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2014 ; 42
(3
): 218-27
Nephropedia Template TP
gab.com Text
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English Wikipedia
Delayed neutralization of interleukin 6 reduces organ injury, selectively
suppresses inflammatory mediator, and partially normalizes immune dysfunction
following trauma and hemorrhagic shock
#MMPMID24978887
Zhang Y
; Zhang J
; Korff S
; Ayoob F
; Vodovotz Y
; Billiar TR
Shock
2014[Sep]; 42
(3
): 218-27
PMID24978887
show ga
An excessive and uncontrolled systemic inflammatory response is associated with
organ failure, immunodepression, and increased susceptibility to nosocomial
infection following trauma. Interleukin 6 (IL-6) plays a particularly prominent
role in the host immune response after trauma with hemorrhage. However, as a
result of its pleiotropic functions, the effect of IL-6 in trauma and hemorrhage
is still controversial. It remains unclear whether suppression of IL-6 after
hemorrhagic shock and trauma will attenuate organ injury and immunosuppression.
In this study, C57BL/6 mice were treated with anti-mouse IL-6 monoclonal antibody
immediately prior to resuscitation in an experimental model combining hemorrhagic
shock and lower-extremity injury. Interleukin 6 levels and signaling were
transiently suppressed following administrations of anti-IL-6 monoclonal antibody
following hemorrhagic shock and lower-extremity injury. This resulted in reduced
lung and liver injury, as well as suppression in the levels of key inflammatory
mediators including IL-10, keratinocyte-derived chemokine, monocyte
chemoattractant protein 1, and macrophage inhibitory protein 1? at both 6 and 24
h. Furthermore, the shift to TH2 cytokine production and suppressed lymphocyte
response were partly prevented. These results demonstrate that IL-6 is not only a
biomarker but also an important driver of injury-induced inflammation and immune
suppression in mice. Rapid measurement of IL-6 levels in the early phase of
postinjury care could be used to guide IL-6-based interventions.