scholarly journals PSV-8 Enriched environment improves the resistance to transport stress in laying hens via modulating the heat shock protective response and inflammation

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 225-225
Author(s):  
Runxiang Zhang ◽  
Chun Li ◽  
Haidong Wei ◽  
Jianhong Li ◽  
Jun Bao
Keyword(s):  
Heat Shock ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Laying Hens ◽  
Enriched Environment ◽  
Inflammatory Factors ◽  
Prostaglandin E ◽  
Protective Response ◽  
Tnf Α ◽  
Transport Stress

Abstract Enriched environment can promote the adaptability of animals to cope with the complex environments. To evaluate how enriched environment experience can help laying hens resist to transport stress, a total of 432 18-week-old laying hens were randomly divided into two treated groups of which one group was housed in conventional battery cages (CC, 24 replicate cages, 3 birds/cage) and the other was in furnished cages (FC, 24 repeated cages, 15 birds/cage). At their 64 weeks of age, one hen per replicate was selected for 4h transportation. The spleen of hens was collected before transportation, after the transportation and 48h for recovery. The expression of heat shock proteins (HSPs), heat shock factors (HSFs) and inflammatory factors were measured. The serum from those birds was collected to detect inflammatory cytokines levels. Variance analysis showed that the expression of most of the detected HSPs and HSFs indicators were decreased after transportation and then elevated later. The mRNA expression of HSP10, 40, 60, 70, 90 and 110, HSF2 and HSF3 and the protein expression of HSP 60, 70 and 90 were higher in FC group than CC after the transportation and recovery (P < 0.05). Moreover, the hens housed in FC group had the lower mRNA expression of pro-inflammatory factors of nuclear transcription factor (NF-κB), cyclooxygenase-2 (COX-2) and prostaglandin E synthase (PTGEs) before and after the transportation compared to CC group (P < 0.05). The mRNA expression of inflammatory cytokines of interleukin-2 (IL-2), -6 (IL-6) and tumor necrosis factor (TNF-α) and serum concentration of IL-1β and TNF-α in FC hens were lower than CC after the transportation (P < 0.05), respectively. Therefore, by regulating the heat shock protective response and inflammatory cytokines expression, the enriched environment can reduce the stress damage of laying hens and improve the resistance to transport stress.

scholarly journals Keel Fracture Causes Stress and Inflammatory Responses and Inhibits the Expression of the Orexin System in Laying Hens

Animals ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 804 ◽  
Author(s):  
Haidong Wei ◽  
Chun Li ◽  
Hongwei Xin ◽  
Shuang Li ◽  
Yanju Bi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Laying Hens ◽  
Inflammatory Responses ◽  
Abdominal Muscle ◽  
Inflammatory Factors ◽  
Prostaglandin E ◽  
Inflammatory Factor ◽  
Tnf Α ◽  
Cox 2 ◽  
The Brain

Keel fracture has negative effects on the health and welfare of laying hens. We investigated effects of keel fracture on stress, inflammation, and the orexin system in laying hens. Ninety 17-week-old Lohmann white laying hens were palpated and euthanatized at 42 weeks old, and marked as normal keel (NK)/fractured keel (FK) from absence/presence of keel fracture. Serum, brain, liver, and abdominal-muscle samples were collected from 10 NK and 10 FK hens to determine the stress and inflammatory responses and the activity of orexin systems by corticosterone content, expression of heat shock proteins (TNF-α 60, 70, 90), and inflammatory factors (tumor necrosis factor (TNF)-α, nuclear factor-kappa Bp65 (NF-κBp65), inducible nitric oxide synthase (iNOS), prostaglandin E synthases (PTGEs), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β)), orexin (ORX), and orexin-receptor 1/2 (ORXR1/ORXR2). The FK hens had higher serum corticosterone content, Hsps, and inflammatory factor mRNA expression levels than NK hens, although levels of iNOS in the liver and TNF-α in the muscle were similar. Protein levels of Hsp70 and Hsp90 in the brain and liver, iNOS and COX-2 in the liver, NF-κBp65, iNOS, and COX-2 in the brain of FK hens were increased compared with NK hens. Furthermore, FK hens had lower mRNA expression of ORX, ORXR1, and ORXR2 than NK hens. Therefore, keel fracture causes stress and inflammation, and inhibits the expression of the orexin system in laying hens.

Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

2020 ◽  
Author(s):  
Xiaoling Wu ◽  
Xinyu Zou ◽  
Mi Zhang ◽  
Haiqiang Hu ◽  
Xueliang Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Inflammatory Reaction ◽  
High Fat Diet ◽  
Laying Hens ◽  
Density Lipoprotein ◽  
Inflammatory Factors ◽  
Pathological Changes ◽  
High Fat ◽  
Tnf Α

Abstract Background: Osteocalcin (OCN), as an energy-regulating hormone, involves in preventing nonalcoholic steatohepatitis. Laying hens have been used as an animal model for investigating liver function and related metabolic disordersas that the synthesis of fat in laying hens is much faster than in mammals with limited adipose tissue. The aim of this study was to investigate the effects of OCN on fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Methods: Thirty 68-week-old White Plymouth laying hens were randomly assigned into conventional single-bird cages, and the cages were randomly allocated into one of three treatments: normal diet (ND + vehicle , ND+V), high-fat diet (HFD + vehicle, HFD+V), and HFD + OCN (3 μg/bird, 1 time/2 days, i.m.) for 40 days. At experimental day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. At the end of experiment, the hens were euthanized followed blood collection. The plasma aspartate transaminase (AST), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using an automatic biochemistry analyzer. Pathological changes in the liver were examined under both light and transmission electron microscopes. The plasma inflammatory factors including interleukin-1 (IL-1), IL-6, and tumor Necrosis Factor-alpha (TNF-α) were analyzed by ELISA, and the gene expressions of these inflammatory factors in the liver were analyzed by Real-time PCR. And oxidative stress was evaluated using Malondialdehyde (MDA) and Glutathione peroxidase (GSH-Px) assay kits. Results: The results showed HFD hens had more severe liver haemorrhage and fibrosis than ND hens. The ultra-microstructural examination showed that hepatocytes of HFD hens appeared necrotic pyknosis associated with great intracellular electron, mitochondrial swelling, shrunk nucleus and absence of autolysosomes. OCN mitigated these pathological changes by improved HFD hens’ insulin resistance via alleviating the glucose intolerence and improving insulin sensitivity; inhibited HFD-induced oxidative stress as evidenced by decreased liver concentrations of MDA but increased GSH-Px; and reduced the inflammatory reaction with reducing blood IL-6 and TNF-α concentrations and mRNA expressions. Conclusion: These results suggest a high-fat diet promotes the FLHS development in aged hens, while OCN prevents the FLHS process through inhibiting insulin resistance, inflammatory reaction, oxidative stress and fibrosis, and acting autophagy.

scholarly journals Post-treatment curcumin reduced ischemia–reperfusion-induced pulmonary injury via the Notch2/Hes-1 pathway

2019 ◽  
Vol 48 (4) ◽  
pp. 030006051989243
Author(s):  
HaiZou bo ◽  
XiaoSun feng
Keyword(s):  
Lung Injury ◽  
Mrna Expression ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Post Treatment ◽  
Inflammatory Factors ◽  
Pulmonary Injury ◽  
Pathological Changes ◽  
Sprague Dawley ◽  
Tnf Α

Objective To investigate the influence of curcumin on the Notch2/Hes-1 pathway after pulmonary injury induction via limb ischemia–reperfusion (I/R). Methods Adult male Sprague–Dawley rats were randomly divided into four groups (n = 30 each): sham, I/R, curcumin post-treatment (I/R+Cur), and inhibitor (I/R+DAPT). Hind-limb ischemia was induced for 4 hours, followed by reperfusion for 4 hours. After ischemia, curcumin (200 mg/kg) or DAPT (0.5 µm) was injected intraperitoneally in the I/R+Cur or I/R+DAPT group, respectively. PaO2 was examined after 4 hours of reperfusion. Pathological changes in the lung and the apoptotic index (AI) were examined. Lung malondialdehyde (MDA), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β levels, the wet/dry (W/D) ratio, semi-quantitative score of lung injury (SSLI), and Notch2 protein and Hes-1 mRNA expression were also examined. Results In the I/R group, inflammatory changes were observed, AI increased, and MDA, SSLI, W/D, TNF-α, IL-1β, Notch2, and Hes1-mRNA expression increased, while PaO2 decreased compared with the Sham group. Pathological changes in the I/R+Cur group were reversed. All indexes in the I/R+DAPT and I/R+Cur group were similar. Conclusion Curcumin post-treatment reduced I/R-induced lung injury in rats. Its mechanism may be related to the inhibition of Notch2/Hes-1 signaling pathway and the release of inflammatory factors.

