Research Reports - Oxidative burst of circulating neutrophils following traumatic brain injury in human

PLoS One. 2013 Jul 24;8(7)

Liao Y, Liu P, Guo F, Zhang ZY, Zhang Z

Besides secondary injury at the lesional site, Traumatic brain injury (TBI) can
cause a systemic inflammatory response, which may cause damage to initially
unaffected organs and potentially further exacerbate the original injury. Here we
investigated plasma levels of important inflammatory mediators, oxidative
activity of circulating leukocytes, particularly focusing on neutrophils, from
TBI subjects and control subjects with general trauma from 6 hours to 2 weeks
following injury, comparing with values from uninjured subjects. We observed
increased plasma level of inflammatory cytokines/molecules TNF-α, IL-6 and CRP,
dramatically increased circulating leukocyte counts and elevated expression of
TNF-α and iNOS in circulating leukocytes from TBI patients, which suggests a
systemic inflammatory response following TBI. Our data further showed increased
free radical production in leukocyte homogenates and elevated expression of key
oxidative enzymes iNOS, COX-2 and NADPH oxidase (gp91(phox)) in circulating
leukocytes, indicating an intense induction of oxidative burst following TBI,
which is significantly greater than that in control subjects with general trauma.
Furthermore, flow cytometry assay proved neutrophils as the largest population in
circulation after TBI and showed significantly up-regulated oxidative activity
and suppressed phagocytosis rate for circulating neutrophils following brain
trauma. It suggests that the highly activated neutrophils might play an important
role in the secondary damage, even outside the injured brain. Taken together, the
potent systemic inflammatory response induced by TBI, especially the intensively
increase oxidative activity of circulating leukocytes, mainly neutrophils, may
lead to a systemic damage, dysfunction/damage of bystander tissues/organs and
even further exacerbate secondary local damage. Controlling these
pathophysiological processes may be a promising therapeutic strategy and will
protect unaffected organs and the injured brain from the secondary damage.
 

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