Expression of innate immunity receptors in an experimental model of Parkinson’s like disease

The innate immunity receptors CD14 ant toll like receptor 4 (TLR4), that function as lipopolysaccharide (LPS) receptor and LPS signal transmitter into the cell respectively, have been recently related to neuroinflammation processes. Parkinson's disease (PD) is a progressive neurodegenerative disorder in which loss of dopaminergic neurons of substantia nigra (SN) occurs, leading to a drastic reduction of dopamine levels in the striatum. Recently it has been found that, both in patients and in experimental animal models of PD, neuroinflammation appears to be an ubiquitous finding. Upregulation of inflammatory response in the brain is associated with a number of neurodegenerative diseases; moreover recently have been found evidences that systemic infections and inflammation can cause exacerbation of symptoms and drive the progression of neurodegeneration in chronic neurodegenerative diseases. Therefore, the aim of this work was to study a possible role of LPS receptor complex in the pathogenesis of 1-methyl-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced parkinsonism. In particular, we investigated the expression of CD14 and TLR4 in SN and striatum in brains obtained from MPTP treated mice, the most commonly used toxic model of PD in mouse. In particular, the analysis of the gene transcripts and protein expression of CD14 and TLR4 showed an augmented expression of both receptors in the SN of MPTP treated mice in comparison to untreated ones. No significant differences were found in the mRNA and protein levels of both CD14 and TLR4 in the striatum of MPTP treated animals if compared with controls. Overall, these results show that innate immunity receptors CD14 and TLR4 are over expressed in distinct anatomical areas of the brain from mice with MPTP induced Parkinson’s-like disease