scholarly journals β-arrestin-2 up-regulates toll-like receptor 2 signaling and inhibits apoptosis in human endometrial cancer heterotransplants in nude mice

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Fanling Hong ◽  
Yujun Zhang ◽  
Wenjin Cheng ◽  
Xiuli Sun ◽  
Jianliu Wang
Keyword(s):  
Inflammatory Cytokines ◽  
Nude Mice ◽  
Caspase 3 ◽  
Glycogen Synthase ◽  
Inflammatory Factors ◽  
Toll Like Receptor ◽  
Caspase 9 ◽  
Serine Threonine Kinase ◽  
Tnf Α ◽  
Toll Like Receptor 2

Abstract Background β-arrestin-2(Arr2) functions as an anti-apoptotic factor and affects cell proliferation, but its downstream molecular pathway in endometrial carcinoma (EC) is still unclear. This study aimed to investigate the effects of the stable overexpression of Arr2 on the proliferation and apoptosis of human EC heterotransplants and the expression of associated molecules, including Toll-like receptor 2(TLR2), serine-threonine kinase Akt (Akt), glycogen synthase kinase-3β(GSK3β) and some typical inflammatory cytokines such as NF-κB p56, TNF-α and IL-6 & IL-8. Methods Human EC cell line Ishikawa, stably transfected with Arr2 full-length plasmid, was injected subcutaneously into nude mice. They were treated with 0, 10, 20 mg/kg paclitaxel and the volume and weight of the tumor tissue were measured and calculated. The necrotic index were assessed by H&E staining and microscopic observation. The levels of caspase-3, caspase-9, TLR2, NF-κB p56, Akt, GSK3β were measured by western blot, and the levels of TNF-α, IL-6, IL-8 were measured by real-time PCR. Results We found that Arr2 overexpression promoted the growth of human EC heterotransplants. Arr2 attenuated the promotion of caspase-3 and caspase-9 by paclitaxel and mediated the increase of TLR2 and several inflammatory cytokines. The levels of Akt and GSK3β were not affected. Conclusion Arr2 overexpression was associated with the increase of TLR2 and several inflammatory factors, meanwhile inhibited paclitaxel-induced anti-tumor effect on human EC heterotransplants.

Crucial Factors of the Inflammatory Microenvironment (IL-1 beta/TNF-alpha/TIMP-1) Promote Maintenance of the Malignant Hemopoietic Clone of Myelofibrosis By Stimulating the in Vitro Survival/Proliferation/Migration of Circulating CD34+ stem/Progenitor Cells

