies suggest that edible insects can modulate lipid and glucose metabolism. The limited number of studies focused on the assessment of anti-coagulation activity of edible insects makes it difficult to draw conclusions. More evidence from dietary intervention studies in humans is needed to support the promising evidence from in vitro and animal models about the functional role of edible insect consumption.

Brucellosis is a widespread zoonosis caused by small bacteria of the genus Brucella. The promoter polymorphisms of IL-10 (-1082 loci, -819 loci and -590 loci) are closely related to the production of IL-10, leading to the alteration of development and pathogenesis of Brucellosis. However, the previous results were controversial. In the present study, we conduct the meta-analysis to get a more precise result of IL-10 polymorphisms with Brucellosis risk. The quality of the studies was assessed according to a predefined scale. The odds ratio (OR) and 95% confidence interval (CI) were counted to evaluate the association strength. No significant association was found between position -1082 loci or -590 loci polymorphism and Brucellosis risk. The significant association was found in Asian population of position -819 (T vs. C: OR 0.60, 95% CI 0.44–0.82, P = 0.001), homozygote comparison (TT vs. CC: OR 0.24, 95% CI 0.09–0.62, P = 0.003) and recessive genetic model (TT vs. TC/CC: OR 0.22, 95% CI 0.05–0.91, P = 0.036). The present meta-analysis demonstrates that IL-10-819 loci polymorphism is not associated with Brucellosis risk of Caucasian population but may contribute a decreased risk to Asian population. And neither IL-10-1082 loci nor -592 loci polymorphism is associated with Brucellosis risk.

Demodex canis infestation in dogs remains one of the main challenges in veterinary dermatology. The exact pathogenesis of canine demodicosis is unknown but an aberration in immune status is considered very significant. No studies have underpinned the nexus between induction of demodicosis and neural immunosuppressive pathways so far. We have evaluated the involvement of cholinergic pathways in association with cytokines regulation as an insight into the immuno-pathogenesis of canine demodicosis in the present study. Remarkable elevations in circulatory immunosuppressive cytokine interleukin-10 and cholinesterase activity were observed in dogs with demodicosis. Simultaneously, remarkable reduction in circulatory pro-inflammatory cytokine tumour necrosis factor-alpha level was observed in dogs with demodicosis. Findings of the present study evidently suggest that Demodex mites might be affecting the cholinergic pathways to induce immunosuppression in their host and then proliferate incessantly in skin microenvironment to cause demodicosis.

Genetic association studies of the cytokine interleukin-10 (IL-10) and sepsis have provided inconsistent results. This work attempts to further quantitatively assess the association of three widely evaluated polymorphisms of IL-10 (−592C/A, −819C/T, −1082A/G) with sepsis susceptibility through a meta-analysis. A search of Pubmed, Web of Science and EMBASE databases was performed. Overall, the three polymorphisms have no strong association with sepsis risk. Subgroup analysis by ethnicity showed there was association between sepsis susceptibility with −592C/A in Caucasians (A vs. C: OR 0·78, 95% CI 0·62–1·00, P = 0·05; AA + CA vs. CC: OR 0·75, 95% CI 0·56–1·00, P = 0·05), and with −1082A/G in Asians (G vs. A: OR 1·41, 95% CI 1·04–1·91, P = 0·03; GG + AG vs. AA: OR 2·11, 95% CI 1·07–4·16, P = 0·03). This meta-analysis suggests that −592C/A and −1082A/G polymorphisms are associated with sepsis susceptibility in Caucasian, and Asian populations, respectively.

We conducted a case-control study involving 150 genotype 3 chronic hepatitis C virus (HCV) patients and 150 healthy controls to investigate the association of polymorphisms in the interleukin-10 (IL-10) gene with chronic HCV infection and the association of these polymorphic variants with the combination of pegylated interferon (Peg-IFN) and ribavirin therapy response. Our data revealed that the GG genotype of IL-10 –1082A/G exhibited significant association with genotype 3 chronic HCV infection compared to controls. Treatment response data also showed a significant increase in risk for the GG genotype of IL-10 –1082A/G in response-relapse patients or non-responder patients compared to sustained virological response patients. Further, a significant increase in risk was also revealed for the CC genotype of IL-10 –592A/C in response-relapse patients or non-responder patients compared to sustained virological response patients, suggesting a role of the GG genotype of IL-10 –1082A/G and CC genotype of IL-10 –592A/C in the treatment outcome of combined Peg-IFN/ribavirin therapy.

Dietary fish oil is considered to have anti-inflammatory effects based primarily on its effects on T-cell proliferation and IL-2 secretion. Its effects on the secretion of T helper (Th) 1-type cytokines vary and few studies have examined its effects on the secretion of Th2-type cytokines. In the present study, we examined the effects of dietary fish oil on the secretion of Th1 and Th2-type cytokines by splenocytes and the mechanism by which dietary fish oil affects Th2-type cytokine secretion. Mice were fed diets supplemented with 18 % fish oil (w/w) +2 % maize oil or 20 % maize oil for 6 weeks. Spleen cells, isolated splenic T cells and accessory cells (splenocytes depleted of T cells) were stimulated with anti-CD3/anti-CD28. The secretion of interferon (IFN)-γ, TNF-α, IL-4 and IL-10 was measured by ELISA. Dietary fish oil decreased the secretion of IFN-γ and TNF-α by total splenocytes and isolated T cells. In contrast, dietary fish oil increased the secretion of IL-4 by total splenocytes but had no effect on IL-4 secretion by isolated T cells. When isolated T cells were cultured with CD11b+ cells (mainly macrophages), cells from mice fed the fish oil diet secreted more IL-4 than cells from mice fed the maize oil diet. These results demonstrate that dietary fish oil directs cytokine secretion by splenocytes towards a Th2 phenotype and that the effects of dietary fish oil on the secretion of a Th2-type cytokine are mediated by its effect on CD11b+ accessory cells.