The Impact of TGF-ß, GM-CSF and Antibody Response for Diagnosis as well as Etiopathology of Lyme Disease

Abstract

In this study the pathogenesis of lyme disease was investigated in vivo by means of the wild-type mouse strains C3H/HeN and FVB/N as well as transgenic mouse strains, which are tissue specific modulated in their TGF-ß or GM-CSF (granulocyte-monocyte colony stimulating factor) activity and sensitivity. The mice were infected intradermally with B. burgdorferi. Progression of lyme disease was monitored using a number of diagnostic tests (recultivation of borrelia from tissue, ELISA, Western blot, histologic analysis). The study confirms the mouse strain FVB/N WT (wild type) to be susceptible to B. burgdorferi infections and that this represents a suitable in vivo model for investigations concerning the progression of a B. burgdorferi infection. We further demonstrate transgenic modification of TGF-ß or GM-CSF activity, and sensitivity in T cells and epithelium respectively, do not affect the pathogenesis of lyme disease. Our data show a positive linear correlation between antibody response and the severity of arthritic processes due to B. burgdorferi infection. Determination of the increase in antibody titer in sera of infected organisms therefore might be a useful tool to predict the progression of inflammatory processes in the course of lyme disease.