scholarly journals Goose Nephritic Astrovirus infection of Goslings Induces Lymphocyte Apoptosis, Reticular Fiber Destruction, and CD8 T-Cell Depletion in Spleen Tissue

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1108
Author(s):  
Rui Ding ◽  
Han Huang ◽  
Hongyu Wang ◽  
Zewen Yi ◽  
Siyu Qiu ◽  
...  
Keyword(s):  
Membrane Integrity ◽  
High Viral Load ◽  
Economic Losses ◽  
Tunel Staining ◽  
White Pulp ◽  
Reticular Cell ◽  
Mrna Levels ◽  
Lymphocyte Apoptosis ◽  
Reticular Fibers ◽  
Reticular Fiber

The emergence of a novel goose nephritic astrovirus (GNAstV) has caused economic losses to the Chinese goose industry. High viral load is found in the spleen of goslings infected with GNAstV, but pathological injuries to the spleen due to GNAstV are largely unknown. In this study, 50 two-day-old goslings were infected orally with GNAstV, and 50 goslings were treated with PBS as control. Spleens were collected at different times following infection to assess damage. GNAstV infection caused visceral gout and urate deposition in joints, and resulted in 16% mortality. GNAstV was found in the lymphocytes and macrophages within the spleen. Lymphocyte loss, especially around the white pulp, and destruction and decline in the number of reticular fibers was observed in GNAstV-infected goslings. Moreover, in GNAstV-infected goslings, ultrahistopathological examination found that splenic lymphocytes exhibited condensed chromatin and apoptotic bodies, and reticular cells displayed damage to plasma membrane integrity and swollen mitochondria. Furthermore, TUNEL staining confirmed apoptosis of lymphocytes, and the mRNA levels of Fas and FasL were significantly increased in the GNAstV-infected goslings. In addition, GNAstV infection reduced the number and protein expression of CD8. In conclusion, GNAstV infection causes lymphocyte depletion, reticular cell necrosis, reticular fiber destruction, lymphocyte apoptosis, and reduction in CD8 levels, which contribute to spleen injury.

scholarly journals Selenium deficiency induces spleen pathological changes in pigs by decreasing selenoprotein expression, evoking oxidative stress, and activating inflammation and apoptosis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shuang Li ◽  
Wenjuan Sun ◽  
Kai Zhang ◽  
Jiawei Zhu ◽  
Xueting Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
The Body ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Antioxidant Systems ◽  
Tunel Staining ◽  
White Pulp ◽  
Sibling Pairs ◽  
Se Deficiency ◽  
Spleen Index

Abstract Background The immune system is one aspect of health that is affected by dietary selenium (Se) levels and selenoprotein expression. Spleen is an important immune organ of the body, which is directly involved in cellular immunity. However, there are limited reports on Se levels and spleen health. Therefore, this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis. Methods Twenty-four pure line castrated male Yorkshire pigs (45 days old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into two equal groups and fed Se-deficient diet (0.007 mg Se/kg) or Se-adequate diet (0.3 mg Se/kg) for 16 weeks. At the end of the trial, blood and spleen were collected to assay for erythroid parameters, the osmotic fragility of erythrocytes, the spleen index, histology, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining, Se concentrations, the selenogenome, redox status, and signaling related inflammation and apoptosis. Results Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes (P < 0.05). The spleen index did not change, but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased, the red pulp increased, and splenocyte apoptosis occurred in the Se deficient group. Se deficiency decreased the Se concentration and selenoprotein expression in the spleen (P < 0.05), blocked the glutathione and thioredoxin antioxidant systems, and led to redox imbalance. Se deficiency activated the NF-κB and HIF-1α transcription factors, thus increasing pro-inflammatory cytokines (IL-1β, IL-6, IL-8, IL-17, and TNF-α), decreasing anti-inflammatory cytokines (IL-10, IL-13, and TGF-β) and increasing expression of the downstream genes COX-2 and iNOS (P < 0.05), which in turn induced inflammation. In addition, Se-deficiency induced apoptosis through the mitochondrial pathway, upregulated apoptotic genes (Caspase3, Caspase8, and Bak), and downregulated antiapoptotic genes (Bcl-2) (P < 0.05) at the mRNA level, thus verifying the results of TUNEL staining. Conclusions These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins, oxidative stress, inflammation and apoptosis.

