Hematoxylin and eosin staining allowed us to compare the morphological characteristics of intestinal villi in goslings treated with intraperitoneal or oral LPS. From 16S sequencing data, we determined the microbiome signatures in the ileum mucosa of LPS-treated goslings (0, 2, 4, and 8 mg/kg BW). The study also assessed alterations in intestinal barrier functions and permeability, the concentration of LPS in the ileum mucosa, plasma, and liver, and the subsequent inflammatory response through Toll-like receptor 4 (TLR4). Subsequently, intraperitoneal injection of LPS resulted in a thickening of the intestinal wall in the ileum within a brief period, with minimal effect on villus height; on the other hand, oral administration of LPS had a more substantial impact on villus height but did not significantly affect intestinal wall thickness. A consequence of oral LPS treatment was a discernible impact on the structure of the intestinal microbiome, observable through modifications in the clustering patterns of the intestinal microbiota. The Muribaculaceae family exhibited an increase in abundance in response to rising lipopolysaccharide (LPS) levels, in contrast to the Bacteroides genus, which showed a decrease when compared to the control group. Moreover, administering 8 mg/kg BW of oral LPS treatment altered the morphology of the intestinal epithelium, compromising the mucosal immune barrier, reducing the expression of tight junction proteins, increasing circulating D-lactate levels, and triggering the release of various inflammatory mediators along with activating the TLR4/MyD88/NF-κB pathway. Goslings subjected to LPS challenges, as detailed in this study, experienced intestinal mucosal barrier damage. This research provides a foundation for finding novel strategies to mitigate the immune response and resultant intestinal injury triggered by LPS exposure.
Granulosa cells (GCs) are impaired due to oxidative stress, a major contributor to ovarian dysfunction. The influence of ferritin heavy chain (FHC) on ovarian function may stem from its capacity to mediate the process of granulosa cell apoptosis. Although this is true, the exact role of FHC as a regulator within follicular germinal center function remains unclear. An oxidative stress model of follicular granulosa cells in Sichuan white geese was developed through the application of 3-nitropropionic acid (3-NPA). Through either gene interference or overexpression of the FHC gene, the study will assess the regulatory effects of FHC on oxidative stress and apoptosis within primary goose GCs. Expression of the FHC gene and protein in GCs significantly decreased (P < 0.005) after 60 hours of siRNA-FHC transfection. Substantial upregulation (P < 0.005) of FHC mRNA and protein expression was detected following 72 hours of FHC overexpression. Following the co-incubation of FHC and 3-NPA, there was a notable impairment of GCs activity, which was statistically significant (P<0.005). When FHC overexpression is coupled with 3-NPA treatment, a significant enhancement of GC activity was observed (P<0.005). Following FHC and 3-NPA treatment, there was a decrease in NF-κB and NRF2 expression (P < 0.005), a notable rise in intracellular ROS (P < 0.005), a fall in BCL-2 expression, a corresponding increase in the BAX/BCL-2 ratio (P < 0.005), a drop in mitochondrial membrane potential (P < 0.005), and a substantial increase in the apoptosis rate of GCs (P < 0.005). FHC overexpression, combined with the presence of 3-NPA, was associated with enhanced BCL-2 protein expression and a reduced BAX/BCL-2 ratio, suggesting a role for FHC in modifying mitochondrial membrane potential and GC apoptosis via modulation of BCL-2 expression. An analysis of our findings reveals that FHC counteracted the suppressive effect of 3-NPA on GC activity. By knocking down FHC, the expression of NRF2 and NF-κB genes was diminished, BCL-2 expression was reduced, the BAX/BCL-2 ratio was amplified, resulting in an accumulation of reactive oxygen species, a disruption of mitochondrial membrane potential, and an augmentation of GC apoptosis.