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4094-4094
Author(s):  
Dorian Forte ◽  
Daria Sollazzo ◽  
Nicola Polverelli ◽  
Romano Marco ◽  
Lara Rossi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Inflammatory Cytokines ◽  
Stromal Cells ◽  
Colony Formation ◽  
Inflammatory Factors ◽  
Inflammatory Microenvironment ◽  
Cd34 Cells ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract Introduction. Myelofibrosis (MF), an acquired clonal disorder of the hematopoietic stem/progenitor cell (HSPC) with a dysregulation in JAK/STAT signalling (mutations in JAK2, MPL and Calreticulin (CALR) genes), is characterized by a state of chronic inflammation. It is argued that the up-regulated production of proinflammatory cytokines by both HSPCs and the surrounding stromal cells generates a microenvironment that selects for the malignant clone. Only recently, it has been hypothesized that the sustained inflammatory microenvironment of MF can alter crucial biological processes, leading to genomic instability and cancer progression. Here we tested the in vitro functional effects of pivotal players of the inflammatory microenvironment (the extracellular ATP nucleotide and selected cytokines, such as Interleukin (IL)-1β, Tumor Necrosis Factor (TNF)-α or the Tissue Inhibitor of Metalloproteinases-1 (TIMP-1)) on the HSPCs from MF patients. Methods: Circulating CD34+/CD34+ CD38- cells from MF patients (JAK2V617F (17 cases) and CALR (9 cases) mutations) or cord blood (CB; 8 samples) were phenotypically and functionally characterized after in vitro incubation with or without ATP (1000 μM), IL-1β (10 ng/mL), TNF-α (10 ng/mL) or TIMP-1 (100 ng/mL) (alone or in combination). Cells were then analyzed for survival/apoptosis (Annexin-V/Propidium Iodide staining), phenotype (evaluation of CD63 (TIMP-1 receptor), CXCR4 and CD38 expression), cell cycle and clonogenic capacity. Migration was assessed first towards a CXCL12 gradient in the presence or absence of the pro-inflammatory factors. In parallel experiments, CD34+ cells from MF patients were co-cultured with normal mesenchymal stromal cells (MSCs) in the presence or absence of the pro-inflammatory cytokines and then evaluated for their ability to migrate towards a CXCL12 gradient. Plasma TIMP-1, TNF-α, IL-1β and CXCL12 were measured by ELISA assay. Results: The plasma levels of TIMP-1, TNF-α, IL-1β, CXCL12 and the number of circulating CD34+, CD34+ CD38-, CD34+ CD63+, CD34+ CD184+ cells were increased in MF patients. According to mutational status, the CD34+ CD63+ cells were higher in the CALR+ patients. The survival of MF CD34+ cells was strongly stimulated by in vitro incubation with TNF-α or IL-1β as compared with the CB-derived CD34+ cells or untreated cells. By multiple cytokine combinations, IL-1β/TIMP-1, IL-1β /ATP or IL-1β /TNF-α treatments significantly promote the survival of MF CD34+ cells as compared with the normal counterparts or the untreated cells. Various combinations with IL-1β were also effective in stimulating survival of CD34+CD38- cells. IL-1β/TIMP-1 and IL-1β/TNF-α/TIMP-1, but not factors alone, significantly increased the CFU-C growth of MF patients as compared with the CB-derived counterparts and the untreated cells. Moreover, comparing CALR+ vs JAK2V617F+ patients, the colony formation of JAK2V617F+ patients was mainly promoted by the IL-1β/TNF-α treatment. Along with clonogenic capacity stimulation, exposure of CD34+ cells from MF patients to IL-1β/TNF-α/TIMP-1 significantly increases the S-phase cells, suggesting that these pro-inflammatory factors stimulated cell-cycle progression in dormant CD34+ MF cells. Migration of CD34+ cells from MF was significantly increased in CXCL12 treated cells. In addition, exposure of MF CD34+ cells to IL-1β/TNF-α, IL-1β/TIMP-1 or IL-1β/TNF-α/TIMP-1 significantly promotes cell migration in comparison with the CB-derived counterparts or SDF-1 alone. MF migrated cells in the presence of IL-1β/TNF-α significantly upregulate CD63 expression. Intriguingly, colony formation of MF migrated CD34+ cells in the presence of IL-1β/TNF-α or IL-1β/TNF-α/TIMP-1 was potently increased. Finally, co-culture systems with normal MSCs in the presence of pro-inflammatory factors revealed that MF CD34+ cells display increased migration ability toward CXCL12 gradient. Conclusions: Altogether our findings suggest that in MF the inflammatory niche plays a key role in the maintenance of the malignant clone. Thus, the interplay between the pro-inflammatory cytokines promote and select the HSPCs with higher proliferative activity, clonogenic potential and migration capability. Targeting these microenvironmental interactions may be a clinically relevant approach. D.F. and D.S. equally contributed Disclosures Martinelli: Pfizer: Consultancy; Ariad: Consultancy; Novartis: Consultancy, Speakers Bureau; MSD: Consultancy; AMGEN: Consultancy; BMS: Consultancy, Speakers Bureau; ROCHE: Consultancy.

scholarly journals Effects of Exercise on Inflammatory Cytokines in Patients with Type 2 Diabetes: A Meta-analysis of Randomized Controlled Trials