scholarly journals Cell Culture-Derived Tilapia Lake Virus-Inactivated Vaccine Containing Montanide Adjuvant Provides High Protection against Viral Challenge for Tilapia

Vaccines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 86
Author(s):  
Weiwei Zeng ◽  
Yingying Wang ◽  
Huzi Hu ◽  
Qing Wang ◽  
Sven M. Bergmann ◽  
...  
Keyword(s):  
Neutralizing Antibodies ◽  
Protective Efficacy ◽  
Interferon Γ ◽  
Economic Losses ◽  
Mrna Levels ◽  
Infectious Dose ◽  
Booster Immunization ◽  
Virus Challenge ◽  
High Level ◽  
Factor Α

Tilapia lake virus (TiLV) is a newly emerging pathogen responsible for high mortality and economic losses in the global tilapia industry. Currently, no antiviral therapy or vaccines are available for the control of this disease. The goal of the present study was to evaluate the immunological effects and protective efficacy of formaldehyde- and β-propiolactone-inactivated vaccines against TiLV in the presence and absence of the Montanide IMS 1312 VG adjuvant in tilapia. We found that β-propiolactone inactivation of viral particles generated a vaccine with a higher protection efficacy against virus challenge than did formaldehyde. The relative percent survivals of vaccinated fish at doses of 108, 107, and 106 50% tissue culture infectious dose (TCID50)/mL were 42.9%, 28.5%, and 14.3% in the absence of the adjuvant and 85.7%, 64.3%, and 32.1% in its presence, respectively. The vaccine generated specific IgM and neutralizing antibodies against TiLV at 3 weeks following immunization that were significantly increased after a second booster immunization. The steady state mRNA levels of the genes tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interferon γ (IFN-γ), cluster of differentiation 4 (CD4), major histocompatibility complex (MHC)-Ia, and MHC-II were all increased and indicated successful immune stimulation against TiLV. The vaccine also significantly lowered the viral loads and resulted in significant increases in survival, indicating that the vaccine may also inhibit viral proliferation as well as stimulate a protective antibody response. The β-propiolactone-inactivated TiLV vaccine coupled with the adjuvant Montanide IMS 1312 VG and booster immunizations can provide a high level of protection from virus challenge in tilapia.

scholarly journals Role of macrophage secretions on rat polycystic ovary: its effect on apoptosis

Reproduction ◽  
2015 ◽  
Vol 150 (5) ◽  
pp. 437-448 ◽  
Author(s):  
Florencia Figueroa ◽  
Alicia Motta ◽  
Mariano Acosta ◽  
Fabian Mohamed ◽  
Liliana Oliveros ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Polycystic Ovary ◽  
Ovarian Response ◽  
Reproductive Age ◽  
Estradiol Valerate ◽  
Tunel Staining ◽  
Prostaglandin E ◽  
Mrna Levels ◽  
Nitric Oxide Release ◽  
Factor Α

