scholarly journals Injury-induced inflammatory signaling and hematopoiesis in Drosophila

2021 ◽  
Author(s):  
Cory J Evans ◽  
Ting Liu ◽  
Juliet R Girard ◽  
Utpal Banerjee
Keyword(s):  
Inflammatory Response ◽  
Blood Cells ◽  
The Body ◽  
Hematopoietic Organ ◽  
Injury Site ◽  
Jnk Signaling ◽  
Jun Kinase ◽  
Stat Signaling ◽  
Blood Cell Type ◽  
Dependent Signal

Inflammatory response in Drosophila to sterile (axenic) injury in embryos and adults has received some attention in recent years, and most concentrate on the events at the injury site. Here we focus on the effect sterile injury has on the hematopoietic organ, the lymph gland, and the circulating blood cells in the larva, the developmental stage at which major events of hematopoiesis are evident. In mammals, injury activates Toll-like receptor (TLR)/NFκB signaling in macrophages, which then express and secrete secondary, pro-inflammatory cytokines. In Drosophila larvae, distal puncture injury of the body wall epidermis causes a rapid activation of Toll and Jun kinase (JNK) signaling throughout the hematopoietic system and the differentiation of a unique blood cell type, the lamellocyte. Furthermore, we find that Toll and JNK signaling are coupled in their activation. Secondary to this Toll/JNK response, a cytokine, Upd3, is induced as a Toll pathway transcriptional target, which then promotes JAK/STAT signaling within the blood cells. Toll and JAK/STAT signaling are required for the emergence of the injury-induced lamellocytes. This is akin to the derivation of specialized macrophages in mammalian systems. Upstream, at the injury site, a Duox- and peroxide-dependent signal causes the activation of the proteases Grass and SPE needed for the activation of the Toll-ligand Spz, but microbial sensors or the proteases most closely associated with them during septic injury are not involved in the axenic inflammatory response.

scholarly journals Mathematical Modeling and Numerical Simulation of Atherosclerosis Based on a Novel Surgeon’s View

2021 ◽  
Author(s):  
Meisam Soleimani ◽  
Axel Haverich ◽  
Peter Wriggers
Keyword(s):  
Mathematical Modeling ◽  
Inflammatory Response ◽  
Phase Field ◽  
Mechanical Response ◽  
Type Equation ◽  
The Body ◽  
Vasa Vasorum ◽  
Diffusion Reaction ◽  
Dust Particles ◽  
Driving Mechanism

AbstractThis paper deals with the mathematical modeling of atherosclerosis based on a novel hypothesis proposed by a surgeon, Prof. Dr. Axel Haverich (Circulation 135(3):205–207, 2017). Atherosclerosis is referred as the thickening of the artery walls. Currently, there are two schools of thoughts for explaining the root of such phenomenon: thickening due to substance deposition and thickening as a result of inflammatory overgrowth. The hypothesis favored here is the second paradigm stating that the atherosclerosis is nothing else than the inflammatory response of of the wall tissues as a result of disruption in wall nourishment. It is known that a network of capillaries called vasa vasorum (VV) accounts for the nourishment of the wall in addition to the natural diffusion of nutrient from the blood passing through the lumen. Disruption of nutrient flow to the wall tissues may take place due to the occlusion of vasa vasorums with viruses, bacteria and very fine dust particles such as air pollutants referred to as PM 2.5. They can enter the body through the respiratory system at the first place and then reach the circulatory system. Hence in the new hypothesis, the root of atherosclerotic vessel is perceived as the malfunction of microvessels that nourish the vessel. A large number of clinical observation support this hypothesis. Recently and highly related to this work, and after the COVID-19 pandemic, one of the most prevalent disease in the lungs are attributed to the atherosclerotic pulmonary arteries, see Boyle and Haverich (Eur J Cardio Thorac Surg 58(6):1109–1110, 2020). In this work, a general framework is developed based on a multiphysics mathematical model to capture the wall deformation, nutrient availability and the inflammatory response. For the mechanical response an anisotropic constitutive relation is invoked in order to account for the presence of collagen fibers in the artery wall. A diffusion–reaction equation governs the transport of the nutrient within the wall. The inflammation (overgrowth) is described using a phase-field type equation with a double well potential which captures a sharp interface between two regions of the tissues, namely the healthy and the overgrowing part. The kinematics of the growth is treated by classical multiplicative decomposition of the gradient deformation. The inflammation is represented by means of a phase-field variable. A novel driving mechanism for the phase field is proposed for modeling the progression of the pathology. The model is 3D and fully based on the continuum description of the problem. The numerical implementation is carried out using FEM. Predictions of the model are compared with the clinical observations. The versatility and applicability of the model and the numerical tool allow.

