Systemic Inflammatory Response Syndrome (Sirs), Multiple Organ Dysfunction Syndrome (Mods), Multiple Organ Failure (Mof)

Baue, Arthur E.; Durham, Rodney M.; Faist, Eugen

doi:10.1097/00024382-199808000-00001

Cited by 424 publications

(258 citation statements)

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“…Recent studies by Heckbert et al (15) have shown that 39% of the trauma patients with a documented episode of hypotension during or shortly after the incident develop infectious complications. Under those conditions, the respiratory system is the most frequently affected organ system, and lung dysfunction is the first step in the development of multiple organ failure (4). Thus the acute respiratory distress syndrome (ARDS) is a major cause of death in surgical intensive care units with an incidence of ϳ10-14 cases per 100,000 people and an associated mortality rate of 36-52% (35).…”

mentioning

confidence: 99%

“…Studies in different experimental animal models have shown that systemic stressors, such as endotoxemia, hemorrhagic shock, or sepsis per se, can modulate the in vivo activity of AM⌽ and their reactivity to a subsequent in vitro stimulation (9,12,39). However, in the usual clinical situation, the patients who are most susceptible to multiple organ failure are the ones who encounter several sequential insults after the initial injury (4,37).…”

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confidence: 99%

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Alveolar macrophage activation after trauma-hemorrhage and sepsis is dependent on NF-κB and MAPK/ERK mechanisms

Jarrar

Kuebler

Rue

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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The acute respiratory distress syndrome (ARDS) is a major cause of morbidity after injury. We hypothesized that alveolar macrophage (AMΦ) chemokine and cytokine release after hemorrhage and sepsis is regulated by NF-κB and MAPK. Adult male rats underwent soft tissue trauma and hemorrhagic shock (∼90 min) followed by crystalloid resuscitation. Sepsis was induced by cecal ligation and puncture (CLP) 20 h after resuscitation. AMΦ were harvested, and TNF-α, IL-6, and macrophage inflammatory protein (MIP)-2 release and serum IL-6 and TNF-α levels were measured at 5 h after HCLP. Lung tissues were analyzed for activation of NF-κB, myeloperoxidase activity, and wet/dry weight ratio. In control animals, AMΦ were stimulated with LPS with or without inhibitors of NF-κB and MAPK. Serum TNF-α and IL-6 levels and spontaneous AMΦ TNF-α and MIP-2 release were elevated ( P < 0.05) after HCLP, concomitantly with the development of lung edema and leukocyte activation. Activation of NF-κB increased in lungs from the hemorrhage and CLP group compared with shams. Inhibition of NF-κB or the upstream MAPK significantly decreased LPS-stimulated AMΦ activation. Because enhanced release of inflammatory mediators by AMΦ may contribute to ARDS after severe trauma, inhibition of intracellular signaling pathways represents a target to attenuate organ injury under those conditions.

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mentioning

confidence: 99%

mentioning

confidence: 99%

Alveolar macrophage activation after trauma-hemorrhage and sepsis is dependent on NF-κB and MAPK/ERK mechanisms

Jarrar

Kuebler

Rue

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Its hallmarks are relatively consistent across patient populations and organ systems. They lead to systemic inflammatory response syndrome, multiple organ dysfunction, and multiple organ failure [1]. A variety of biomolecules is known to be involved in this response.…”

Section: Effects Of Hemorrhagic Shockmentioning

confidence: 99%

“…It has been shown to cause systemic inflammatory response syndrome, multiple organ dysfunction, and multiple organ failure [1]. It is an old problem and to find useful remedies that are capable of reducing its casualty is a most important task in combat medicine and trauma injury [2].…”

Section: Introductionmentioning

confidence: 99%

Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury

Kiang

2004

Cell Res

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Inducible heat shock protein 70 kD (HSP-70i) has been shown to protect cells, tissues, and organs from harmful assaults in in vivo and in vitro experimental models. Hemorrhagic shock followed by resuscitation is the principal cause of death among trauma patients and soldiers in the battlefield. Although the underlying mechanisms are still not fully understood, it has been shown that nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression play important roles in producing injury caused by hemorrhagic shock including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B 4 (LTB 4 ) generation. Moreover, transcription factors responsible for iNOS expression are also altered by hemorrhage and resuscitation. It has been evident that either up-regulation of HSP-70i or down-regulation of iNOS can limit tissue injury caused by ischemia/reperfusion or hemorrhage/resuscitation. In our laboratory, geldanamycin, a member of ansamycin family, has been shown to induce HSP70i overexpression and then subsequently to inhibit iNOS expression, to reduce cellular caspase-3 activity, and to preserve cellular ATP levels. HSP-70i is found to couple to iNOS and its transcription factor. Therefore, the complex formation between HSP-70i and iNOS may be a novel mechanism for protection from hemorrhage/resuscitation-induced injury.

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“…Following wide acceptance of the concept of systemic inflammatory reaction syndrome (SIRS), the association between acute pancreatitis and SIRS was extensively investigated (1,2).…”

Section: Introductionmentioning

confidence: 99%

The regulatory role of immunosuppressants on immune abnormalities in acute pancreatitis

Duan

Chi

et al. 2013

Biomedical Reports

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Abstract. The uncontrolled progression of the inflammatory cascade is the main cause underlying the development of multiple organ dysfunction syndrome (MODS) in acute pancreatitis. In this study, we investigated the effects of several immunosuppressants on mitigating the systemic inflammatory reaction syndrome (SIRS) and the compensatory anti-inflammatory response syndrome (CARS) associated with acute pancreatitis. A total of 93 male Sprague Dawley rats were divided into 5 groups: group 1 was the sham group and group 2 underwent laparoscopic intrapancreatic duct injection of sodium taurocholate to induce pancreatitis. The remaining 3 groups were the same as group 2, with the addition of methylprednisolone, cyclophosphamide or methotrexate treatment (metastab, CTX or MTX groups, respectively). Following establishment of the acute pancreatitis model, the serum levels of inflammatory and anti-inflammatory cytokines in groups 2, 3, 4 and 5 were found to be significantly elevated. Following immunosuppressant administration, the levels of all inflammatory and anti-inflammatory cytokines investigated in groups 3, 4 and 5 were decreased compared to those in group 2. The pancreatic amylase levels and pancreatic wet weight (PWW) were also decreased in groups 3, 4 and 5 compared to those in group 2. Therefore, immunosuppressants may reduce inflammation-related cytokine levels in acute pancreatitis and relieve disease progression.

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Systemic Inflammatory Response Syndrome (Sirs), Multiple Organ Dysfunction Syndrome (Mods), Multiple Organ Failure (Mof)

Cited by 424 publications

References 0 publications

Alveolar macrophage activation after trauma-hemorrhage and sepsis is dependent on NF-κB and MAPK/ERK mechanisms

Alveolar macrophage activation after trauma-hemorrhage and sepsis is dependent on NF-κB and MAPK/ERK mechanisms

Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury

The regulatory role of immunosuppressants on immune abnormalities in acute pancreatitis

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