Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats

Mahasweta Das, Christopher C. Leonardo, Saniya Rangooni, Shyam S. Mohapatra, Subhra Mohapatra, Keith R. Pennypacker

Research output: Contribution to journalArticlepeer-review

60 Scopus citations


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 24h 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.Conclusion: 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.

Original languageEnglish
Article number148
JournalJournal of Neuroinflammation
StatePublished - Oct 31 2011

Bibliographical note

Funding Information:
This work is supported by a VA career scientist award to Shyam Mohapatra, a USF Health development grant to Subhra Mohapatra and 5R21NS060907 to Keith Pennypacker. We would like to acknowledge Xiaoyuan Kong, Jordan Heft and Sowndharya Rajavel for technical assistance and James Musso (III) for assistance in initial experiments.


  • Ccl20
  • Cortex
  • Hippocampus
  • Inflammation
  • Lfpi
  • Neural damage
  • Spleen
  • Tbi

ASJC Scopus subject areas

  • General Neuroscience
  • Immunology
  • Neurology
  • Cellular and Molecular Neuroscience


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