Clock gene-independent daily regulation of haemoglobin oxidation in red blood cells

2021 ◽  
Author(s):  
Andrew D. Beale ◽  
Priya Crosby ◽  
Utham K. Valekunja ◽  
Rachel S. Edgar ◽  
Johanna E. Chesham ◽  
...  
Keyword(s):  
Circadian Rhythms ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Human Subjects ◽  
Developmental Regulation ◽  
Physiological Role ◽  
Cell Types ◽  
The Body

AbstractCellular circadian rhythms confer daily temporal organisation upon behaviour and physiology that is fundamental to human health and disease. Rhythms are present in red blood cells (RBCs), the most abundant cell type in the body. Being naturally anucleate, RBC circadian rhythms share key elements of post-translational, but not transcriptional, regulation with other cell types. The physiological function and developmental regulation of RBC circadian rhythms is poorly understood, however, partly due to the small number of appropriate techniques available. Here, we extend the RBC circadian toolkit with a novel biochemical assay for haemoglobin oxidation status, termed “Bloody Blotting”. Our approach relies on a redox-sensitive covalent haem-haemoglobin linkage that forms during cell lysis. Formation of this linkage exhibits daily rhythms in vitro, which are unaffected by mutations that affect the timing of circadian rhythms in nucleated cells. In vivo, haemoglobin oxidation rhythms demonstrate daily variation in the oxygen-carrying and nitrite reductase capacity of the blood, and are seen in human subjects under controlled laboratory conditions as well as in freely-behaving humans. These results extend our molecular understanding of RBC circadian rhythms and suggest they serve an important physiological role in gas transport.

EFEKTIVITAS PEMBERIAN INFUSED WATER KURMA TERHADAP PENINGKATAN KADAR HEMOGLOBIN REMAJA PUTRI KEBIDANAN POLTEKKES MEDAN TAHUN 2020

2021 ◽  
Vol 2 (1) ◽  
pp. 64-69
Author(s):  
HIJRA HIDAYANA ◽  
Suswati Suswati
Keyword(s):  
Red Blood Cells ◽  
Adolescent Girls ◽  
Blood Cells ◽  
The Body ◽  
Rank Test ◽  
Plain Water ◽  
P Value ◽  
Signed Rank ◽  
Wilcoxon Signed Rank Test ◽  
Signed Rank Test

Hemoglobin is the red pigment-protein contained in red blood cells. The function of hemoglobin is to transport oxygen from the lungs and in the bloodstream to be carried to the tissues. Hemoglobin can increase by increasing the intake of iron in the body. One way to increase hemoglobin can be done by giving method Infused Water Dates. Infused water is a drink consisting of plain water with fresh fruit added and soaking or settling together for a certain time. The making of infused water is carried out by soaking for a period of 0 to 12 hours, so that the infused water becomes a liquid medium that carries more nutrients than ordinary water and will be more easily absorbed by cells and distributed throughout the body (Sidauruk, 2018 ). In several studies, it is stated that dates can increase hemoglobin levels in the blood. Where dates contain iron, vitamin A, vitamin C, protein to form red blood cells. With the method, Infused Water the date palm water becomes alkaline so that it can accelerate the absorption process in the body. The purpose of this study was to determine the effectiveness of dates infused water provision to increase hemoglobin levels of midwifery adolescent girls at Medan Health Polytechnic in 2020. This research was quasi-experimental study using the One Group Pretest-Posttest Without Control Design approach. The sample in this study were 20 respondents of midwifery adolescent girls from Medan Health Polytechnic, using the technique of purposive sampling. The statistical test used wa the Wilcoxon Signed Rank Test because the data was not normal. The results of the Wilcoxon Signed Rank Test obtained the value of P-Value = 0.001. So it can be concluded that the date infused water  is effective in increasing hemoglobin levels of midwifery adolescent girls at Medan Health Polytechnic in 2020.   Keywords: Dates Infused Water, Increased Hemoglobin Levels, Girls Adolescent

