Kinetics of polymorphonuclear neutrophil infiltration after a traumatic brain injury in rat

Abstract

The aim of our study was to assess polymorphonuclear neutrophil infiltration into the injured parenchyma after a traumatic brain injury (TBI). Myeloperoxidase (MPO) activity was assayed on the hippocampus, temporal and parietal cortex 6, 24, 48, 72, and 120 h post-trauma. MPO activity occurred in these structures from 6 h post-trauma and was maximum at 24-48 h. It was resolved by 72 h in the hippocampus and the parietal cortex, but persisted in the temporal cortex until 120 h after trauma. This suggests that neutrophil infiltration is a delayed phenomenon in the physiopathology of TBI. Considering that a large therapeutic window may be crucial in the management of TBI, inhibition of neutrophil infiltration needs to be further investigated following cerebral trauma.

Acute Brain Injury Triggers MyD88-Dependent, TLR2/4-Independent Inflammatory Responses

“…CNS-specific overexpression of KC/CXCL-1 produced substantial neutrophil infiltration into perivascular, meningeal, and parenchymal sites, 60 and neutralization of LIX/CXCL5 significantly inhibited neutrophil influx into the cornea during LPS keratitis. 61 Our immunohistochemical findings together with previous reports 41,42,62 imply that leukocyte infiltration is a relatively delayed phenomenon in the pathogenesis of aseptic brain injury, occurring later than 4 hours and reaching its maximum between 24 and 48 hours after injury. Thus, CNS resident cells are the most likely source of cytokines and chemokines like KC/CXCL1 and LIX/CXCL5 at early time points after injury.…”

“…41,42 The presence of neutrophils in the injured brain was indicated by immunohistochemistry using an anti GR-1 antibody (RB6-8C5 Ab). GR-1-positive cells were found in the lesioned cortex at 24 hours (Figure 1) after cold injury but were absent in brains from sham-operated controls.…”

Novel Docosanoids Inhibit Brain Ischemia-Reperfusion-mediated Leukocyte Infiltration and Pro-inflammatory Gene Expression

“…Thus exogenous administration of 10,17S-docosatriene directly into the cerebroventricular system through continuous infusion during the initial 2 days of reperfusion did indeed exert neuroprotection. During 24 -72 h of reperfusion is when most brain leukocyte infiltration occurs (7,8,29,30). Leukocytes accumulate in an area surrounding the brain infarct (Fig.…”

“…Inhibited by 10,17S-Docosatriene-We monitored PMN infiltration, a major factor in mediating brain ischemia-reperfusion damage (7,8,29,30). PMN infiltration is a complex multistep process that is modulated by the coordinated expression of adhesion and signaling molecules (26).…”

Strategies for CNS repair following TBI

“…The invasion of the central nervous system by inflammatory cells is partially dependent upon blood brain barrier breakdown. Polymorphonuclear cells can be found to invade the brain parenchyma as early as 6 hours after injury, peaking at approximately 24 hours and remaining present for 3-5 days (Royo et al, 1999;Williams et al, 2007). While T cells have a less well delineated role in the pathophysiology of TBI, T lymphocyte invasion is also found to peak around 24 hours following a CCI insult (Clausen et al, 2007).…”