scholarly journals The role of neuronal NO synthase in the respiratory effects of the proinflammatory cytokine TNF-α

2021 ◽  
Vol 2 (2) ◽  
pp. 157-164
Author(s):  
Anna A. Klinnikova ◽  
Nina P. Aleksandrova
Keyword(s):  
Proinflammatory Cytokine ◽  
No Synthase ◽  
Respiratory Effects ◽  
Neuronal No Synthase ◽  
Tnf Α

scholarly journals Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits withPseudomonas aeruginosapneumonia

2009 ◽  
Vol 296 (2) ◽  
pp. L198-L209 ◽  
Author(s):  
Kiyoyasu Kurahashi ◽  
Teiji Sawa ◽  
Maria Ota ◽  
Osamu Kajikawa ◽  
Keelung Hong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Proinflammatory Cytokine ◽  
Systemic Infection ◽  
Dry Weight ◽  
Reticuloendothelial System ◽  
Bacterial Clearance ◽  
Blood Samples ◽  
Tnf Α ◽  
Inflammatory Modulation

Phagocytes of the reticuloendothelial system are important in clearing systemic infection; however, the role of the reticuloendothelial system in the response to localized infection is not well-documented. The major goals of this study were to investigate the roles of phagocytes in the reticuloendothelial system in terms of bacterial clearance and inflammatory modulation in sepsis caused by Pseudomonas pneumonia. Macrophages in liver and spleen were depleted by administering liposome encapsulated dichloromethylene diphosphonate (clodronate) intravenously 36 h before the instillation of Pseudomonas aeruginosa into the lungs of anesthetized rabbits. Blood samples were analyzed for bacteria and cytokine concentrations. Lung injury was assessed by the bidirectional flux of albumin and by wet-to-dry weight ratios. Blood pressure and cardiac outputs decreased more rapidly and bacteremia occurred earlier in the clodronate-treated rabbits compared with the nondepleted rabbits. Plasma TNF-α (1.08 ± 0.54 vs. 0.08 ± 0.02 ng/ml) and IL-8 (6.8 ± 1.5 vs. 0.0 ± 0.0 ng/ml) were higher in the depleted rabbits. The concentration of IL-10 in liver of the macrophage-depleted rabbits was significantly lower than in normal rabbits at 5 h. Treatment of macrophage-depleted rabbits with intravenous IL-10 reduced plasma proinflammatory cytokine concentrations and reduced the decline in blood pressure and cardiac output. These results show that macrophages in the reticuloendothelial system have critical roles in controlling systemic bacteremia and reducing systemic inflammation, thereby limiting the systemic effects of a severe pulmonary bacterial infection.

scholarly journals The Role of TNF-α as a Proinflammatory Cytokine in Pathological Processes

2019 ◽  
Vol 13 (1) ◽  
pp. 332-338
Author(s):  
Luciano B. Silva ◽  
Alexandrino P. dos Santos Neto ◽  
Sandra M.A.S. Maia ◽  
Carolina dos Santos Guimarães ◽  
Iliana L. Quidute ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Literature Review ◽  
Adaptive Immunity ◽  
Proinflammatory Cytokine ◽  
Antigen Presenting Cells ◽  
Tnf Α ◽  
Antigen Presenting

TNF-α is a member of the vast cytokine family being considered a proinflammatory substance produced many by macrophages and other cells belonging to the innate immunity, many of them classified as indeed Antigen Presenting Cells (APCs) involved in the complex chemotactic process of activation of the adaptive immunity. The aim of this work was to accomplish a literature review concerning the main pathologies that have TNF-α as a modulating agent in other to bring light to the main interactions present in the inflammation installed.

scholarly journals Blockade of neuronal nitric oxide synthase alters the baroreflex control of heart rate in the rabbit

1998 ◽  
Vol 274 (1) ◽  
pp. R181-R186 ◽  
Author(s):  
Hiroshi Murakami ◽  
Jun-Li Liu ◽  
Hirohito Yoneyama ◽  
Yasuhiro Nishida ◽  
Kenji Okada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
No Synthase ◽  
Baroreflex Control ◽  
Neuronal No Synthase ◽  
Significant Difference ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Oxide Synthase

In previous studies we used N G-nitro-l-arginine (l-NNA) to investigate the role of nitric oxide (NO) in baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA).l-NNA increased resting mean arterial pressure (MAP), decreased HR, and did not change or slightly decreased RSNA. These changes complicated the assessment of the central effects of NO on the baroreflex control of HR and RSNA. Therefore, in the present study the effects of the relatively selective neuronal NO synthase inhibitor 7-nitroindazole (7-NI) on the baroreflex control of HR and RSNA were investigated in rabbits. Intraperitoneal injection of 7-NI (50 mg/kg) had no effect on resting HR, MAP, or RSNA. 7-NI significantly reduced the lower plateau of the HR-MAP baroreflex curve from 140 ± 4 to 125 ± 4 and from 177 ± 10 to 120 ± 9 beats/min in conscious and anesthetized preparations, respectively ( P < 0.05). In contrast, there was no significant difference in the RSNA-MAP curves before and after 7-NI administration in conscious or anesthetized preparations. These data suggest that blockade of neuronal NO synthase influences baroreflex control of HR but not of RSNA in rabbits.

