Concentration of TGF-beta1 in the supernatant of peripheral blood mononuclear cells cultures from patients with early disseminated and chronic lyme borreliosis.

 Adv Med Sci. 2007;52:174-8. Concentration of TGF-beta1 in the supernatant of 
peripheral blood mononuclear cells cultures from patients with early disseminated and 
chronic lyme borreliosis. Grygorczuk S, Chmielewski T, Zajkowska J, Swierzbi·ska R, Pancewicz
S, Kondrusik M, Tylewska-Wierzbanowska S, Hermanowska-Szpakowicz T. Department of 
Infectious Diseases and Neuroinfections, Medical University of Bia·ystok, ul. Zurawia 14, 15-540 
Bia·ystok, Poland. neuroin@amb.edu.pl
PURPOSE: The aberrant inflammatory response is probably involved in the pathogenesis of 
chronic Lyme borreliosis, including chronic Lyme arthritis and neuroborreliosis. Transforming 
growth factor-beta 1, TGF-beta1, is an important anti-inflammatory and immunomodulatory
cytokine and its deficient synthesis is linked to exaggerated inflammation and immune response. 
MATERIAL AND METHODS: Peripheral blood mononuclear cells, PBMC, from 25 patients 
with Lyme borreliosis and 6 controls were incubated for 7 days with suspension of Borrelia afzeli, 
B. garinii and B. burgdorferi sensu stricto spirochetes. TGF-beta1 concentration in culture 
supernatants was measured with ELISA. Results were analyzed according to disease duration, 
group I--chronic borreliosis, n=20; group II--early borreliosis, n=5, and clinical form, 
LA--arthritis, NB--neuroborreliosis. RESULTS: TGF-beta1 concentration was increased in 
supernatants of PBMC cultures of patients with early neuroborreliosis, in comparison with 
chronic borreliosis and controls. In chronic, but not in early borreliosis, there was a tendency 
70for decrease of TGF-beta1 synthesis under stimulation with B. burgdorferi spirochetes. 
CONCLUSIONS: Impaired synthesis of TGF-beta1 by mononuclear cells seems to be present 
in patients with chronic forms of Lyme borreliosis when compared to those with early stage of 
the disease. It may be a factor contributing to the persistence of inadequate inflammatory 
response in patients in whom chronic form of the disease develops




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