A stable Bacillus subtilis strain expressing a chicken NK-lysin peptide (B.) has been recently identified. learn more Subtilis-cNK-2, a vehicle for oral delivery of an antimicrobial peptide, demonstrates therapeutic effectiveness in combating Eimeria parasites affecting broiler chickens. A study was designed to examine the impact of an elevated dosage of B. subtilis-cNK-2 oral treatment on coccidiosis, intestinal health, and gut microbiota composition. A randomized, controlled trial was performed on 100 fourteen-day-old broiler chickens, allocating them into four treatment groups: 1) uninfected control (CON), 2) infected control without B. subtilis (NC), 3) B. subtilis with empty vector (EV), and 4) B. subtilis with the cNK-2 treatment (NK). All chickens, save for the CON group, were inoculated with 5000 sporulated Eimeria acervulina (E.). learn more Oocysts of acervulina were present on day 15. Chickens, supplemented with B. subtilis (EV and NK), were orally gavaged with 1 × 10^12 cfu/mL daily, commencing on day 14 and concluding on day 18. Growth characteristics were monitored on days 6, 9, and 13 post-infection. To ascertain the gut microbiota and gauge the gene expression of markers for intestinal integrity and local inflammation, spleen and duodenal samples were collected on day 6 post-inoculation (dpi). Oocyst shedding was assessed by collecting fecal samples on days 6 through 9 following infection. Blood samples were collected 13 days post-inoculation to ascertain the levels of serum 3-1E antibodies. Chickens in the NK group exhibited a substantial enhancement in growth performance, gut integrity, and mucosal immunity, and a decrease in fecal oocyst shedding, significantly (P<0.005) better than those in the NC group. Interestingly, the NK group's gut microbiota profile underwent a marked transformation when compared to those of the NC and EV chickens. The percentage of Firmicutes decreased and the percentage of Cyanobacteria increased in response to the presence of E. acervulina. Despite variations in the Firmicutes to Cyanobacteria ratio in CON chickens, a consistent ratio was maintained in NK chickens, comparable to CON chickens' ratio. Oral B. subtilis-cNK-2, supplemented by NK treatment, proved effective in restoring the dysbiosis resulting from E. acervulina infection, showcasing its general protective impact in coccidiosis cases. Broiler chicken health is improved by the reduction in fecal oocyst shedding, augmented local protective immunity, and the preservation of gut microbiota balance.
In chickens infected with Mycoplasma gallisepticum (MG), this study examined the anti-inflammatory and antiapoptotic actions of hydroxytyrosol (HT) and explored the related molecular mechanisms. Post-MG infection, chicken lung tissue exhibited profound ultrastructural pathologies, including inflammatory cell infiltration, thickened alveolar walls, noticeable cellular swelling, mitochondrial cristae disruption, and ribosomal shedding. MG potentially initiated the nuclear factor kappa-B (NF-κB)/nucleotide-binding oligomerization domain-like receptor 3 (NLRP3)/interleukin-1 (IL-1) signaling cascade in the lung. Furthermore, the adverse effects of MG on lung tissue were significantly improved by undergoing HT treatment. In the context of MG infection, HT intervention effectively decreased the extent of pulmonary injury by minimizing apoptosis and regulating pro-inflammatory cytokine discharge. learn more Substantial inhibition of NF-κB/NLRP3/IL-1 signaling pathway gene expression was observed in the HT-treated group compared to the MG-infected group, with significant decreases in the expression of NF-κB, NLRP3, caspase-1, IL-1β, IL-2, IL-6, IL-18, and TNF-α (P < 0.001 or P < 0.005). In summary, HT's impact on the MG-induced inflammatory response and apoptotic processes in chicken lungs is significant, achieved through the inhibition of the NF-κB/NLRP3/IL-1 signaling cascade and mitigation of MG-related tissue damage. The current study uncovered evidence supporting HT's suitability and efficacy as an anti-inflammatory treatment for MG disease in chickens.
During the late laying period of Three-Yellow breeder hens, this study examined the influence of naringin on the development of hepatic yolk precursors and antioxidant capabilities. Randomized assignments of 54-week-old three-yellow breeder hens (480 total) to four groups (six replicates of 20 hens each) were performed. The groups received dietary treatments, comprising a control diet (C), and a control diet supplemented with 0.1% (N1), 0.2% (N2), and 0.4% (N3) naringin, respectively. Results from the eight-week dietary study, featuring naringin supplementation at concentrations of 0.1%, 0.2%, and 0.4%, indicated improved cell proliferation and a reduction in hepatic fat accumulation. Measurements in liver, serum, and ovarian tissues indicated a statistically significant (P < 0.005) rise in triglyceride (TG), total cholesterol (T-CHO), high-density lipoprotein cholesterol (HDL-C), and very low-density lipoprotein (VLDL), while low-density lipoprotein cholesterol (LDL-C) levels were decreased in comparison to the C group. Treatment with naringin (0.1%, 0.2%, and 0.4%) over 8 weeks was associated with a substantial rise (P < 0.005) in serum estrogen (E2) levels, along with elevated expression levels of estrogen receptor (ER) proteins and genes. Naringin's influence on the gene expressions pertaining to the development of yolk precursors was noteworthy and statistically significant (P < 0.005). The addition of dietary naringin elevated antioxidant levels, decreased oxidation products, and augmented the transcriptional activity of antioxidant genes in liver tissues (P < 0.005). The results demonstrated that incorporating naringin into the diet could positively impact hepatic yolk precursor development and antioxidant defenses in Three-Yellow laying hens during their late production period. Regarding efficacy, the 0.2% and 0.4% doses are superior to the 0.1% dose.
The strategies employed for detoxification are transforming from physical procedures to biological approaches, aiming to completely abolish toxins. This research endeavored to compare the effects of newly developed toxin deactivators, Magnotox-alphaA (MTA) and Magnotox-alphaB (MTB), and the commercially available Mycofix PlusMTV INSIDE (MF) toxin binder on alleviating aflatoxin B1 (AFB1) impacts on laying hens.