scholarly journals Effect of 25-hydroxycholecalciferol supplementation on turkey performance and immune cell parameters in a coccidial infection model

2019 ◽  
Vol 98 (3) ◽  
pp. 1127-1133 ◽  
Author(s):  
Revathi Shanmugasundaram ◽  
Antrison Morris ◽  
Ramesh K Selvaraj
Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3382 ◽  
Author(s):  
Chi-Lung Yang ◽  
Ho-Cheng Wu ◽  
Tsong-Long Hwang ◽  
Chu-Hung Lin ◽  
Yin-Hua Cheng ◽  
...  

One new dibenzocycloheptene, validinol (1), and one butanolide firstly isolated from the natural source, validinolide (2), together with 17 known compounds were isolated from the stem of Cinnamomum validinerve. Among the isolates, lincomolide A (3), secosubamolide (7), and cinnamtannin B1 (19) exhibited potent inhibition on both superoxide anion generation (IC50 values of 2.98 ± 0.3 µM, 4.37 ± 0.38 µM, and 2.20 ± 0.3 µM, respectively) and elastase release (IC50 values of 3.96 ± 0.31 µM, 3.04 ± 0.23 µM, and 4.64 ± 0.71 µM, respectively) by human neutrophils. In addition, isophilippinolide A (6), secosubamolide (7), and cinnamtannin B1 (19) showed bacteriostatic effects against Propionibacterium acnes in in vitro study, with minimal inhibitory concentration (MIC) values at 16 μg/mL, 16 μg/mL, and 500 μg/mL, respectively. Further investigations using the in vivo ear P. acnes infection model showed that the intraperitoneal administration of the major component cinnamtannin B1 (19) reduced immune cell infiltration and pro-inflammatory cytokines TNF-α and IL-6 at the infection sites. The results demonstrated the potential of cinnamtannin B1 (19) for acne therapy. In summary, these results demonstrated the anti-inflammatory potentials of Formosan C. validinerve during bacterial infections.


Author(s):  
Michael A. Makara ◽  
Ky V. Hoang ◽  
Latha P. Ganesan ◽  
Elliot D. Crouser ◽  
Mahmood Khan ◽  
...  

Background Sepsis patients with cardiac dysfunction have significantly higher mortality. Although several pathways are associated with myocardial damage in sepsis, the precise cause(s) remains unclear and treatment options are limited. This study was designed to develop a new model to investigate the early events of cardiac damage during sepsis progression. Methods and Results Francisella tularensis subspecies novicida ( Ft.n ) is a Gram‐negative intracellular pathogen causing severe sepsis syndrome in mice. BALB /c mice (N=12) were sham treated or infected with Ft.n through the intranasal route. Serial electrocardiograms were recorded at multiple time points until 96 hours. Hearts were then harvested for histology and gene expression studies. Similar to septic patients, we illustrate both cardiac electrical and structural phenotypes in our murine Ft.n infection model, including prominent R' wave formation, prolonged QRS intervals, and significant left ventricular dysfunction. Notably, in infected animals, we detected numerous microlesions in the myocardium, previously observed following nosocomial Streptococcu s infection and in sepsis patients. We show that Ft.n ‐mediated microlesions are attributed to cardiomyocyte apoptosis, increased immune cell infiltration, and expression of inflammatory mediators (tumor necrosis factor, interleukin [ IL] ‐1β, IL ‐8, and superoxide dismutase 2). Finally, we identify increased expression of microRNA‐155 and rapid degradation of heat shock factor 1 following cardiac Ft.n infection as a primary cause of myocardial inflammation and apoptosis. Conclusions We have developed and characterized an Ft.n infection model to understand the pathogenesis of cardiac dysregulation in sepsis. Our findings illustrate novel in vivo phenotypes underlying cardiac dysfunction during Ft.n infection with significant translational impact on our understanding of sepsis pathophysiology.