scholarly journals Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Yan Chen ◽  
Yan-Jun Wang ◽  
Ying Zhao ◽  
Jin-Cheng Wang
Keyword(s):  
Diabetes Mellitus ◽  
Inflammatory Response ◽  
Mesangial Cells ◽  
Binding Protein ◽  
The Body ◽  
Mrna Levels ◽  
Diabetic Mice ◽  
Response Element ◽  
Tnf Α ◽  
Element Binding Protein

Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix–loop–helix leucine zipper transcription factor that primarily mediates glucose homeostasis in the body. The present study investigated the role of ChREBP in the pathogenesis of DN. The expression of ChREBP was detected in patients with type 2 diabetes mellitus (T2DM), diabetic mice, and mesangial cells. ELISA was used to measure cytokine production in mesangial cells. Flow cytometry analysis was performed to detect the apoptosis of mesangial cells in the presence of high glucose. The expression levels of ChREBP and several cytokines (TNF-α, IL-1β, and IL-6) were up-regulated in T2DM patients. The mRNA and protein levels of ChREBP were also significantly elevated in the kidneys of diabetic mice. Moreover, glucose treatment promoted mRNA levels of TNF-α, IL-1β, and IL-6 in mesangial cells. Glucose stimulation induced significant apoptosis of SV40 MES 13 cells. In addition, transfection with ChREBP siRNA significantly inhibited ChREBP expression. Consequently, the inflammatory responses and apoptosis were inhibited in SV40 MES 13 cells. These results demonstrated that ChREBP could mediate the inflammatory response and apoptosis of mesangial cells, suggesting that ChREBP may be involved in the pathogenesis of DN.

scholarly journals Systemic inflammatory response syndrome and multiple-organ damage / dysfunction in complicated canine babesiosis

2001 ◽  
Vol 72 (3) ◽  
Author(s):  
C. Welzl ◽  
A.L. Leisewitz ◽  
L.S. Jacobson ◽  
T. Vaughan-Scott ◽  
E. Myburgh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Renal Involvement ◽  
Organ Damage ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
The Body ◽  
Increased Risk

This study was designed to document the systemic inflammatory response syndrome (SIRS) and multiple-organ dysfunction syndrome (MODS) in dogs with complicated babesiosis, and to assess their impact on outcome. Ninety-one cases were evaluated retro-spectively for SIRS and 56 for MODS. The liver, kidneys, lungs, central nervous system and musculature were assessed. Eighty-seven percent of cases were SIRS-positive. Fifty-two percent of the cases assessed for organ damage had single-organ damage and 48 % had MODS. Outcome was not significantly affected by either SIRS or MODS, but involvement of specific organs had a profound effect. Central nervous system involvement resulted in a 57 times greater chance of death and renal involvement in a 5-fold increased risk compared to all other complications. Lung involvement could not be statistically evaluated owing to co-linearity with other organs, but was associated with high mortality. Liver and muscle damage were common, but did not significantly affect outcome. There are manysimilarities between the observations in this study and previous human and animal studies in related fields, lending additional support to the body of evidence for shared underlying pathophysiological mechanisms in systemic inflammatory states.

scholarly journals A parasitoid wasp of Drosophila employs preemptive and reactive strategies to deplete its host’s blood cells