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Xiaoke Chen ◽  
Xinzheng Sun ◽  
Chenghao Wang ◽  
Hui He
Keyword(s):  
Type 2 Diabetes ◽  
Randomized Controlled Trials ◽  
Inflammatory Cytokines ◽  
Exercise Intervention ◽  
Meta Analysis ◽  
Inflammatory Factors ◽  
Controlled Trials ◽  
Randomized Controlled ◽  
Tnf Α

Objective. Inflammation is involved in the pathogenesis of type 2 diabetes (T2DM) and the occurrence of insulin resistance. The purpose of this study was to investigate the effects of exercise on inflammatory factors in patients with T2DM. Methods. A systematic review was conducted on five databases, Cochrane, Embase, Pubmed, Web of Science, and EBSCO. All randomized controlled trials (RCTs) published between establishment of the database and November 2020 without restrictions on language were included. Studies evaluated the effects of exercise intervention on inflammatory cytokines in patients with T2DM were selected. Results. Twenty-three randomized controlled trials (1350 patients) were included in our meta-analysis. Exercise can significantly reduce the level of C-reactive protein (CRP) (MD: −0.79, 95% CI: −1.26 to −0.33, p = 0.0008 ), tumor necrosis factor-α (TNF-α) (MD: −2.33, 95% CI: −3.39 to −1.27, p < 0.0001 ), and interleukin-6 (IL-6) (MD: −0.42, 95% CI: −0.60 to −0.24, p < 0.0001 ) in T2DM patients. Conclusion. The findings of this review suggest that exercise reduces inflammatory cytokines (CRP, TNF-α, and IL-6) in T2DM patients. More studies with high methodological qualities and large sample sizes need to be done to confirm which forms of exercise are most effective.

scholarly journals Metformin ameliorates scleroderma via inhibiting Th17 cells and reducing mTOR-STAT3 signaling in skin fibroblasts

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jeonghyeon Moon ◽  
Seon-yeong Lee ◽  
Jeong Won Choi ◽  
A Ram Lee ◽  
Jin Hee Yoo ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Th17 Cells ◽  
Skin Fibroblasts ◽  
Inflammatory Factors ◽  
Metformin Treatment ◽  
Protective Effects ◽  
Stat3 Signaling ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

AbstractScleroderma is an autoimmune disease that causes dermal fibrosis. It occurs when collagen accumulates in tissue as a result of persistent inflammation. Th17 cells and pro-inflammatory cytokines such as IL-1β, IL-6, IL-17, and TNF-α play important roles in the pathogenesis of scleroderma. Because metformin, a medication used to treat diabetes, has effective immunoregulatory functions, we investigated its therapeutic function in scleroderma. Mice in a model of bleomycin-induced scleroderma were treated with metformin for 2 weeks. Histological assessment demonstrated protective effects of metformin against scleroderma. Metformin decreased the expression of pro-inflammatory factors in dermal tissue and lymphocytes. It also decreased mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, IL-17, and TNF-α) and fibrosis-inducing molecules both in vivo and in vitro. These results suggest that metformin treatment has anti-inflammatory effects on lymphocytes via the inhibition of IL-17 and cytokines related to Th17 differentiation, such as IL-1β, IL-6, and TNF-α. To investigate how metformin modulates the inflammatory process in skin fibroblasts, we measured mTOR-STAT3 signaling in skin fibroblasts and found that phosphorylated mTOR and phosphorylated STAT3 protein expression were decreased by metformin treatment. These results suggest that metformin has potential to treat scleroderma by inhibiting pro-inflammatory cytokines and anti-inflammatory activity mediated by mTOR-STAT3 signaling.

scholarly journals Formulation of Huangqin Decoction Influence Immune Function and Fecal Microbiome of Chicks Suffered Escherichia Coli O78 Challenge

2021 ◽  
Author(s):  
Junyan Wang ◽  
Rui Li ◽  
Yong Liu ◽  
Chensheng Gu ◽  
Haili Wang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Mortality Rate ◽  
Mrna Expression ◽  
Relative Abundance ◽  
Inflammatory Factors ◽  
Fecal Microbiome ◽  
E Coli ◽  
Liver Index ◽  
Tnf Α ◽  
Spleen Index