Polycystic ovarian syndrome is the most common endocrine disorder among women of reproductive age. Little is known about its etiology, although the evidence suggests an intrinsic ovarian abnormality in which endocrine, metabolic, neural and immune factors would be involved. In this work, the effects of macrophage (MO) secretion on ovarian apoptosis in a polycystic ovary syndrome rat model (PCO rat) induced by estradiol valerate are studied. Spleen MO secretions were used to stimulate ovaries and ovarian interstitial and granulosa cells from both PCO and control rats. Ovarian hormones and prostaglandin E2(PGE2) were measured by RIA; ovarian mRNA levels of Bax, Bcl2 and NFkB by RT-PCR; and ovarian inducible nitric oxide synthase (iNOS) by western blot. The number of apoptotic cells was evaluated by TUNEL. In the PCO ovary, the MO secretions from PCO rats increased the Bax and NFkB mRNA expressions and increased TUNEL staining in both granulosa and theca cells. In addition, the PCO MO secretions produced a decrease of nitric oxide release, iNOS protein level and PGE2content in the PCO ovary, and it also induced an increase of androstenedione production by PCO interstitial cells, in comparison with control MO secretions. Considering these results and knowing that testosterone stimulates tumour necrosis factor-α production by PCO MO modifying ovarian response by increasing androstenedione, it is reasonable to suggest that the increase of androgens stimulated in ovarian cells by PCO MO secretions could in turn stimulate the cytokine production from MO, thus maintaining an apoptotic vicious cycle in the PCO ovary.

Effects of different heat stress periods on various blood and meat quality parameters in young Arbor Acer broiler chickens

2013 ◽  
Vol 93 (4) ◽  
pp. 453-460 ◽  
Author(s):  
Shu Tang ◽  
Jimian Yu ◽  
Miao Zhang ◽  
Endong Bao
Keyword(s):  
Heat Stress ◽  
Meat Quality ◽  
Shear Force ◽  
Broiler Chickens ◽  
Plasma Concentrations ◽  
Membrane Integrity ◽  
Muscle Metabolism ◽  
Quality Parameters ◽  
Economic Losses ◽  
Clear Understanding

Tang, S., Yu, J., Zhang, M. and Bao, E. 2013. Effects of different heat stress periods on various blood and meat quality parameters in young Arbor Acer broiler chickens. Can. J. Anim. Sci. 93: 453–460. Heat stress can influence muscle metabolism and meat quality in animals reared for food production. From a commercial perspective, understanding the mechanism of this effect is clearly necessary. The aim of this study was to investigate the effects of different heat stress periods on serum metabolites and chicken meat quality (n=120). Plasma indicators creatine kinase (CK), glutamic-pyruvic transaminase (GPT), glutamic-oxaloacetic transaminase (GOT), insulin and glucagon and meat quality (pH, expressible moisture, cooking losses, shear force values) were evaluated. Compared with controls, the concentrations of CK and GPT increased (P<0.01) after 2 and 3 h of heat stress, respectively, whereas plasma insulin and glucagon decreased after 1 and 5 h of heat stress, respectively. The immediate pH (pHi) and ultimate pH (pHu) of the pectoralis muscles decreased (P<0.01) after 1 and 2 h of exposure to heat stress, respectively. Cooking loss, expressible moisture and shear force value increased (P<0.01) after 3, 2, and 1 h of heat stress, respectively. These data indicate that elevated plasma concentrations of CK and GPT can be used as parameters for assessing the stress level to which broilers are exposed before slaughter. The preslaughter exposure of broiler chickens to heat stress can alter muscle metabolism and membrane integrity, leading to undesirable meat characteristics. Thus, a clear understanding of the mechanisms underlying these processes will contribute to the determination of prevention strategies and the avoidance of the associated economic losses.

scholarly journals Electroacupuncture Ameliorates Cerebral I/R-Induced Inflammation through DOR-BDNF/TrkB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Yue Geng ◽  
Yeting Chen ◽  
Wei Sun ◽  
Yingmin Gu ◽  
Yongjie Zhang ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Cytokine Gene Expression ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Mrna Levels ◽  
Anti Inflammatory

