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

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.

A Co(II)-mediated coordination polymer: treatment capability on post-traumatic osteoarthritis via reducing inflammatory response

2020 ◽  
Vol 51 (1) ◽  
pp. 63-69
Author(s):  
Xi-Biao Zhang ◽  
Zhi-Cai Jia ◽  
Hao-Guang Ma ◽  
Hua Pan ◽  
Xiang-Bo Lin ◽  
...  
Keyword(s):  
Coordination Polymer ◽  
Inflammatory Response ◽  
Post Traumatic

Mechanism of Salutary Effects of Finasteride on Post-traumatic Immune/Inflammatory Response

2007 ◽  
Vol 246 (5) ◽  
pp. 836-843 ◽  
Author(s):  
Michael Frink ◽  
Ya-Ching Hsieh ◽  
Shunhua Hu ◽  
Chi-Hsun Hsieh ◽  
Hans-Christoph Pape ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Post Traumatic

scholarly journals Role of Hypothalamic Pituitary Adrenal (HPA) Axis and Tumor Necrosis Factor (TNF) in Development of Post-Traumatic Nosocomial Pneumonia

2017 ◽  
Vol 2 (1) ◽  
Keyword(s):  
Hip Fracture ◽  
Inflammatory Response ◽  
Nosocomial Pneumonia ◽  
Serum Cortisol ◽  
Cardiovascular Death ◽  
Cardiovascular Complications ◽  
Large Individual ◽  
Cardiovascular Patients ◽  
Investigation Period ◽  
Post Traumatic

Background and purpose: Infection after experimental focal ischemia may result from brain-induced immune depression. A strong cytokine mediated anti-inflammatory response was recently observed in stroke patients at higher risk of infection, although infection due to the decreased pro-inflammatory mediators can be expected as well. To investigate this question the following experiment was performed. Methods: 105 over 60 years hip fracture patients were included in the study. Sera and lympho/monocytes were separated from blood samples taken on different days (day 1, 3, 6, 9). Isolated lympho/ monocytes were cultured for one day with or without endotoxin (LPS). TNFα levels in sera and in the culture supernatants were determined by bioassays using WEHI 164 cells. Plasma ACTH and cortisol values were measured by RIA kits. Results: From 105 hip fracture patients 7 nosocomial pneumonia patients were found, (4 survivors and 3 nonsurvivors) furthermore 2 non-survivors with cardiovascular death without infection. On the day of trauma the level of circulating TNFα activity was extremely low in nosocomial pneumonia patients in comparison to uneventful healing patients. In pneumonia patients TNFα started to increase on day 3, increased till day 9 then reached the values of uneventful healing group. In two patients with later cardiovascular complications, extremely high TNF alpha activities were detected throughout the entire observation period. The plasma cortisol values were high in nosocomial pneumonia patients in comparison to uneventful healing persons, and decreased slightly by the 9th post-trauma day. In the two cardiovascular patients, serum cortisol was extremely low on the day of trauma and increased gradually during the investigation period. ACTH level was stable in the sera of uneventfully healing patients, while showed large individual and also time-dependent fluctuations people with post-traumatic complications. Conclusions: An excessive decrease in pro-inflammatory response is a key facilitating factor for the development of infection.

scholarly journals 4260 Hollow, Degradable poly(N-Isopropylacrylamide) Derived Nanoparticles for the Delivery of Anti-Inflammatory Peptides for the Treatment and Prevention of Post-Traumatic Osteoarthritis

2020 ◽  
Vol 4 (s1) ◽  
pp. 109-109
Author(s):  
Marcus A Deloney ◽  
Kyra Smart ◽  
Blaine Christiansen ◽  
Alyssa Panitch
Keyword(s):  
Articular Cartilage ◽  
Inflammatory Response ◽  
Sustained Release ◽  
Sodium Dodecylsulfate ◽  
Joint Space ◽  
The Core ◽  
Post Traumatic ◽  
Cyclic Degradation

OBJECTIVES/GOALS: Knocking down the inflammatory response following joint trauma may halt the cytokine cascade and prevent the resulting cyclic degradation of articular cartilage. MK2 inhibiting (MK2i) peptides are an emerging and promising class of pharmaceutical to treat post-traumatic osteoarthritis (PTOA); however, these peptides are susceptible to proteolytic degradation in the extracellular space. Our objective is to encapsulate MK2i in thermoresponsive hollow nanoparticles (hNPs) to knockdown the inflammatory cytokine IL-6 to prevent the cyclic degradation of articular cartilage. METHODS/STUDY POPULATION: NP Synthesis: N-isopropyl acrylamide (NIPAm) cores was initiated by potassium persulfate (KPS) in aqueous solution with sodium dodecylsulfate (SDS) at 70°C under a nitrogen for 2 hours. Then exposed to oxygen for 45 min, followed by a nitrogen purge. NIPAm, 2-acrylamindo-2-methyl-1-propanesulfonic acid (AMPS), N,N’-bis(acryoyl)cystamine (BAC), and Acrylic Acid (AAc), in fluorescent batches rhodamine b isothiocyanate (RBITC), were polymerized around the core to form the shell. NPs were purified using tangential flow filtration. The NPs were dialyzed at 4°C for 14 days to remove the core and form hNPs. Loading & Release: hNPs and MK2i were incubated at 1 mg/ml at 4°C for 24 h. MK2i released into 1x PBS and analyzed on HPLC. IL-6 Expression: Bovine chondrocytes seeded at 10,000 cell/cm2 were stimulated with 20 ng/ml IL-1b daily and treated once with 100 µg/ml MK2i loaded-NP or 100 µg/ml free MK2i treatment on day 2. Analyzed on bovine IL-6 ELISA. In Vivo Intra Articular Injections: 75 µl of 2 mg/ml hNPsRHB or a PBS control was injected into the right knee of 4-month old Fischer 344 (Envigo) rats. Rats were imaged daily for 7 days then euthanized, legs dissected, and imaged. RESULTS/ANTICIPATED RESULTS: Core removal facilitated increased MK2i release from hNPs, Fig 1A, allowing up to 63% after 5 days in PBS. The hNPs generated here offer a continual sustained release of MK2i and hNPs are non-cytotoxic (data not shown) up to 12 mg/ml. MK2i loaded-NPs significantly knocked down IL-6 production after a single treatment after 2 days, Figure 1B, and continued knockdown for up to 4 days. hNPsRBITC was successfully injected into rat joint space and was retained for at least 7-days compared to pre-injection and PBS control, Fig 1 B-C. DISCUSSION/SIGNIFICANCE OF IMPACT: hNPs protect MK2i from ECM degradation and offer continual sustained release into chondrocytes. Core removal allows for MK2i release in vitro with further sustained release compared to previous non-degradable model. The single MK2i treatment lead to a significant IL-6 knockdown bovine chondrocytes for up to 4 days in hNPs. We were able to successfully inject and retain fluorescently labeled hNPs within rat knees for 7 days. Our translational therapeutic shows the promise of delivering a degradable, non-cytotoxic hNP into the joint space to knockdown the inflammatory response to halt the cyclic progression of articular cartilage degradation and progression of PTOA. CONFLICT OF INTEREST DESCRIPTION: The authors declare the following competing financial interest(s): Moerae Matrix, Inc. has a worldwide exclusive license to the CPP (MK2 inhibitor peptide). A. Panitch owns greater than 5% of Moerae Matrix, Inc.

Sign in / Sign up

Export Citation Format

Share Document