2021 ◽  
Author(s):  
Johnny R. Ramroop ◽  
Mary Ellen Heavner ◽  
Zubaidul H. Razzak ◽  
Shubha Govind
Keyword(s):  
Extracellular Vesicles ◽  
Cellular Immunity ◽  
Blood Cells ◽  
Insect Pests ◽  
Lymph Gland ◽  
Parasite Development ◽  
Parasitoid Wasps ◽  
Parasitic Wasps ◽  
Hematopoietic Organ ◽  
Leptopilina Heterotoma

AbstractThe wasps Leptopilina heterotoma parasitize and ingest their Drosophila hosts. They produce extracellular vesicles (EVs) in the venom that are packed with proteins, some of which perform immune suppressive functions. EV interactions with blood cells of host larvae are linked to hematopoietic depletion, immune suppression, and parasite success. But how EVs disperse within the host, enter and kill hematopoietic cells are not well understood. Using an antibody marker for L. heterotoma EVs, we show that these parasite-derived structures are readily distributed within the hosts’ hemolymphatic system. EVs converge around the tightly clustered cells of the posterior signaling center (PSC) of the larval lymph gland, a small hematopoietic organ in Drosophila. The PSC serves as a source of developmental signals in naïve animals. In wasp-infected animals, the PSC directs the differentiation of lymph gland progenitors into lamellocytes. These lamellocytes are needed to encapsulate the wasp egg and block parasite development. We found that L. heterotoma infection disassembles the PSC and PSC cells disperse into the disintegrating lymph gland lobes. Genetically manipulated PSC-less lymph glands remain non-responsive and largely intact in the face of L. heterotoma infection. We also show that the larval lymph gland progenitors use the endocytic machinery to internalize EVs. Once inside, L. heterotoma EVs damage the Rab7- and LAMP1-positive late endocytic and phagolysosomal compartments. Rab5 maintains hematopoietic and immune quiescence as Rab5 knockdown results in hematopoietic over-proliferation and ectopic lamellocyte differentiation. Thus, both aspects of anti-parasite immunity, i.e., (a) phagocytosis of the wasp’s immune-suppressive EVs, and (b) progenitor differentiation for wasp egg encapsulation reside in the lymph gland. These results help explain why the lymph gland is specifically and precisely targeted for destruction. The parasite’s simultaneous and multipronged approach to block cellular immunity not only eliminates blood cells, but also tactically blocks the genetic programming needed for supplementary hematopoietic differentiation necessary for host success. In addition to its known functions in hematopoiesis, our results highlight a previously unrecognized phagocytic role of the lymph gland in cellular immunity. EV-mediated virulence strategies described for L. heterotoma are likely to be shared by other parasitoid wasps; their understanding can improve the design and development of novel therapeutics and biopesticides as well as help protect biodiversity.Author summaryParasitoid wasps serve as biological control agents of agricultural insect pests and are worthy of study. Many parasitic wasps develop inside their hosts to emerge as free-living adults. To overcome the resistance of their hosts, parasitic wasps use varied and ingenious strategies such as mimicry, evasion, bioactive venom, virus-like particles, viruses, and extracellular vesicles (EVs). We describe the effects of a unique class of EVs containing virulence proteins and produced in the venom of wasps that parasitize fruit flies of Drosophila species. EVs from Leptopilina heterotoma are widely distributed throughout the Drosophila hosts’ circulatory system after infection. They enter and kill macrophages by destroying the very same subcellular machinery that facilitates their uptake. An important protein in this process, Rab5, is needed to maintain the identity of the macrophage; when Rab5 function is reduced, macrophages turn into a different cell type called lamellocytes. Activities in the EVs can eliminate lamellocytes as well. EVs also interfere with the hosts’ genetic program that promotes lamellocyte differentiation needed to block parasite development. Thus, wasps combine specific preemptive and reactive strategies to deplete their hosts of the very cells that would otherwise sequester and kill them. These findings have applied value in agricultural pest control and medical therapeutics.

