Environmental Cadmium Exposure Perturbs Gut Microbial Dysbiosis in Ducks.

Ore extraction, chemical production, and agricultural fertilizers may release significant amounts of heavy metals, which may eventually accumulate widely in the environment and organisms over time, causing global ecological and health problems. As a recognized environmental contaminant, cadmium has been demonstrated to cause osteoporosis and renal injury, but research regarding the effects of cadmium on gut microbiota in ducks remains scarce. Herein, we aimed to characterize the adverse effects of cadmium on gut microbiota in ducks. Results indicated that cadmium exposure dramatically decreased gut microbial alpha diversity and caused significant changes in the main component of gut microbiota. Moreover, we also observed significant changes in the gut microbial composition in ducks exposed to cadmium. A microbial taxonomic investigation showed that Firmicutes, Bacteroidota, and Proteobacteria were the most preponderant phyla in ducks regardless of treatment, but the compositions and abundances of dominant genera were different. Meanwhile, a Metastats analysis indicated that cadmium exposure also caused a distinct increase in the levels of 1 phylum and 22 genera, as well as a significant reduction in the levels of 1 phylum and 36 genera. In summary, this investigation demonstrated that cadmium exposure could disturb gut microbial homeostasis by decreasing microbial diversity and altering microbial composition. Additionally, under the background of the rising environmental pollution caused by heavy metals, this investigation provides a crucial message for the assessment of environmental risks associated with cadmium exposure.

Comparative analysis of the gut microbiota of wild wintering whooper swans (Cygnus Cygnus), captive black swans (Cygnus Atratus), and mute swans (Cygnus Olor) in Sanmenxia Swan National Wetland Park of China.

The gastrointestinal microbiota, a complex ecosystem, is involved in the physiological activities of hosts and the development of diseases. Birds occupy a critical ecological niche in the ecosystem, performing a variety of ecological functions and possessing a complex gut microbiota composition. However, the gut microbiota of wild and captive birds has received less attention in the same region. We profiled the fecal gut microbiome of wild wintering whooper swans (Cygnus Cygnus; Cyg group, n = 25), captive black swans (Cygnus Atratus; Atr group, n = 20), and mute swans (Cygnus Olor; Olor group, n = 30) using 16S rRNA gene sequencing to reveal differences in the gut microbial ecology. The results revealed that the three species of swans differed significantly in terms of the alpha and beta diversity of their gut microbiota, as measured by ACE, Chao1, Simpson and Shannon indices, principal coordinates analysis (PCoA) and non-metricmulti-dimensional scaling (NMDS) respectively. Based on the results of the linear discriminant analysis effect size (LEfSe) and random forest analysis, we found that there were substantial differences in the relative abundance of Gottschalkia, Trichococcus, Enterococcus, and Kurthia among the three groups. Furthermore, an advantageous pattern of interactions between microorganisms was shown by the association network analysis. Among these, Gottschalkia had the higher area under curve (AUC), which was 0.939 (CI = 0.879-0.999), indicating that it might be used as a biomarker to distinguish between wild and captive black swans. Additionally, PICRUSt2 predictions indicated significant differences in gut microbiota functions between wild and captive trumpeter swans, with the gut microbiota functions of Cyg group focusing on carbohydrate metabolism, membrane transport, cofactor, and vitamin metabolism pathways, the Atr group on lipid metabolism, and the Olor group on cell motility, amino acid metabolism, and replication and repair pathways. These findings showed that the gut microbiota of wild and captive swans differed, which is beneficial to understand the gut microecology of swans and to improve regional wildlife conservation strategies.

Evaluation of different combination of pam2CSK4, poly (I:C) and imiquimod enhance immune responses to H9N2 avian influenza antigen in dendritic cells and duck.

Current commercial H9 avian influenza viruses (AIVs) vaccines cannot provide satisfactory antibody titers and protective immunity against AIVs in duck. Toll like receptors (TLR) ligand as AIVs adjuvants can activate dendritic cells to improve immune responses in multiple animals, while the studies were absent in duck. Therefore, we investigated TLR ligands pam2CSK4, poly (I:C) and/or imiquimod enhance immune responses to inactivated H9N2 avian influenza antigen (H9N2 IAIV) in peripheral blood monocyte-derived dendritic cells (MoDCs) and duck. In vitro, we observed that transcription factor NF-κB, Th1/Th2 type cytokines (IFN-γ, IL-2 and IL-6) and the ability of catching H9N2 IAIV antigen were significantly up-regulated when H9N2 IAIV along with TLR ligands (pam2CSK4, poly (I:C) and imiquimod, alone or combination) in duck MoDCs. Also, the best enhancement effects were showed in combination of pam2CSK4, poly (I:C) and imiquimod group, whereas IFN-α showed no significant enhancement in all experimental groups. In vivo, the results demonstrated that the percentages of CD4+/ CD8+ T lymphocytes, the levels of Th1/Th2 type cytokines and H9N2 HI titers were significant enhanced in combination of pam2CSK4, poly (I:C) and imiquimod group. However, pam2CSK4 alone or combining with imiquimod showed no enhancement or additive effects on Th1 cytokines (IFN-γ and IL-2), Th2 cytokines (IL-6) and HI titers in Muscovy duck, respectively. Taken together, our results concluded that not all TLR ligands showed enhancement of immune responses to H9N2 IAIV in duck. The combination of poly (I:C), imiquimod and pam2CSK4 that can be an effectively adjuvant candidate for H9N2 AIVs inactivated vaccine in duck, which provide novel insights in explore waterfowl vaccine.

IFN-τ Plays an Anti-Inflammatory Role in Staphylococcus aureus-Induced Endometritis in Mice Through the Suppression of NF-κB Pathway and MMP9 Expression.

Interferon-tau (IFN-τ) is a type I interferon and considered as a pregnancy recognition signal in ruminants. Our previous reports have confirmed that IFN-τ has a potential anti-inflammatory effect in macrophage. However, the anti-inflammatory effect of IFN-τ on endometritis has never been reported. Thus, the aim of this study was to investigate the effects of IFN-τ in a mouse model of Staphylococcus aureus-induced endometritis. The histopathological and myeloperoxidase activity results showed that IFN-τ could protect the uterus from S. aureus damage. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction results revealed that IFN-τ inhibited TNF-α, IL-1ß, and IL-6 production. TLR2, involved in the S. aureus infection, was downregulated by IFN-τ and directly activated nuclear transcription factor kappa-B (NF-κB) pathway. Then, we measured the phosphorylation of IκBα and NF-κB p65 by Western blotting. Western blotting results indicated that IFN-τ inhibited the phosphorylation of IκBα and NF-κB p65 in the S. aureus-induced endometritis. Matrix metalloproteinase (MMP)9, which has been reported to be regulated by NF-κB, was also suppressed by IFN-τ, but its inhibitors, tissue inhibitor of metalloproteinases1 level, increased. All of these findings suggested that IFN-τ plays an anti-inflammatory role in S. aureus-induced endometritis by suppressing NF-κB pathway and MMP9 expression.