Missense mutations in the Leucine Rich Repeat Kinase 2 (LRRK2) gene result in late-onset Parkinson’s disease (PD). The incomplete penetrance of LRRK2 mutations in humans and LRRK2 murine models of PD suggests that the disease may result from a complex interplay of genetic predispositions and persistent exogenous insults. To examine molecular pathways that might be affected by mutant LRRK2 in peripheral leukocytes, we performed mass spectrometry analysis (tandem mass tagging, TMT) on peripheral blood mononuclear cells obtained from intact and acute LPS-challenged WT and R1441G mutant mice.