1989 ◽  
Vol 17 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Michael Maes ◽  
Eugène Bosmans ◽  
Eduard Suy ◽  
Bob Minner ◽  
Jef Raus

Author(s):  
V.V Zheltkova ◽  
D.A. Zheltkov ◽  
G.A. Bocharov

Mathematical modelling can be very useful in studying complex objects in modern systems immunology. In this work we studied the problem of modelling immune cell population dynamics for HIV infection through the set of models with different levels of complexity, which include several characteristics of HIV infection dynamics (antigen presenting, cell and humoral immune reactions, the effect of regulatory T-lymphocytes). We formulated and solved the parameter estimation problem using maximal likelihood approach, for two variants of modelling error quantifying. The global sensitivity analysis was implemented with LHS-PRCC method. Models were compared by the residual functional values and using the information-theoretical framework. We present the extended Marchuk-Petrov model for HIV infection with delays. For solving the parameter estimation problem for this model we compared a number of numerical optimization methods.


2020 ◽  
Author(s):  
Einar B. Ólafsson ◽  
Arne L. ten Hoeve ◽  
Xiaoze Li Wang ◽  
Linda Westermark ◽  
Manuel Varas-Godoy ◽  
...  

AbstractRas-Erk MAPK signaling controls many of the principal pathways involved in metazoan cell motility, drives metastasis of multiple cancer types and is targeted in chemotherapy. Yet, its putative roles in immune cell functions or in infections have remained elusive. Here, using primary dendritic cells (DCs) in an infection model with the protozoan Toxoplasma gondii, we show that two pathways activated by infection converge on Ras-Erk MAPK signaling to promote migration of parasitized DCs. We identify signaling through the receptor tyrosine kinase Met (also known as HGFR) as a driver of T. gondii-induced DC hypermotility. Further, we show that voltage-gated Ca2+channel (VGCC, subtype CaV1.3) signaling impacts the migratory activation of DCs via calmodulin-calmodulin kinase II. We report that VGCC and Met signaling converge on Ras GTPase to drive Erk1/2 phosphorylation and migratory activation of T. gondii-infected DCs. The data provide a molecular basis for the hypermigratory mesenchymal-to-amoeboid transition (MAT) of parasitized DCs. The emerging concept suggests that parasitized DCs acquire metastasis-like migratory properties to promote infection-related dissemination.


2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Julia Sbierski-Kind ◽  
David Goldeck ◽  
Nikolaus Buchmann ◽  
Joachim Spranger ◽  
Hans-Dieter Volk ◽  
...  

Abstract Background Obesity is associated with chronic low-grade inflammation leading to metabolic and cardiovascular diseases, but a subset of obese individuals is considered insulin sensitive (IS). The underlying pathophysiologic mechanisms remain elusive and clinical studies on the relationship between inflammatory markers and metabolically healthy obesity (MHO) are scarce. Methods In this cross-sectional analysis, we included a sample of 437 older participants (60–84 years) from the Berlin Aging Study II (BASE-II). Peripheral blood mononuclear cells were isolated, immune cell subsets were analyzed with multiparameter flow cytometry and systemic cytokine levels were measured. Immune cell parameters were correlated with metabolic measures and multiple linear regression analysis was conducted and adjusted for various demographic and clinical factors. Results We found that frequencies of naïve and memory CD4+ and CD8+ T cells inversely correlated with measures for insulin sensitivity in the older population. Moreover, the percentages of naïve CD4+ and CD8+ T cells were significantly higher, whereas activated T cells and IL-6 levels were lower in IS compared to insulin resistant (IR) obese individuals. The percentages of naïve CD4+ and CD8+ T cells were predictive for impaired insulin sensitivity (ß = 0.16, p = 0.01 and ß = 0.11, p = 0.04), and the association of naïve CD4+ T cells with insulin sensitivity persisted after multivariate adjustment (ß = 0.14, p = 0.02). Conclusions These findings support the hypothesis that parameters of systemic inflammation can differentiate IS from IR obese individuals that are at higher risk for cardiometabolic diseases and may have clinical implications with regard to obesity treatment stratification. Trial registration DRKS00009277. Registered 31 August 2015 - Retrospectively registered.