The beneficial effects of electroacupuncture (EA) at Shuigou (GV26) and Neiguan (PC6) on poststroke rehabilitation are critically related to the activation of the delta-opioid receptor (DOR). The underlying anti-inflammatory mechanisms in DOR activation and EA-mediated neuroprotection in cerebral ischemia/reperfusion (I/R) injury were investigated in the current study. Cell proliferation and apoptosis were detected by morphological changes, cell counting kit-8 (CCK-8) assay, lactate dehydrogenase (LDH) release, and TUNEL staining. The mRNA levels were evaluated by using real-time quantitative polymerase chain reaction (RT-qPCR), and the protein expression was measured by western blot or enzyme-linked immunosorbent assay (ELISA) in vitro. Infarct volume was examined by cresyl violet (CV) staining, neurologic recovery was assessed by neurological deficit scores, and pro- and anti-inflammatory cytokines were determined by immunofluorescence in vivo. DOR activation greatly ameliorated morphological injury, reduced LDH leakage and apoptosis, and increased cell viability. It reversed the oxygen-glucose deprivation/reoxygenation- (OGD/R-) induced downregulation of DOR mRNA and protein, as well as BDNF protein. DOR activation also reduced proinflammatory cytokine gene expression, including TNF-α, IL-1β, and IL-6, and at the same time, increased anti-inflammatory cytokines IL-4 and IL-10 in OGD/R challenged PC12 cells. EA significantly reduced middle cerebral artery occlusion/reperfusion- (MCAO/R-) induced infarct volume and attenuated neurologic deficit scores. It markedly increased the expression of IL-10 and decreased IL-1β, while sham EA did not have any protective effect in MCAO/R-injured rats. DOR activation plays an important role in neuroprotection against OGD/R injury by inhibiting inflammation via the brain-derived neurotrophic factor/tropomyosin-related kinase B (BDNF/TrkB) pathway. The neuroprotective efficacy of EA at Shuigou (GV26) and Neiguan (PC6) on cerebral I/R injury may be also related to the inhibition of inflammatory response through the DOR-BDNF/TrkB pathway.

Endotoxin infusion in rats induces apoptotic and survival pathways in hearts

2000 ◽  
Vol 279 (5) ◽  
pp. H2053-H2061 ◽  
Author(s):  
Treena E. McDonald ◽  
Michelle N. Grinman ◽  
Chris M. Carthy ◽  
Keith R. Walley
Keyword(s):  
Fold Increase ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Mrna Levels ◽  
Apoptotic Pathway ◽  
Protein Levels ◽  
Bax Protein ◽  
Survival Pathways ◽  
Baseline Values

Inflammatory mediators of sepsis induce apoptosis in many cell lines. We tested the hypothesis that lipopolysaccharide (LPS) injection in vivo results in induction of early apoptotic and survival pathways as well as evidence of late-stage apoptosis in the heart. Hearts were collected from control rats and at 6, 12, and 24 h after LPS injection (4 mg/kg). Activation of an apoptotic pathway was identified by a 1,000-fold increase in caspase-3 activity at 24 h ( P < 0.05). Confirmation of these results occurred when terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining identified myocardial cells undergoing DNA fragmentation with significant levels at 24 h post-LPS injection. LPS also caused early proapoptotic mRNA (Bax) to increase (16% at 24 h, P < 0.05), whereas the Bax protein initially decreased (35% at 6 h, P < 0.05) and then returned to baseline values by 24 h. Six hours after LPS injection, Bcl-2 (early prosurvival) mRNA levels increased, whereas its protein levels decreased (70%, P < 0.05) and then returned to baseline levels by 24 h. Mitochondrial cytochrome c levels decreased, suggestive of mitochondrial involvement. Thus involvement of proapoptotic and prosurvival pathways in the heart occurs during a septic inflammatory response.