The role of prostaglandins in the realization of respiratory effects of TNF-α in case of hypoxia

2021 ◽  
Author(s):  
G.А. Danilova ◽  
A.A. Klinnikova ◽  
N.P. Aleksandrova
Keyword(s):  
Ventilatory Response ◽  
Minute Volume ◽  
Respiratory Effects ◽  
Cox Inhibitor ◽  
Tnf Α ◽  
Before And After ◽  
Factor Α ◽  
And Control ◽  
Rebreathing Method

At the present time very little is known about interactions between systemic inflammation and control of respiration. The aim of this study was to compare the respiratory effects of the main inflammatory cytokine TNF - α before and after pretreatment with diclofenac, a nonspecific cyclooxygenase (COX) inhibitor. In experiments on anesthetized, tracheostomized rats, pneumotachometry method was used to measure peak airflow and respiratory rate. The ventilatory response to hypoxia was investigated by the rebreathing method. It is shown that an increase in the systemic level of TNF – α causes a significant increase in the minute volume of respiration, tidal volume, the average speed of the inspiratory flow. In contrast the slope of the hypoxic ventilatory response decreased after administration of TNF-α. Diclofenac pretreatment eliminated these respiratory effects of TNF - α. The data indicate that the ability of TNF - α to enhance basal ventilation and to reduce the ventilatory hypoxic response is mediated by the cyclooxygenase pathway. Key words: tumor necrosis factor – α, hypoxia, prostaglandins, peripheral chemoreception, respiration.

scholarly journals MiR-26a inhibits the inflammatory response of microglia by targeting HMGA2 in intracerebral hemorrhage

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052092961 ◽  
Author(s):  
Jun Jin ◽  
Feng Zhou ◽  
Jie Zhu ◽  
Weixian Zeng ◽  
Yong Liu
Keyword(s):  
Inflammatory Response ◽  
Intracerebral Hemorrhage ◽  
Test Performance ◽  
Proinflammatory Cytokine ◽  
Potential Role ◽  
Microglial Cells ◽  
Secondary Brain Injury ◽  
Rotarod Test ◽  
Tnf Α

Objective Intracerebral hemorrhage (ICH) is a common cerebrovascular disease with high mortality and poor prognosis. Therefore, the biological function and underlying molecular mechanism of miR-26a in inflammatory injury following ICH was investigated. Methods The potential role of miR-26a was investigated in lipopolysaccharide (LPS)-treated microglial cells by quantitative real-time PCR. To explore the potential role of HMGA2 in the miR-26a-regulated inflammatory response, LPS-induced microglial cells were cotransfected with an miR-26a mimic and pcDNA-HMGA2. Then, lentivirus-mediated overexpression of an miR-26a mimic in mouse microglial cells was performed, and the effects of miR-26a treatment on IL-6, IL-1β, and TNF-α expression in the mouse brain, neurological behavior, and rotarod test performance of mice after ICH were observed. Results MiR-26a was significantly downregulated in LPS-treated microglia and ICH mouse models. MiR-26a markedly reduced IL-6, IL-1β, and TNF-α expression in LPS-treated microglial cells. Furthermore, HMGA2 was verified as a direct target of miR-26a. In vivo, miR-26a overexpression in mouse microglial cells significantly suppressed proinflammatory cytokine expression in mouse brains and markedly improved the neurological behavior and rotarod test performance of mice after ICH. Conclusion MiR-26a remarkably inhibited proinflammatory cytokine release by targeting HMGA2, indicating that miR-26a could protect against secondary brain injury following ICH.

Role of Hsp90- and Hsp70-chaperones in regulation of neuronal NO-synthase ubiquitination and proteasomal degradation

Nitric Oxide ◽  
2012 ◽  
Vol 27 ◽  
pp. S5-S6 ◽  
Author(s):  
Yoichi Osawa ◽  
Hwei-Ming Peng ◽  
Kelly M. Clapp ◽  
Miranda Lau ◽  
Yoshihiro Morishima
Keyword(s):  
Proteasomal Degradation ◽  
No Synthase ◽  
Neuronal No Synthase

scholarly journals MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) CONCENTRATIONS IN CARRAGEENAN-INDUCED GASTROENTEROCOLITIS

2017 ◽  
pp. 64-67
Author(s):  
A. S. Tkachenko ◽  
O. A. Nakonechnaya ◽  
T. V. Gorbach ◽  
A. I. Onischenko ◽  
T. N. Chubukova
Keyword(s):  
Oxidative Stress ◽  
Blood Serum ◽  
Proinflammatory Cytokine ◽  
Food Additive ◽  
Control Group ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Tnf Α

Aim: to study MCP-1 concentrations in chronic carrageenan-induced gastroenterocolitis and the role of this protein in the development and progression of the disease. Material and methods . Thirty female WAG rats were divided into three groups (each group consisted of ten individuals): 1) introduction of 1% carrageenan solution for 14 days; 2) introduction of 1 % carrageenan solution for 28 days; 3) the control group. The animals of the first two groups were developing gastroenterocolitis. The MCP-1 and TNF-α concentrations were measured in the blood serum by ELISA. Results. Development of carrageenan-induced gastroenterocolitis was accompanied by increased levels of both MCP-1 and TNF-α in the blood serum. The level of the increase of both the parameters was more evident after four-week oral taking of the food additive carrageenan. Conclusion. The increased MCP-1 production in carrageenan-induced gastroenterocolitis may be directly due to the toxic effect of carrageenan on the macrophages of the gastrointestinal tract, development of oxidative stress, as well as due to the stimulating effect of the proinflammatory cytokine TNF-α.

Role of cytokines in caerulein-induced acute pancreatilis of IL-1, IL-6 and TNF-α knockoul mice

2001 ◽  
Vol 120 (5) ◽  
pp. A541-A541
Author(s):  
K KITAMURA ◽  
J NIIKAWA ◽  
T IMAMURA ◽  
A TAKAHASHI ◽  
A IKEGAMI ◽  
...  
Keyword(s):  
Tnf Α
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