scholarly journals Inflammatory Response to Traumatic Injury: Clinical and Animal Researches in Inflammation

2015 ◽  
Vol 2015 ◽  
pp. 1-2 ◽  
Author(s):  
Huang-Ping Yu ◽  
Irshad H. Chaudry ◽  
Mashkoor A. Choudhry ◽  
Chung-Hsi Hsing ◽  
Fu-Chao Liu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Traumatic Injury

FLUID RESUSCITATION INCREASES INFLAMMATORY RESPONSE TO TRAUMATIC INJURY

2004 ◽  
Vol 57 (6) ◽  
pp. 1378 ◽  
Author(s):  
Jennifer M. Watters ◽  
Terisa Jackson ◽  
Patrick J. Muller ◽  
Darren Malinoski ◽  
S Rob Todd ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Fluid Resuscitation ◽  
Traumatic Injury

scholarly journals A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome

2022 ◽  
Vol 13 ◽  
Author(s):  
Samuel Houle ◽  
Olga N. Kokiko-Cochran
Keyword(s):  
Risk Factors ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Genetic Risk ◽  
Traumatic Injury ◽  
Genetic Risk Factors ◽  
Post Injury ◽  
Immune Stress ◽  
Age Related

Increasing evidence demonstrates that aging influences the brain's response to traumatic brain injury (TBI), setting the stage for neurodegenerative pathology like Alzheimer's disease (AD). This topic is often dominated by discussions of post-injury aging and inflammation, which can diminish the consideration of those same factors before TBI. In fact, pre-TBI aging and inflammation may be just as critical in mediating outcomes. For example, elderly individuals suffer from the highest rates of TBI of all severities. Additionally, pre-injury immune challenges or stressors may alter pathology and outcome independent of age. The inflammatory response to TBI is malleable and influenced by previous, coincident, and subsequent immune insults. Therefore, pre-existing conditions that elicit or include an inflammatory response could substantially influence the brain's ability to respond to traumatic injury and ultimately affect chronic outcome. The purpose of this review is to detail how age-related cellular and molecular changes, as well as genetic risk variants for AD affect the neuroinflammatory response to TBI. First, we will review the sources and pathology of neuroinflammation following TBI. Then, we will highlight the significance of age-related, endogenous sources of inflammation, including changes in cytokine expression, reactive oxygen species processing, and mitochondrial function. Heightened focus is placed on the mitochondria as an integral link between inflammation and various genetic risk factors for AD. Together, this review will compile current clinical and experimental research to highlight how pre-existing inflammatory changes associated with infection and stress, aging, and genetic risk factors can alter response to TBI.

scholarly journals Developing a Minimally Invasive Cell-Based Model to Predict Response to Major Trauma

2020 ◽  
Vol 3 ◽  
Author(s):  
Kayla Gates ◽  
Rebecca Nunge ◽  
Jamila Adom ◽  
Mark Kaplan ◽  
Todd McKinley
Keyword(s):  
Cell Death ◽  
Inflammatory Response ◽  
Traumatic Injury ◽  
Control Group ◽  
Immunologic Response ◽  
Post Injury ◽  
Predictive Tool ◽  
Severity Of Injury ◽  
Inflammatory Stimuli

Background. Physical trauma results in a systemic inflammatory response.  Preliminary research in orthopedic trauma patients suggests that patients with similar demographics and severity of injury vary in their response to traumatic injury.  Analysis of the immunological response post-injury showed a sustained pro-inflammatory response with delayed reparative cytokine expression in trauma sensitive patients, while the trauma tolerant patients had an early inflammatory expression with resolution by 72 hours post-injury.  Thus, we hypothesize that differential response to non-traumatic injury might serve as a predictive tool for the identification of trauma tolerant and sensitive patients prior to injury.  The goal of this research is to test whether immunological changes to inflammatory stimuli can predict tolerance or sensitivity to trauma using an-vitro cell-based assay.  Methods. Splenocytes were isolated from naive C57BL/6 mice and subjected to biological trauma in vitro using LPS (100 ng/mL) or hypoxic trauma using hydrogen peroxide (50 µM, 100 µM, and 200 µM) with or without proinflammatory cytokines, IL-1β (1 ng/mL) , IL-6 (200 ng/mL), and IL-33 (150 ng/mL). Inflammation and hypoxia were assessed using IL-6 and HIF-1ɑ expression respectively via qPCR 24 hours post-treatment. Cell death and pro-inflammatory cytokine production using multiplex analysis were used to measure outcomes.   Results. Both types of treatments showed increased cell death compared to the control group. qPCR data is pending.  Conclusion. With these studies as a core of the experimental approach, this in vitro cell-based assay will be used to assess immunologic response to inflammatory stimuli across the genetic variation of mouse strains. Findings from this project could enable the development of a clinical test that accurately predicts immunologic response to trauma and related-complications based on patients’ sensitivity to pre-traumatic injury.   

