scholarly journals Protein from Hevea brasiliensis “Hev b 13” latex attenuates systemic inflammatory response and lung lesions in rats with sepsis

2017 ◽  
Vol 78 (2) ◽  
pp. 271-280 ◽  
Author(s):  
L. A. Araújo ◽  
P. R. Melo-Reis ◽  
F. Mrue ◽  
C. M. Gomes ◽  
M. A. P. Oliveira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Hevea Brasiliensis ◽  
Rubber Tree ◽  
Cecal Ligation ◽  
Neutrophil Infiltration ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Lung Lesions ◽  
Male Wistar Rats ◽  
Anti Inflammatory

Abstract Sepsis induces a severe systemic inflammatory response that may result in multiple organ dysfunction and death. Studies using a protein derived from natural Hevea brasiliensis (rubber tree) latex, denominated Hev b 13, have demonstrated important anti-inflammatory effects, but no data have been published regarding its effects on sepsis. The aim of this study was to investigate the effects of Hev b 13 on the inflammatory response and lung lesions of septal rats. Male Wistar rats were submitted to cecal ligation and puncture (CLP), randomized into groups and treated with subcutaneously administered doses of 0.5/2.0/3.0 mg/Kg of Hev b 13. Next, animals were subdivided into three different points in time (1, 6 and 24 hours after treatments) for collection of blood samples and euthanasia accompanied by organ removal. Total and differential leukocyte counts, cytokine dosage and histological assessment were analyzed. Treatment with Hev b 13 resulted in a significant decline in total and differential leukocytes as well as suppression of TNF-α and IL-6 production, associated with the increase in IL-10 and IL-4 in plasma and lung tissue. Moreover, it reduced morphological and pathological changes found in the lungs, including neutrophil infiltration, edema and alveolar thickening. The present study concluded that Hev b 13 exerts anti-inflammatory effects and attenuates lung lesions in septal rats, showing potential for clinical application.

scholarly journals Synthetic leu-enkefalin analogue prevents activation of neutrophils induced by a bacterial component

2019 ◽  
Vol 47 (3) ◽  
pp. 228-235
Author(s):  
O. A. Grebenchikov ◽  
A. K. Shabanov ◽  
A. A. Kosov ◽  
Yu. V. Skripkin ◽  
A. G. Yavorovsky ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Human Neutrophils ◽  
Synthetic Analogue ◽  
Dependent Manner ◽  
Activated Neutrophils ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Background: Neutrophil activation is a  mandatory stage and a  sensitive marker of systemic inflammatory response. The development of this condition is associated with subsequent multiple organ failure which is the main indication for the patients stay in the intensive care unit. The search for drugs that could prevent the development of systemic inflammatory response and reduce mortality remains an urgent task of anesthesiology/resuscitation.Aim: To study the anti-inflammatory effect of dalargin, a synthetic analogue of lei-enkephalin, on human neutrophils in vitro.Materials and methods: The study was performed on blood neutrophils isolated from 5 healthy donors. A proportion of neutrophils were activated by 10 mkM formil-Met-Leu-Pro (fMLP) and 100 ng/mL lipopolysaccharide (LPS) with subsequent assessment of their activity by fluorescent antibodies to the degranulation markers CD11b and CD66b. Thereafter intact and activated neutrophils were treated with dalargin solution at concentrations of 50 and 100 mcg/mL.Results: Dalargin at 100 mcg/mL reduced the expression of CD11b molecules on the surface of intact neutrophils by 5.5-fold (p=0.008). On the contrary, LPS at a  dose of 100  ng/mL increased the expression of the same molecules by 46% (p=0.08). The addition of dalargin at 50 mcg/mL to LPS-activated neutrophils reduced the expression of CD11b molecules (p=0.016). The addition of dalargin at 50  mcg/mL to fMLP-activated neutrophils significantly (p=0.008) reduced the expression of CD11b molecules and reversed their expression virtually to the level of the control. The addition of dalargin at 100  mcg/mL to neutrophils activated by fMLP at 10 mkM reduced the expression of CD11b on their surface to a level below the control by 23% (p=0.08).Conclusion: Dalargin at the studied concentrations has an anti-inflammatory effect on both intact and pre-activated bacterial components of neutrophils, thus inhibiting the process of activation and degranulation in a dose-dependent manner. 

scholarly journals Dependence of the severity of the systemic inflammatory response on resistance to hypoxia in male Wistar rats

2019 ◽  
Vol Volume 12 ◽  
pp. 73-86 ◽  
Author(s):  
Dzhuliia Sh. Dzhalilova ◽  
Anna M Kosyreva ◽  
Mikhail E. Diatroptov ◽  
Elena A. Ponomarenko ◽  
Ivan S. Tsvetkov ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Wistar Rats ◽  
Systemic Inflammatory Response ◽  
Resistance To Hypoxia ◽  
Male Wistar Rats

Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome

2003 ◽  
Vol 31 (4) ◽  
pp. 1048-1052 ◽  
Author(s):  
Takeshi Motoyama ◽  
Kazufumi Okamoto ◽  
Ichirou Kukita ◽  
Masamichi Hamaguchi ◽  
Yoshihiro Kinoshita ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Oxidant Stress ◽  
Multiple Organ ◽  
Systemic Inflammatory Response

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 Sepsis, mitochondrial failure and multiple organ dysfunction

2014 ◽  
Vol 37 (2) ◽  
pp. 58 ◽  
Author(s):  
Josefina Duran-Bedolla ◽  
Marco A Montes de Oca-Sandoval ◽  
Vianey Saldaña-Navor ◽  
José A Villalobos-Silva ◽  
Maria Carmen Rodriguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Physiological State ◽  
Redox Balance ◽  
Multiple Organ ◽  
Reactive Species ◽  
Systemic Inflammatory Response ◽  
Antioxidant Systems ◽  
Multiple Organ Dysfunction

Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis. Principal findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure. In a physiological state, reactive species and antioxidant systems are in redox balance. The loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic inflammatory response. The loss of the redox balance, together with a systemic inflammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion: Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of effective therapies and better prognosis for patients with sepsis and organ dysfunction.

Article Commentary: Sepsis, Systemic Inflammatory Response, and Multiple Organ Dysfunction: The Mystery Continues

2012 ◽  
Vol 78 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Donald E. Fry
Keyword(s):  
Clinical Trials ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Invasive Infection ◽  
Multiple Organ Dysfunction ◽  
Human Sepsis ◽  
Critical Organ

Human sepsis is thought to be systemic inflammatory response syndrome (SIRS) that is activated by invasive infection. The multiple organ dysfunction syndrome (MODS) is the identified failure of critical organ function in patients that have sustained SIRS. Because SIRS and MODS are consequences of the excessive activation of inflammation, extensive research and numerous clinical trials have pursued treatments that would modify the inflammatory response. This presentation reviews the normal local mechanisms of inflammation and provides a theoretical framework for the transition of the inflammatory process to a systemic level. Clinical trials with biomodulators to block or inhibit inflammation have generally failed to improve the outcomes in patients with severe sepsis, septic shock, and MODS. The role of counter-inflammatory signaling and the newer concept of the cholinergic anti-inflammatory pathway are being investigated, and newer hypotheses are focusing upon the balancing of proinflammatory and counter-inflammatory mechanisms as important directions for newer therapies. It is concluded that failure to define novel and effective treatments reflects fundamental gaps in our understanding of inflammation and its regulation.

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