scholarly journals BIOLOGICAL EFFECTS OF SILICON OXIDE NANOPARTICLES ON BROILER CHICKEN

2020 ◽  
Vol 5 (2) ◽  
pp. 63-71
Author(s):  
Vladimir Nikulin ◽  
Aleksandra Mustafina
Keyword(s):  
Red Blood Cells ◽  
Total Protein ◽  
Blood Cells ◽  
Broiler Chickens ◽  
Broiler Chicken ◽  
Silicon Oxide ◽  
The Body ◽  
Control Group ◽  
The Third ◽  
Experimental Group

The aim of the study is to increase the productive qualities of broiler chickens by including ultrafine silicon oxide into main diet. During the experiment, the biological effect of ultrafine silicon oxide on broiler chickens was estab-lished. Use of ultrafine SiO2 particles for poultry feeding contributed to an increase in the number of red blood cells and content of total protein and albumins. By the end of the experiment, the number of red blood cells in birds in-creased by 17.43% (P≤0.001) – in the blood of birds of the first experimental group, 16.51% (P≤0.01) – the second one, 20.80% (P≤0.001) – the third experimental and 21.71% (P≤0.001) – the fourth experimental group, compared with the indicator of the control group. The amount of total protein in blood serum of chickens of the first and the second experimental groups increased by 1.36-1.39 %, in the third and fourth ones there was a significant (P≤0.05) increase by 5.45 and 3.05%, respectively. The blood glucose content of chickens in the experimental groups is higher by 8.04-23.65% compared to this indicator with ones in the control group. During the experiment feed con-sumption per 1 kg gain of live weight decreased: in the first experimental group by 3.00 % in the second by – 0.50 %, the third – 6.00 % the fourth– by 4.50 %, compared to this with the control group. The chicken’s vibrancy of the first the experimental group was higher by 4.77 %, the second – by 6.20 %, the third – by 19.25 % and the fourth– by 11.59% than in the control one. Consequently, when converting the feed energy into the body energy of a broiler chicken, the energy conversion coefficient of the experimental group of poultry is higher than that of the control one by 7.16-21.76 %. Thus, the most optimal dose for further research was determined.

scholarly journals The Effects of Combined Therapy With Metformin and Hydroxypropyl-β-Cyclodextrin in a Mouse Model of Niemann-Pick Disease Type C1

2022 ◽  
Vol 12 ◽  
Author(s):  
Jiang Du ◽  
Xinlei Liu ◽  
Yan Zhang ◽  
Xiaojing Han ◽  
Chunya Ma ◽  
...  
Keyword(s):  
Body Weight ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Survival Time ◽  
Free Cholesterol ◽  
Disease Type ◽  
The Body ◽  
Niemann Pick Disease ◽  
Niemann Pick ◽  
Pick Disease

Niemann–Pick disease type C1 (NPC1) is a neurodegenerative disorder characterized by lysosomal storage of free cholesterol. 2-Hydroxypropyl-β-cyclodextrin (HPβCD) is a cyclic oligosaccharide derivative that is being developed to treat NPC1. Recently, metformin was reported to be beneficial in various neurodegenerative diseases, such as Alzheimer’s and Huntington’s diseases. In this study, we examined the effects of combined treatment with HPβCD and metformin on Npc1−/− mice. Unfortunately, body weight and survival rates showed that cotreatment with metformin did not extend survival time and increase the body weight of HPβCD-treated Npc1−/− mice. However, cotreatment with metformin reduced inflammatory response and inhibited the proinflammatory cytokine release in the brain, liver and spleen of HPβCD-treated Npc1−/− mice. Furthermore, metformin did not reduce the free cholesterol levels in Npc1−/− brain tissue or fibroblasts. In conclusion, our results demonstrate that metformin does not show beneficial effects on body weight or survival time but reduced the inflammatory response in a mouse model of NPC1 when combined with HPβCD.

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