Complement activation and clearance in acute illness and injury: Evidence for C5a as a cell-directed mediator of the adult respiratory distress syndrome in man

Solomkin, Joseph S.; Cotta, Leala A.; Satoh, Paul S.

doi:10.1097/00005373-198602000-00029

Cited by 39 publications

(50 citation statements)

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“…In vivo, the chemotactic responses of neutrophils obtained from patients with sepsis or multisystem trauma with adult respiratory distress syndrome were found to be specifically deactivated to C5a or deactivated to both C5a and fMLP depending on clinical severity and time after trauma or onset of sepsis. In contrast, no alteration in neutrophil function was found in patients who did not develop adult respiratory distress syndrome (28). Our recent studies in the CLP model indicate that the H 2 O 2 response of neutrophils to PMA is impaired (14), suggesting a broad defect in postreceptor signaling pathways.…”

Section: Discussionmentioning

confidence: 78%

Role of C5a in Multiorgan Failure During Sepsis

Huber‐Lang

Sarma

et al. 2001

The Journal of Immunology

208

178

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In humans with sepsis, the onset of multiorgan failure (MOF), especially involving liver, lungs, and kidneys, is a well known complication that is associated with a high mortality rate. Our previous studies with the cecal ligation/puncture (CLP) model of sepsis in rats have revealed a C5a-induced defect in the respiratory burst of neutrophils. In the current CLP studies, MOF occurred during the first 48 h with development of liver dysfunction and pulmonary dysfunction (falling arterial partial pressure of O2, rising partial pressure of CO2). In this model an early respiratory alkalosis developed, followed by a metabolic acidosis with increased levels of blood lactate. During these events, blood neutrophils lost their chemotactic responsiveness both to C5a and to the bacterial chemotaxin, fMLP. Neutrophil dysfunction was associated with virtually complete loss in binding of C5a, but binding of fMLP remained normal. If CLP animals were treated with anti-C5a, indicators of MOF and lactate acidosis were greatly attenuated. Under the same conditions, C5a binding to blood neutrophils remained intact; in tandem, in vitro chemotactic responses to C5a and fMLP were retained. These data suggest that, in the CLP model of sepsis, treatment with anti-C5a prevents development of MOF and the accompanying onset of blood neutrophil dysfunction. This may explain the protective effects of anti-C5a in the CLP model of sepsis.

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Section: Discussionmentioning

confidence: 78%

Role of C5a in Multiorgan Failure During Sepsis

Huber‐Lang

Sarma

et al. 2001

The Journal of Immunology

208

178

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“…13 Systemic activation of the complement system, as known from patients suffering from sepsis, severe burns or injuries, could induce autodestructive inflammatory reactions, such as adult respiratory distress syndrome (ARDS) or multiple organ failure (MOF). [14][15][16][17][18] Both types of clinical symptom complexes have been observed in the patient who died during the OTCD trial, which suggests an involvement of the complement system. In this article, we will discuss prophylactic measures which might help to control or avoid excess activation of the complement system after adenoviral gene therapy in humans.…”

Section: The Complement Systemmentioning

confidence: 92%

Complement activation by recombinant adenoviruses

et al. 2001

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“…17 Although the clinical implication of this complement activation is unclear, it may be important, because it has been associated with pulmonary edema. [18][19][20] Furthermore, the effect of LCT/MCT on complement activation has not been examined. In this report, injection pain, bradykinin generation and complement activation with use of LCT emulsive propofol and LCT/MCT emulsive propofol were compared to identify the mechanism for reduced pain when using LCT/MCT propofol.…”

Section: Résultatsmentioning

confidence: 99%

Mechanism of injection pain with long and longmedium chain triglyceride emulsive propofol

Ohmizo

Obara

Iwama

2005

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : t has been suggested that long-medium chain triglyceride (LCT/MCT) emulsive propofol causes less injection pain than long chain triglyceride (LCT) emulsive propofol because of the decreased propofol concentration in the aqueous phase. Alternatively, LCT propofol generates bradykinin causing the injection pain and activates complement, but these effects when using LCT/MCT propofol have not been examined. To identify the mechanism for reduced pain with LCT/MCT propofol, injection pain, bradykinin generation and complement activation with use of both propofol products were compared.M Me et th ho od ds s: : Two hundred adult patients randomly allocated to two groups were given 1.5 mg·kg -1 iv of either LCT propofol or LCT/MCT propofol at a rate of 200 mg·min -1 in a double-blind manner and were asked to grade pain scores. In another study, bradykinin and activated complement 3 (C3a) concentrations were measured using blood obtained from 13 healthy volunteers mixed with saline, LCT propofol or LCT/MCT propofol.R Re es su ul lt ts s: : There was a significant difference in pain scores between groups, showing a lower incidence of injection pain in the LCT/MCT propofol group. The bradykinin concentrations in blood mixed with LCT and LCT/MCT propofol were significantly higher than in blood mixed with saline. The C3a concentrations showed similar results.C Co on nc cl lu us si io on ns s: : LCT/MCT propofol causes less pain on injection compared with LCT propofol. Bradykinin generation and complement activation are similar with both LCT and LCT/MCT propofol. Thus, the reason for less pain on injection with LCT/MCT propofol may be attributed to a decreased concentration of propofol in the aqueous phase. Objectif : On a pensé qu'une émulsion de propofol avec une chaîne mi-longue de triglycéride (CLT/CMT) cause moins de douleur à l'injection qu'une émulsion à chaîne longue (CLT) parce que la concentration de propofol diminue pendant la phase aqueuse. Aussi, le propofol avec CLT génère de la bradykinine, causant de la douleur à l'injection, et active le complément, mais ces effets n'ont pas été étudiés avec le propofol CLT/CMT. Pour définir le mécanisme qui réduit la douleur avec le propofol CLT/CMT, nous avons comparé la douleur à l'injection, la génération de bradykinine et l'activation du complément avec l'usage des deux produits de propofol. Méthode : Deux cents patients adultes ont été répartis au hasard en deux groupes et ont reçu 1,5 mg·kg -1 iv de propofol CLT ou CLT/CMT

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Complement activation and clearance in acute illness and injury: Evidence for C5a as a cell-directed mediator of the adult respiratory distress syndrome in man

Cited by 39 publications

References 0 publications

Role of C5a in Multiorgan Failure During Sepsis

Role of C5a in Multiorgan Failure During Sepsis

Complement activation by recombinant adenoviruses

Mechanism of injection pain with long and longmedium chain triglyceride emulsive propofol

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