scholarly journals Different experimental multiple trauma models induce comparable inflammation and organ injury

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Borna Relja ◽  
Bing Yang ◽  
Katrin Bundkirchen ◽  
Baolin Xu ◽  
Kernt Köhler ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Multiple Trauma ◽  
Inflammatory Cells ◽  
Organ Damage ◽  
Organ Injury ◽  
Local Inflammatory Response ◽  
Healthy Control ◽  
Post Traumatic ◽  
Tissue Trauma ◽  
Trauma Group

AbstractMultiple injuries appear to be a decisive factor for experimental polytrauma. Therefore, our aim was to compare the inflammatory response and organ damage of five different monotrauma with three multiple trauma models. For this, mice were randomly assigned to 10 groups: Healthy control (Ctrl), Sham, hemorrhagic shock (HS), thoracic trauma (TxT), osteotomy with external fixation (Fx), bilateral soft tissue trauma (bsTT) or laparotomy (Lap); polytrauma I (PT I, TxT + HS + Fx), PT II (TxT + HS + Fx + Lap) and one multi-trauma group (MT, TxT + HS + bsTT + Lap). The inflammatory response and organ damage were quantified at 6 h by analyses of IL-6, IL-1β, IL-10, CXCL1, SAA1, HMGB1 and organ injury. Systemic IL-6 increased in all mono and multiple trauma groups, while CXCL1 increased only in HS, PT I, PT II and MT vs. control. Local inflammatory response was most prominent in HS, PT I, PT II and MT in the liver. Infiltration of inflammatory cells into lung and liver was significant in all multiple trauma groups vs. controls. Hepatic and pulmonary injury was prominent in HS, PT I, PT II and MT groups. These experimental multiple trauma models closely mimic the early post-traumatic inflammatory response in human. Though, the choice of read-out parameters is very important for therapeutic immune modulatory approaches.

scholarly journals Proinflammatory Role of Angiotensin II in the Aorta of Normotensive Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Rariane Silva de Lima ◽  
Juliane Cristina de Souza Silva ◽  
Cintia Taniguti Lima ◽  
Leandro Ezequiel de Souza ◽  
Maikon Barbosa da Silva ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Control Group ◽  
Positive Staining ◽  
Perivascular Adipose Tissue ◽  
Local Inflammatory Response ◽  
Applied Dose ◽  
And Migration

Angiotensin II plays important functions in cardiovascular system mediating actions leading to inflammatory responses such as activation of VSMC in order to produce ROS, inflammatory cytokines, chemokines, and adhesion molecules. Changes in angiotensin II production could stimulate the recruitment and activation of myeloid cells initiating local inflammatory response without effect on BP. We aimed to verify if angiotensin II induces an inflammatory response in the aorta and if it correlates with variations in BP. C57Bl/6 mice treated with saline solution (0.9%, control group) or angiotensin II (30ng/kg, Ang II group) were used. BP and HR levels were measured. Immunohistochemistry for IL1-β, TGF-β, iNOS, CD45, andα-actin was performed in the aorta. BP and HR do not change. A biphasic response was observed both for IL1-βand TGF-βexpression and also for the presence of CD45 positive cells, with an acute increase (between 30 and 60 minutes) and a second increase, between 24 and 48 hours. Positive staining for iNOS increased in the earlier period (30 minutes) in perivascular adipose tissue and in a longer period (48 hours) in tunica adventitia. Immunoblotting toα-actin showed no alterations, suggesting that the applied dose of angiotensin II does not alter the aortic VSMCs phenotype. The results suggest that angiotensin II, even at doses that do not alter BP, induces the expression of inflammatory markers and migration of inflammatory cells into the aorta of normotensive mice. Thus, angiotensin II may increase the propensity to develop a cardiovascular injury, even in normotensive individuals.

scholarly journals Effect of Lipopolysaccharides (LPS) and Lipoteichoic acid (LTA) on the Inflammatory Response in Rumen Epithelial Cells (REC) and the Impact of LPS on Claw Explants

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 2058
Author(s):  
Nicole Reisinger ◽  
Dominik Wendner ◽  
Nora Schauerhuber ◽  
Elisabeth Mayer
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Structural Integrity ◽  
Animal Health ◽  
Lipoteichoic Acid ◽  
Local Inflammatory Response ◽  
Tissue Integrity ◽  
Separation Force ◽  
The Impact ◽  
Rumen Epithelial Cells