Uteroplacental insufficiency increases apoptosis and alters p53 gene methylation in the full-term IUGR rat kidney

2003 ◽  
Vol 285 (5) ◽  
pp. R962-R970 ◽  
Author(s):  
Tho D. Pham ◽  
Nicole K. MacLennan ◽  
Christina T. Chiu ◽  
Gisella S. Laksana ◽  
Jennifer L. Hsu ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Molecular Mechanisms ◽  
Cpg Methylation ◽  
Full Term ◽  
Tunel Staining ◽  
Mrna Levels ◽  
Fetal Origins ◽  
P53 Expression ◽  
Pregnant Rat ◽  
Related Proteins

Uteroplacental insufficiency causes intrauterine growth retardation (IUGR), which is associated with adult onset diseases such as hypertension. Previous studies demonstrate that growth retardation in humans and rats decreases glomeruli number; however, the molecular mechanisms responsible for this reduction are unknown. Apoptosis plays a key role in renal organogenesis. We therefore hypothesized that the in utero deprivation associated with uteroplacental insufficiency decreases glomeruli, increases apoptosis, and alters the mRNA levels of key apoptosis-related proteins in full-term IUGR kidneys. To prove this hypothesis, we induced asymmetric IUGR through bilateral uterine artery ligation of the pregnant rat. We found that uteroplacental insufficiency significantly reduced glomeruli number while increasing TUNEL staining and caspase-3 activity in the IUGR kidney. A significant decrease in Bcl-2 mRNA and a significant increase in Bax and p53 mRNA further characterized the IUGR kidney. Because altered p53 CpG methylation affects p53 expression, we analyzed p53 promoter CpG methylation using methylation-sensitive restriction enzymes and real-time PCR. Uteroplacental insufficiency specifically decreased CpG methylation of the renal p53 BstU I site promoter without affecting the Hha I or the Aci I sites. Uteroplacental insufficiency also induced a relative hypomethylation from exon 5 to exon 8, which was associated with deceased mRNA levels of DNMT1. We conclude that uteroplacental insufficiency alters p53 DNA CpG methylation, affects mRNA levels of key apoptosis-related proteins, increases renal apoptosis, and reduces glomeruli number in the IUGR kidney. We speculate that these changes represent mechanisms that contribute to the fetal origins of adult disease.

Localization of Silver in the Spleen of Argyric Rats by Energy Dispersive X-Ray Analysis Coupled with Scanning and Transmission Electron Microscopy

1977 ◽  
Vol 35 ◽  
pp. 504-506
Author(s):  
G. Pereira
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Computer Assisted ◽  
White Pulp ◽  
Reticular Cell ◽  
X Ray ◽  
Transmission Electron ◽  
Freeze Dried ◽  
Scanning Electron

Previous electron microscopic observations of the spleen have revealed the white pulp to be completely separated from the extravasated blood in the surrounding marginal zone by a strategically-located, double layer of reticular cells ensheathing a coarse reticular fiber. Similarly, a single reticular cell layer has been observed to form a continuous investment for all white pulp capillaries. To test the significance of this apparent isolation of the splenic white pulp from the blood, the distribution and composition of silver deposits in the spleen of argyric rats were determined by transmission and scanning electron microscopy coupled with computer-assisted x-ray analysis.Young male albino rats were made argyric by supplying them for many months with drinking water to which 1.5gm per liter of silver nitrate had been added. Specimens from the spleens of control and argyric animals were prepared for conventional transmission electron microscopy by glutaraldehyde-osmium fixation. For scanning electron microscopy, other specimens were fixed in buffered glutaraldehyde, freeze-dried in vacuo, coated with a thin film of gold- palladium and examined in a Cambridge Stereoscan Mark II.