AGING AND THE INFLAMMATORY RESPONSE AFTER TRAUMATIC INJURY

Shock ◽  
2006 ◽  
Vol 25 (Supplement 1) ◽  
pp. 13
Author(s):  
E.J. Kovacs ◽  
T.P. Plackett ◽  
L. Ramirez ◽  
C.R. Gomez
Keyword(s):  
Inflammatory Response ◽  
Traumatic Injury

The host response to trauma and burns in the critically ill

2016 ◽  
Author(s):  
Edward A. Bittner ◽  
Shawn P. Fagan
Keyword(s):  
Inflammatory Response ◽  
Host Response ◽  
Expression Patterns ◽  
Traumatic Injury ◽  
Recovery Process ◽  
Organ Injury ◽  
Severe Injury ◽  
Poor Correlation ◽  
Severe Traumatic Injury ◽  
Anti Inflammatory

Following severe traumatic injury, patients enter a state of immune dysregulation consisting of both exaggerated inflammation and immune suppression. Traditionally, the host response has been viewed as an early systemic inflammatory response syndrome (SIRS) followed temporally by a compensatory anti-inflammatory or immune-suppressive response syndrome (CARS). While this paradigm has been widely accepted across both medical and scientific fields, recent advances have challenged this concept. The Glue grant investigators recently characterized both the initial inflammatory response to injury and the dynamic evolving recovery process. They found: (1) severe injury produces a rapid (< 12 hours) genomic reprioritization in which 80% of the leukocyte transcriptome is altered; (2) similarities in gene expression patterns between different injuries reveal an apparently fundamental response to severe inflammatory stress, which is far more common than different; (3) alterations in the expression of classical inflammatory and anti-inflammatory as well as adaptive immunity genes occur simultaneously, not sequentially after severe injury; (4) the temporal nature of the current SIRS/CARS paradigm is not supported at the level of the leukocyte transcriptome. Complications are not associated with genomic evidence of a ‘second hit’ and differ only in the magnitude and duration of this genomic reprioritization. Furthermore, the delayed clinical recovery with organ injury is not associated with dramatic qualitative differences in the leukocyte transcriptome. Finally, poor correlation between human and rodent inflammatory genomic responses will alter how the host response is studied in the future.

scholarly journals Tanshinone IIA Attenuates the Inflammatory Response and Apoptosis after Traumatic Injury of the Spinal Cord in Adult Rats

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e38381 ◽  
Author(s):  
Xin Yin ◽  
Yue Yin ◽  
Fa-Le Cao ◽  
Yu-Fei Chen ◽  
Ye Peng ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Inflammatory Response ◽  
Traumatic Injury ◽  
Tanshinone Iia ◽  
Adult Rats

Low-level laser therapy attenuates the acute inflammatory response induced by muscle traumatic injury

2016 ◽  
Vol 50 (5) ◽  
pp. 503-513 ◽  
Author(s):  
Paulo Cesar Lock Silveira ◽  
Debora da Luz Scheffer ◽  
Viviane Glaser ◽  
Aline Pertile Remor ◽  
Ricardo Aurino Pinho ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Laser Therapy ◽  
Traumatic Injury ◽  
Low Level Laser Therapy ◽  
Acute Inflammatory Response ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser

Update: Behavioral Management of Unilateral Vocal Fold Paralysis and Paresis

2019 ◽  
Vol 4 (3) ◽  
pp. 474-482
Author(s):  
Sarah L. Schneider
Keyword(s):  
Vocal Fold ◽  
Treatment Plan ◽  
Traumatic Injury ◽  
Voice Therapy ◽  
Valuable Insight ◽  
Behavioral Management ◽  
Use Patterns ◽  
Vocal Quality ◽  
And Function ◽  
Voice Use

PurposeVocal fold motion impairment (VFMI) can be the result of iatrogenic or traumatic injury or may be idiopathic in nature. It can result in glottic incompetence leading to changes in vocal quality and ease. Associated voice complaints may include breathiness, roughness, diplophonia, reduced vocal intensity, feeling out of breath with talking, and vocal fatigue with voice use. A comprehensive interprofessional voice evaluation includes auditory-perceptual voice evaluation, laryngeal examination including videostroboscopy, acoustic and aerodynamic voice measures. These components provide valuable insight into laryngeal structure and function and individual voice use patterns and, in conjunction with stimulability testing, help identify candidacy for voice therapy and choice of therapeutic techniques.ConclusionA comprehensive, interprofessional evaluation of patients with VFMI is necessary to assess the role of voice therapy and develop a treatment plan. Although there is no efficacy data to support specific voice therapy techniques for treating VFMI, considerations for various techniques are provided.

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