Endotoxins play a crucial role in ruminant health due to their deleterious effects on animal health. The study aimed to evaluate whether LPS and LTA can induce an inflammatory response in rumen epithelial cells. For this purpose, epithelial cells isolated from rumen tissue (RECs) were stimulated with LPS and LTA for 1, 2, 4, and 24 h. Thereafter, the expression of selected genes of the LPS and LTA pathway and inflammatory response were evaluated. Furthermore, it was assessed whether LPS affects inflammatory response and structural integrity of claw explants. Therefore, claw explants were incubated with LPS for 4 h to assess the expression of selected genes and for 24 h to evaluate tissue integrity via separation force. LPS strongly affected the expression of genes related to inflammation (NFkB, TNF-α, IL1B, IL6, CXCL8, MMP9) in RECs. LTA induced a delayed and weaker inflammatory response than LPS. In claw explants, LPS affected tissue integrity, as there was a concentration-dependent decrease of separation force. Incubation time had a strong effect on inflammatory genes in claw explants. Our data suggest that endotoxins can induce a local inflammatory response in the rumen epithelium. Furthermore, translocation of LPS might negatively impact claw health.

scholarly journals DECRYPT trial: study protocol for a phase II randomised controlled trial of cognitive therapy for post-traumatic stress disorder (PTSD) in youth exposed to multiple traumatic stressors

BMJ Open ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. e047600
Author(s):  
Leila Allen ◽  
Polly-Anna Ashford ◽  
Ella Beeson ◽  
Sarah Byford ◽  
Jessica Chow ◽  
...  
Keyword(s):  
Young People ◽  
Cognitive Therapy ◽  
Multiple Trauma ◽  
Traumatic Stress ◽  
Controlled Trial ◽  
Post Traumatic Stress ◽  
Children And Young People ◽  
Post Traumatic ◽  
Randomised Controlled ◽  
Post Randomisation

BackgroundPost-traumatic stress disorder (PTSD) is a distressing and disabling condition that affects significant numbers of children and adolescents. Youth exposed to multiple traumas (eg, abuse, domestic violence) are at particular risk of developing PTSD. Cognitive therapy for PTSD (CT-PTSD), derived from adult work, is a theoretically informed, disorder-specific form of trauma-focused cognitive–behavioural therapy. While efficacious for child and adolescent single-event trauma samples, its effectiveness in routine settings with more complex, multiple trauma-exposed youth has not been established. The Delivery of Cognitive Therapy for Young People after Trauma randomised controlled trial (RCT) examines the effectiveness of CT-PTSD for treating PTSD following multiple trauma exposure in children and young people in comparison with treatment as usual (TAU).Methods/designThis protocol describes a two-arm, patient-level, single blind, superiority RCT comparing CT-PTSD (n=60) with TAU (n=60) in children and young people aged 8–17 years with a diagnosis of PTSD following multiple trauma exposure. The primary outcome is PTSD severity assessed using the Children’s Revised Impact of Event Scale (8-item version) at post-treatment (ie, approximately 5 months post-randomisation). Secondary outcomes include structured interview assessment for PTSD, complex PTSD symptoms, depression and anxiety, overall functioning and parent-rated mental health. Mid-treatment and 11-month and 29-month post-randomisation assessments will also be completed. Process–outcome evaluation will consider which mechanisms underpin or moderate recovery. Qualitative interviews with the young people, their families and their therapists will be undertaken. Cost-effectiveness of CT-PTSD relative to TAU will be also be assessed.Ethics and disseminationThis trial protocol has been approved by a UK Health Research Authority Research Ethics Committee (East of England–Cambridge South, 16/EE/0233). Findings will be disseminated broadly via peer-reviewed empirical journal articles, conference presentations and clinical workshops.Trial registrationISRCTN12077707. Registered 24 October 2016 (http://www.isrctn.com/ISRCTN12077707). Trial recruitment commenced on 1 February 2017. It is anticipated that recruitment will continue until June 2021, with 11-month assessments being concluded in May 2022.

Localized pancreatic NF-κB activation and inflammatory response in taurocholate-induced pancreatitis

2001 ◽  
Vol 280 (6) ◽  
pp. G1197-G1208 ◽  
Author(s):  
Eva Vaquero ◽  
Ilya Gukovsky ◽  
Vjekoslav Zaninovic ◽  
Anna S. Gukovskaya ◽  
Stephen J. Pandol
Keyword(s):  
Transcription Factor ◽  
Inflammatory Response ◽  
Pancreatic Head ◽  
Pancreatic Injury ◽  
Nuclear Factor Κb ◽  
Saline Infusion ◽  
Activator Protein 1 ◽  
Local Inflammatory Response ◽  
Monocyte Chemoattractant Protein 1 ◽  
Factor Α

Transcription factor nuclear factor-κB (NF-κB) is activated in cerulein pancreatitis and mediates cytokine expression. The role of transcription factor activation in other models of pancreatitis has not been established. Here we report upregulation of NF-κB and inflammatory molecules, and their correlation with local pancreatic injury, in a model of severe pancreatitis. Rats received intraductal infusion of taurocholate or saline, and the pancreatic head and tail were analyzed separately. NF-κB and activator protein-1 (AP-1) activation were assessed by gel shift assay, and mRNA expression of interleukin-6, tumor necrosis factor-α, KC, monocyte chemoattractant protein-1, and inducible nitric oxide synthase was assessed by semiquantitative RT-PCR. Morphological damage and trypsin activation were much greater in the pancreatic head than tail, in parallel with a stronger activation of NF-κB and cytokine mRNA. Saline infusion mildly affected these parameters. AP-1 was strongly activated in both pancreatic segments after either taurocholate or saline infusion. NF-κB inhibition with N-acetylcysteine ameliorated the local inflammatory response. Correlation between localized NF-κB activation, cytokine upregulation, and tissue damage suggests a key role for NF-κB in the development of the inflammatory response of acute pancreatitis.

