Isolated closed minor-muscle injury of the lower leg did not cause an obvious systemic immune response

Schmitz, Daniel; Bangen, Joerg M.; Herborn, Christoph U.; Husain, Baher; Lendemans, Sven; Flohé, Stefanie B.; Metz, K.; Schade, F. Ulrich; Taeger, G.; Oberbeck, J.R.; Kobbe, Philipp; Waydhas, Christian; Flohé, Sascha

doi:10.1007/s00011-009-0081-z

Cited by 9 publications

(16 citation statements)

References 20 publications

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“…In addition, Kobbe et al. [28] also showed that the soft tissue injury with no bone components injection neither increased the cytokines levels nor induced pulmonary injury, similar with other studies demonstrating that soft tissue injury alone does not cause systemic inflammation [44] or remote organ failure.…”

Section: Discussionsupporting

confidence: 58%

Orthopedic Trauma-Induced Pulmonary Injury in the Obese Zucker Rat

Xiang¹,

Hester²,

Fuller³

et al. 2010

Microcirculation

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Objective Obese subjects with orthopedic trauma exhibit increased inflammation and an increased risk of pulmonary edema. PGE2 production is elevated during inflammation and associated with increased vascular permeability. We hypothesize that pulmonary edema in obesity following orthopedic trauma is due to elevated PGE2 and resultant increases in pulmonary permeability. Methods Orthopedic trauma was induced in both hindlimbs in lean (LZ) and obese Zucker rats (OZ). On the following day, plasma IL-6 and PGE2 levels, pulmonary edema, and pulmonary gas exchange capability were compared between groups: LZ, OZ, LZ with trauma (LZT), and OZ with trauma (OZT). Vascular permeability in isolated lungs was measured in LZ and OZ before and after application of PGE2. Results As compared with the other groups, the OZT exhibited elevated plasma IL-6 and PGE2 levels, increased lung wet/dry weight ratio and bronchoalveolar protein concentration, and an impaired pulmonary gas exchange. Indomethacin treatment normalized plasma PGE2 levels and pulmonary edema. Basal pulmonary permeability in isolated lungs was higher in OZ than LZ, with a further increase in permeability following treatment with PGE2. Conclusions These results suggest that pulmonary edema in OZ following orthopedic trauma is due to an elevated PGE2 and resultant increases in pulmonary permeability.

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Section: Discussionsupporting

confidence: 58%

Orthopedic Trauma-Induced Pulmonary Injury in the Obese Zucker Rat

Xiang¹,

Hester²,

Fuller³

et al. 2010

Microcirculation

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“…In order to link our ex vivo observations to an in vivo function of BMP signals during muscle regeneration we analyzed regenerating gastrocnemius muscles of mice after induction of a blunt closed minor soft tissue trauma (Figure 8) [35]. Histological analysis of trauma tissue revealed the invasion of leukocytes into the injured region 24 hours after trauma induction (Figure 8B).…”

Section: Resultsmentioning

confidence: 99%

“…8-10 weeks old male BALB/c mice were obtained from Harlan. Muscle trauma in anaesthetized BALB/c mice was induced as previously described [35]. Briefly, a drop-mass of 20 g (height 1.20 m) delivered a single impact on the posterior part of the gastrocnemius muscle without fracture of the bone.…”

Section: Methodsmentioning

confidence: 99%

BMP signaling balances proliferation and differentiation of muscle satellite cell descendants