Current Biomarkers of Apoptosis Process in Chronically Inflamed Nasal Sinus Epithelium: Representatives of BAX, Bcl-2 and miRNA Group

2021 ◽  
Author(s):  
Monika Morawska-Kochman ◽  
Agnieszka Smieszek ◽  
Klaudia Marcinkowska ◽  
Krzysztof Marycz ◽  
Kamil Nelke ◽  
...  
Keyword(s):  
Treatment Strategies ◽  
Tunel Staining ◽  
Mrna Levels ◽  
Upper Respiratory Tract ◽  
Nasal Sinus ◽  
Expression Levels ◽  
Apoptosis Markers ◽  
Cell Proliferative Activity ◽  
Characteristic Features ◽  
Apoptosis Process

Abstract In chronic upper respiratory tract diseases, increased cell proliferative activity is observed, which is coordinated by Bcl-2 proteins as well as by small non-coding RNAs.The aim of this study was to determine the expression of critical apoptosis markers at the mRNA and miRNA level in patients with chronic rhinosinusitis with nasal polyps (CSRwNP).The study group consisted of 10 patients with CSRwNP and 10 healthy controls. TUNEL staining was performed to detect in situ apoptosis in the maxillary sinus mucosa. The levels of selected mRNA transcripts associated with cell survival and apoptosis: BAX, p53, p21, CASP3, CASP9, c-MYC, CCND1, BRIC5 and APAF1 and miRNAs: miR-17-5p, miR-145-5p, miR-146a-5p and miR-203a-3p were determined by RT-qPCR. CSRwNP patients showed increased apoptosis determined by TUNEL assay accompanied by increased expression of BAX, P21, P53, CASP3, CASP9, c-MYC, APAF-1 transcripts and decreased mRNA levels of BCL-2 and BIRC5. There were increased expression levels of miR-203a-3p and decreased expression levels of miR-17-5p and miR-145-5p. These findings appear to be characteristic features of apoptosis in CRSwNP. The proapoptotic effect of miR-203a-3p may be crucial for future treatment strategies for CRSwNP.

Contribution of the immune system and astrocytes to spinal muscular atrophy pathology

2018 ◽  
Author(s):  
◽  
Marie-Therese Khairallah
Keyword(s):  
Immune System ◽  
Spinal Muscular Atrophy ◽  
Motor Neuron ◽  
Muscular Atrophy ◽  
Membrane Integrity ◽  
Survival Motor Neuron ◽  
White Pulp ◽  
Functional Impairments ◽  
Altered Expression ◽  
The Impact

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease and the leading genetic cause of infant mortality. SMA is caused by afunctional loss of the survival motor neuron-1 (SMN1) gene and the subsequent deficiency of the ubiquitously expressed survival motor neuron (SMN) protein. SMA presents by motor neuron loss and muscle atrophy, and historically was considered an autonomous disease of the a-lower motor neuron (LMN). In this work we investigated effects of low levels of SMN outside the LMNs. Specifically, we looked in the spleen to determine the impact of SMN deficiency on the spleen development and the integrity of the splenic immune cells. Additionally, we analyzed astrocytes to determine if they exhibit functional impairments that could compromise their role in supporting the survival and function of LMNs. First, we reported spleen hypoplasia in multiple SMA mouse models with alteration of the splenic architecture due to a severe reduction in the red pulp zone and relative conservation of the white pulp area. We found alterations in the relative abundance of splenic mediators of the immune response, where the resident macrophage subset was depleted starting at early pre-symptomatic time (post-natal day 2), whereas the B- and T-lymphocytes, and CD11b+ macrophages had higher frequency at the late symptomatic age (post-natal day 12). Secondly, we showed that primary astrocytes derived from the spinal cord of a SMA mouse model had compromised efficiency in their glutamate uptake capacity. Moreover, SMA spinal cords had altered expression in the level of flottilin-1, a lipid raft protein necessary for cell membrane integrity and for the function of receptors and transporters. Furthermore, we showed a higher expression of the NR2B, a subunit of the glutamate receptor NMDAR that signals mainly toward apoptosis. In summary, this work characterized new pathologies in two non-neuronal tissues in the CNS and in the periphery, demonstrated that the spleen and the immune system are likely contributing to the overall clinical pathology of SMA, and found altered mechanisms in astrocytes function that might explain their effect on LMNs in SMA.

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