scholarly journals Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Shi ◽  
Zhirong Zhang ◽  
Danli Cai ◽  
Jing Kuang ◽  
Shuifang Jin ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Animal Model ◽  
Inflammatory Response ◽  
Inflammatory Cell ◽  
Pulmonary Thromboembolism ◽  
Thrombus Formation ◽  
Inflammatory Cells ◽  
Hemodynamic Instability ◽  
Synergistic Action ◽  
Determining Factor

Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

Post-traumatic inflammatory response: perhaps a succession of phases with a nutritional purpose

2004 ◽  
Vol 63 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Maria-Angeles Aller ◽  
Jorge-Luis Arias ◽  
Jaime Arias
Keyword(s):  
Inflammatory Response ◽  
Post Traumatic

Use of Vicryl (Polyglactin 910) Mesh to Limit Epidural Scar Formation after Laminectomy

Neurosurgery ◽  
1990 ◽  
Vol 26 (4) ◽  
pp. 649-654 ◽  
Author(s):  
Charles E. Nussbaum ◽  
Joseph V. McDonald ◽  
Raymond B. Baggs
Keyword(s):  
Inflammatory Response ◽  
Subcutaneous Fat ◽  
Inflammatory Cells ◽  
Scar Formation ◽  
Good Survival ◽  
Polyglactin 910 ◽  
Chronic Inflammatory Response ◽  
Fat Grafts ◽  
Free Grafts ◽  
Vicryl Mesh

Abstract A variety of substances have been used at laminectomy sites to prevent postoperative epidural scarring. Free grafts of autologous subcutaneous fat are commonly used both clinically and experimentally. The free fat grafts usually survive, but decrease in size by about 50%. Postoperatively, subcutaneous seroma has been observed with the use of fat grafts, as well as recurrent symptoms of neural compression by the graft that required additional operations. When compared to the use of free fat grafts after laminectomy in dogs, Vicryl mesh produced slightly more scarring, but consistently less than that observed in control animals. The Vicryl mesh was resorbed by a minimal chronic inflammatory response over about 45 days. Seven of 11 fat-grafted zones showed signs of necrosis, at times with a greater collection of inflammatory cells than that associated with the Vicryl mesh. Of the 4 fat-grafted zones that showed good survival. 2 had gross evidence of neural compression. No surgical zone treated with Vicryl mesh exhibited evidence of neural compression. In view of these results, the use of Vicryl mesh at laminectomy sites may be a safer method of limiting postoperative epidural scar formation.

Prospective PC-interactive Pressure Algesimetry of Post-Traumatic Neck pain after Whiplash Injury

Cephalalgia ◽  
2005 ◽  
Vol 25 (3) ◽  
pp. 205-213 ◽  
Author(s):  
K Nebel ◽  
P Stude ◽  
C Lüdecke ◽  
H Wiese ◽  
H-C Diener ◽  
...  
Keyword(s):  
Muscle Pain ◽  
Whiplash Injury ◽  
Acute Stage ◽  
Acute Injury ◽  
Systematic Analysis ◽  
Pressure Pain ◽  
Healthy Control ◽  
Post Traumatic ◽  
Recovery Dynamics ◽  
Whiplash Syndrome

Cervical pain is a prominent symptom in both acute whiplash injury and late whiplash syndrome. However, no systematic analysis of post-traumatic pain development covering several weeks has yet been performed in whiplash patients. It was the aim of the present study to analyse the duration and course of post-traumatic muscle pain due to whiplash injury in a prospective follow-up examination with short investigation intervals. A recovery of initially increased muscle pain after whiplash injury within 1 month was hypothesized. Pressure pain of the splenius and trapezius muscles was recorded using PC-interactive pressure algesimetry. Whiplash patients were investigated during the acute injury stage and after 3, 4, and 6 weeks and compared with matched controls. We found significantly increased pressure pain of the splenius and trapezius muscles in the acute stage of whiplash injury. After 4 weeks patients' scores of pain parameters were comparable to those of healthy control subjects. Within the patient group the first changes of pressure pain were observed within 3 (splenius) and 4 weeks (trapezius). For most patients the recovery dynamics lasted 4-6 weeks. A minority of patients did not show any improvement after 6 weeks. The present study shows that the dynamics of pressure pain due to whiplash injury can be quantified by means of PC-interactive pressure algesimetry. Our results confirm the clinical experience that the acute post-traumatic cervical syndrome normally subsides within weeks.

Sign in / Sign up

Export Citation Format

Share Document