title: Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats.
abstract: BACKGROUND
  Traumatic brain injury (TBI) evokes a systemic immune response including leukocyte migration into the brain and release of pro-inflammatory cytokines; however, the mechanisms underlying TBI pathogenesis and protection are poorly understood. Due to the high incidence of head trauma in the sports field, battlefield and automobile accidents identification of the molecular signals involved in TBI progression is critical for the development of novel therapeutics.
  
  
  METHODS
  In this report, we used a rat lateral fluid percussion impact (LFPI) model of TBI to characterize neurodegeneration, apoptosis and alterations in pro-inflammatory mediators at two time points within the secondary injury phase. Brain histopathology was evaluated by fluoro-jade (FJ) staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay, polymerase chain reaction (qRT PCR), enzyme linked immunosorbent assay (ELISA) and immunohistochemistry were employed to evaluate the CCL20 gene expression in different tissues.
  
  
  RESULTS
  Histological analysis of neurodegeneration by FJ staining showed mild injury in the cerebral cortex, hippocampus and thalamus. TUNEL staining confirmed the presence of apoptotic cells and CD11b+ microglia indicated initiation of an inflammatory reaction leading to secondary damage in these areas. Analysis of spleen mRNA by PCR microarray of an inflammation panel led to the identification of CCL20 as an important pro-inflammatory signal upregulated 24 h after TBI. Although, CCL20 expression was observed in spleen and thymus after 24 h of TBI, it was not expressed in degenerating cortex or hippocampal neurons until 48 h after insult. Splenectomy partially but significantly decreased the CCL20 expression in brain tissues.
  
  
  CONCLUSIONS
  These results demonstrate that the systemic inflammatory reaction to TBI starts earlier than the local brain response and suggest that spleen- and/ or thymus-derived CCL20 might play a role in promoting neuronal injury and central nervous system inflammation in response to mild TBI.
authors: Department of Internal Medicine, University of South Florida College of Medicine, 12901 Bruce B Downs Blvd, Tampa, FL 33612, USA.
authors: Mahasweta
authors: M
authors: Das
authors: Christopher C
authors: CC
authors: Leonardo
authors: Saniya
authors: S
authors: Rangooni
authors: Keith R
authors: KR
authors: Pennypacker
authors: Subhra
authors: S
authors: Mohapatra
authors: Shyam S
authors: SS
authors: Mohapatra
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001921:Brain / Q000033:anatomy & histology / Q000276:immunology* / Q000473:pathology*; D001930:Brain Injuries / Q000276:immunology* / Q000473:pathology*; D054418:Chemokine CCL20 / Q000235:genetics / Q000276:immunology*; D053938:DNA Fragmentation; D006801:Humans; D020287:In Situ Nick-End Labeling; D007249:Inflammation / Q000276:immunology / Q000473:pathology*; D008297:Male; D009410:Nerve Degeneration / Q000276:immunology / Q000473:pathology*; D010474:Percussion / Q000009:adverse effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000276:immunology; D013156:Splenectomy; D013950:Thymus Gland / Q000276:immunology
chemical_list: D054418:Chemokine CCL20