Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
-
Traumatic injury to the spinal cord activates B cells, which culminates in the synthesis of autoantibodies. The functional significance of this immune response is unclear. Antibodies produced after SCI caused pathology, in part by activating intraspinal complement and cells bearing Fc receptors. These data indicate that B cells, through the production of antibodies, affect pathology in SCI. There is increasing appreciation of the important role of B cells in spinal cord trauma and consequently, increasing interest in treating these disorders through B cell-depletion therapy. The purpose of this study was to investigate the effects of anti-CD20 mAb B cell depletion therapy within the first 24 hours of SCI. ⋯ Our data demonstrate an important role of B cells, which could possibly lead to B cell-based strategies for the treatment of SCI.
-
The purpose of the study is to evaluate the effect of a severe hemorrhagic shock on murine fracture healing. ⋯ : A hemorrhagic shock has a negative effect on the fracture healing. In this context the amount of the removed blood in terms of a '30% threshold' plays a decisive role.
-
The purpose of this study was to investigate fracture-associated local inflammation in regard to therapeutic hypothermia and gain information about the early inflammatory stages after polytrauma. ⋯ Induced hypothermia seems to influence the early immunologic milieu of fracture hematoma in regard to a prolonged pro-inflammatory and decreased anti-inflammatory state. These changes might influence induction of early bone healing.
-
Septic shock causes diffuse microvascular leakage leading to interstitial edema, and hypovolemia. In a resuscitated murine CLP-induced septic shock model that the adrenomedullin antibody HAM1101 reduced norepinephrine requirements, increased urine flow, ameliorated kidney dysfunction and organ injury. To dissect the mechanisms by which endothelial barrier injury may contribute to kidney dysfunction we plotted creatinine clearance as a function of bio-markers for barrier dysfunction. ⋯ We were able to demonstrate a direct link between microvascular leakage and kidney function, further highlighting the important role of vascular integrity in septic shock-related renal failure.
-
Postinjury multiple organ failure results from an inappropriate overwhelming immune response to injury. During trauma and hemorrhagic shock (T/HS), mesenteric ischemia causes gut mucosal breakdown with disruption of the intestinal barrier. It has been proposed that this releases the gut microbiota systemically via postshock mesenteric lymph (PSML), engendering infectious complications. ⋯ Thus, we confirmed that bacterial translocation does not exist in PSML after resuscitation from T/HS-associated mesenteric ischemia. However, T/HS does increase the presence of mitochondrial DAMPs in PSML. These results support our current position that PSML elaborates remote organ injury by multiple inflammatory mechanisms, including lipid-mediated proinflammatory stimuli, and by contribution from gut-derived DAMPs.