Andrologia ◽  
2003 ◽  
Vol 35 (1) ◽  
pp. 6-7
Author(s):  
S. Graenz ◽  
A. Lewen ◽  
M. P. Hedger ◽  
J. Seitz ◽  
G. Aumüller ◽  
...  

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1742
Author(s):  
Pao-Chia Chou ◽  
Pei-Chi Lin ◽  
Shu-Wei Wu ◽  
Chien-Kai Wang ◽  
Thau-Kiong Chung ◽  
...  

Past immunological studies in broilers focused on juveniles within the rapid pre-slaughter growth period and may not reflect adult immune responses, particularly in breeders managed with chronic feed restriction (R). The study aimed to assess innate immune cell functions in respect to R vs. ad libitum (Ad) feed intake in breeder hens with and without dietary 25-hydroxycholecalciferol (25-OH-D3) supplementation. Ad-feed intake consistently suppressed IL-1β secretion, respiratory burst, and cell livability in peripheral heterophils and/or monocytes along the feeding trial from the age of 51 to 68 weeks. Supplemental 25-OH-D3 repressed IL-1β secretion and respiratory burst of both cells mostly in R-hens, but promoted monocyte phagocytosis, chemotaxis, and bacterial killing activity in Ad-hens in accompany with relieved hyperglycemia, hyperlipidemia, and systemic inflammation. Overnight cultures with leukocytes from R-hens confirmed the differential effects of 25-OH-D3 to rescue immune functions altered by glucose and/or palmitic acid exposure. Studies with specific inhibitors further manifested the operative mechanisms via glucolipotoxicity in a cell type- and function-dependent manner. The results concluded no predominant changes between R- vs. Ad-feed intake on leukocyte defense against pathogens despite some differential differences, but supplemental 25-OH-D3 exerts more pronounced effects in Ad-hens.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Irene Martínez de Toda ◽  
Carmen Vida ◽  
Luis Sanz San Miguel ◽  
Mónica De la Fuente

According to the oxidative-inflammatory theory of aging, there is a link between the function, the oxidative-inflammatory stress state of immune cells, and longevity. However, it is unknown which immune cell parameters can predict lifespan and if there would be any changes in this prediction, depending on the age of the subject. Therefore, a longitudinal study in mice was performed analysing immune function (chemotaxis of macrophages and lymphocytes, phagocytosis of macrophages, natural killer (NK) activity, and lymphoproliferation capacity), antioxidant (catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) activities as well as reduced glutathione (GSH) concentrations), oxidant (oxidized glutathione (GSSG), superoxide anion, and malondialdehyde (MDA) concentrations), and inflammation-related markers (basal release of IL-1β, IL-6, TNF-α, and IL-10) in peritoneal leukocytes from mice at the adult, mature, old, very old, and long-lived ages (40, 56, 72, 96, and 120±4 weeks of age, respectively). The results reveal that some of the investigated parameters are determinants of longevity at the adult age (lymphoproliferative capacity, lymphocyte chemotaxis, macrophage chemotaxis and phagocytosis, GPx activity, and GSH, MDA, IL-6, TNF-α, and IL-10 concentrations), and therefore, they could be proposed as markers of the rate of aging. However, other parameters are predictive of extreme longevity only at the very old age (NK activity, CAT and GR activities, and IL-6 and IL-1β concentrations), and as such, they could reflect some of the adaptive mechanisms underlying the achievement of high longevity. Nevertheless, although preliminary, the results of the present study provide a new perspective on the use of function, redox, and inflammatory parameters in immune cells as prognostic tools in aging research and represent a novel benchmark for future work aimed at prediction of lifespan.


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