Abstract Ethnopharmacological relevance: Huangqin Decoction (HQD), a traditional Chinese medicine formula from the Shang Han Lun written by Zhang Zhongjing, has been used in China for nearly two thousand years. According to traditional Chinese medicine and a previous literature, HQD has the effect of clearing heat and removing toxin, antidiarrhea, and relieving pain. Therefore, HQD were used to prevent or cure many diseases, such as inflammation, diarrhea, malaria, and other acute or chronic gastrointestinal diseases. Materials and methods: HQD consist of four components: Scutellariae Radix (huangqin, HQ), Paeoniae Radix Alba (shaoyao, SY), Jujubae Fructus (dazao, DZ), Licorice (gancao, GC). A total of 80 1-day-old male Esa brown chicks were divided into eight groups (n=10): Control group (CG), model group (MG), Enrofloxacin group (ENR, 10 mg/kg·BW), HQD group (HQD, 500 mg/kg·BW), HQD-GC group (GC absent HQD, 500 mg/kg·BW), HQD-HQ group (HQ absent HQD, 500 mg/kg·BW), HQD-DZ group (DZ absent HQD, 500 mg/kg·BW) and HQD-SY group (SY absent HQD, 500 mg/kg·BW). The chicks, which were given HQD, herb absent HQD, or enrofloxacin orally at 19 days of age for 7 days, and then were intraperitoneally injected with inoculum of E. coli O78，fed continuously for 5 days as before. Results: It showed that E. coli O78 challenge decreased the average daily gain (ADG) and increased the mortality rate of chicks, increased the heart index and the liver index, decreased the bursal index, and had no effect on the spleen index. E. coli O78 challenge increased the serum lysozyme (LZM) and IL-1β, TNF-α, IL-10, IL-6, up-regulated the mRNA expression of TLR4, TLR5 and TLR15 in the spleen, and had no effect on the bursal compared with CG. E. coli O78 challenge increased the Operational Taxonomic Unit (OTU), increased the relative abundance of harmful bacteria Proteobacteria, and decreased the relative abundance of probiotics Bacteroidetes and Firmicutes at the phylum levels. E. coli O78 challenge increased the relative abundance of harmful bacteria Escherichia-Shigella and Pseudomonas at the genus levels. HQD supplementation showed higher ADG and reduced the mortality rate caused by E. coli O78 challenge, decreased the heart index and liver index, and increased the bursal index and spleen index. HQD supplementation decreased the serum LZM, IL-1β, TNF-α, IL-10, IL-6 levels, down-regulated the mRNA expression of TLR4, TLR5 and TLR15 in the spleen in E. coli O78 challenged chicks, and up-regulated the mRNA expression of TLR4, TLR5 and TLR15 in the bursal in that. At the phylum levels, HQD supplementation reversed the increased of OTUs, decreased the relative abundance of harmful bacteria Proteobacteria, increased the relative abundance of probiotics Bacteroidetes and Firmicutes. At the genus levels, HQD decreased the relative abundance of harmful bacteria Escherichia-Shigella and Pseudomonas. It means that HQD reversed the change of the gut microbiota structure. Compared with HQD, HQD-DZ and HQD-HQ increased the mortality rate. HQD-HQ decreased the ADG and liver index. HQD-GC decreased the spleen index. HQD-DZ, HQD-HQ, HQD-SY and HQD-GC increased the serum TL-6, but only the HQD-HQ and HQD-SY increased the serum TNF-α. All herb absent HQD did not activate the toll-like receptors signaling pathways in spleen and bursal of chicks. HQD-DZ and HQD-HQ increased the harmful bacteria Escherichia-Shigella, and HQD-DZ increased the harmful bacteria Proteobacteria levels. Conclusions: Dietary supplementation with HQD, by down-regulating the mRNA expression of TLR4, TLR5 and TLR15 in the spleen, further decreasing the serum LZM and IL-1β, TNF-α, IL-10, IL-6 levels, improves the immune function and reverse the change of fecal microbiome in chicks challenged with E. coli O78. About herb absent groups, the results shown that SY and DZ play a key role in reducing the level of inflammatory factors and keeping fecal microbiome balance respectively. what’s more, we highlighted that HQ is indispensable in HQD, HQ not only play a key role in reducing the level of inflammatory factors, but also keep the balance of fecal microflora.

Sign in / Sign up

Export Citation Format

Share Document