et al. 2011

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BackgroundThe capacity of muscle to grow or to regenerate after damage is provided by adult stem cells, so called satellite cells, which are located under the basement lamina of each myofiber. Upon activation satellite cells enter the cell cycle, proliferate and differentiate into myoblasts, which fuse to injured myofibers or form new fibers. These processes are tightly controlled by many growth factors.ResultsHere we investigate the role of bone morphogenetic proteins (BMPs) during satellite cell differentiation. Unlike the myogenic C2C12 cell line, primary satellite cells do not differentiate into osteoblasts upon BMP signaling. Instead BMP signaling inhibits myogenic differentiation of primary satellite cells ex vivo. In contrast, inhibition of BMP signaling results in cell cycle exit, followed by enhanced myoblast differentiation and myotube formation. Using an in vivo trauma model we demonstrate that satellite cells respond to BMP signals during the regeneration process. Interestingly, we found the BMP inhibitor Chordin upregulated in primary satellite cell cultures and in regenerating muscles. In both systems Chordin expression follows that of Myogenin, a marker for cells committed to differentiation.ConclusionOur data indicate that BMP signaling plays a critical role in balancing proliferation and differentiation of activated satellite cells and their descendants. Initially, BMP signals maintain satellite cells descendants in a proliferating state thereby expanding cell numbers. After cells are committed to differentiate they upregulate the expression of the BMP inhibitor Chordin thereby supporting terminal differentiation and myotube formation in a negative feedback mechanism.

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“…Accordingly, it was suggested that hemorrhage-associated ischemia and reperfusion injury is probably the predominant pathophysiological effector in trauma models that use a combination of minor injury and hemorrhage (29). Thus, little information is currently available about the influence of major trauma, hemorrhage and their combination on the systemic release of inflammation markers.…”

Section: Introductionmentioning

confidence: 99%

Systemic release of cytokines and heat shock proteins in porcine models of polytrauma and hemorrhage*

Baker

Romero

Bach

et al. 2012

Critical Care Medicine

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Objective To define systemic release kinetics of a panel of cytokines and heat shock proteins (HSP) in porcine polytrauma/hemorrhage models and to evaluate whether they could be useful as early trauma biomarkers. Design and Setting Prospective study in a research laboratory. Subjects Twenty-one Yorkshire pigs. Measurements and Main Results Pigs underwent polytrauma (femur fractures/lung contusion, P), hemorrhage (mean arterial pressure 25-30mmHg, H), polytrauma plus hemorrhage (P/H) or sham procedure (S). Plasma was obtained at baseline, in 5-15min intervals during a 60min shock period without intervention and in 60-120min intervals during fluid resuscitation for up to 300min. Plasma was assayed for IL-1β, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12/IL-23p40, IL-13, IL-17, IL-18, IFNγ, TGFβ, TNFα, HSP40, HSP70 and HSP90 by ELISA. All animals after S, P and H survived (n=5/group). Three of six animals after P/H died. IL-10 increased during shock after P and this increase was attenuated after H. TNFα increased during the shock period after P, H and also after S. P/H abolished the systemic IL-10 and TNFα release and resulted in 20-30% increased levels of IL-6 during shock. As fluid resuscitation was initiated TNFα and IL-10 levels decreased after P, H and P/H, HSP 70 increased after P, IL-6 levels remained elevated after P/H and also increased after P and S. Conclusions Differential regulation of the systemic cytokine release after polytrauma and/or hemorrhage, in combination with the effects of resuscitation, can explain the variability and inconsistent association of systemic cytokine/HSP levels with clinical variables in trauma patients. Insults of major severity (P/H) partially suppress the systemic inflammatory response. The plasma concentrations of the measured cytokines/HSPs do not reflect injury severity or physiological changes in porcine trauma models and are unlikely to be able to serve as useful trauma biomarkers in patients.

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Isolated closed minor-muscle injury of the lower leg did not cause an obvious systemic immune response

Abstract: We describe a standardized trauma model for minor soft tissue injury in mice. Systemic effects on the immune system by traumatized lower leg were not found on the level of circulating cytokines or cellular responses to endotoxin.

Cited by 9 publications

References 20 publications

Orthopedic Trauma-Induced Pulmonary Injury in the Obese Zucker Rat

Orthopedic Trauma-Induced Pulmonary Injury in the Obese Zucker Rat

BMP signaling balances proliferation and differentiation of muscle satellite cell descendants

Systemic release of cytokines and heat shock proteins in porcine models of polytrauma and hemorrhage*

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