Evaluation of CXCL8, CXCL10, CXCL11, CXCL12 and CXCL13 in serum and cerebrospinal fluid of patients with neuroborreliosis.

PURPOSE: Knowledge of the role of chemokines in the inflammation during neuroborreliosis (NB) is limited. We evaluated the pre- and post-treatment concentration of CXCL8, CXCL10, CXCL11, CXCL12, and CXCL13 in serum (s) and cerebrospinal fluid (csf) in patients with NB. RESULTS: There was a statistically significant increase in pre-treatment s CXCL8, CXCL10, CXCL11, CXCL12, CXCL13 and csf CXCL8, CXCL11, CXCL12, CXCL13 in patients with early form of NB. CXCL8, CXCL11, CXCL12 and CXCL13 increase was the highest in csf. After treatment, a significant decrease in csf chemokine levels (except CXCL10) and s levels (except CXCL11) was observed. CONCLUSIONS: CXCL8, CXCL10, CXCL11, CXCL12, CXCL13 are involved in the pathomechanism of NB but their role is different in s and csf. CXCL13 seems to be a good biomarker for NB. In early NB, it may facilitate the diagnosis and monitoring of therapy. However tick-borne encephalitis needs to be excluded as it also increases chemokine concentration. Decrease in all examined chemokines in s and csf after treatment suggests that chemokines may be useful in monitoring response to NB therapy.

[Presence of antibodies against gangliosides among patients with Lyme borreliosis--preliminary study]. / Wystepowanie przeciwcial przeciw gangliozydom w surowicy chorych na borelioze z Lyme--badania wstepne.

UNLABELLED: THE AIM of the study was the evaluation of autoantibody reaction against endogenous gangliosides in the course of Lyme borreliosis. MATERIAL AND METHODS: Antibodies against profile of gangliosides composed of GM1, GM2, GM3, GD1a,GD1b,GT1b, GQ1b were evaluated in serum patients with early disseminated (neuroborreliosis) Lyme disease (n = 16), patients with long lasting serologic response against Borrelia burgdorferi (n = 32) and in healthy subjects (n = 16). Immunoblot test for IgG was used. RESULTS: Antibodies were detected in all evaluated groups. In group of neuroborreliosis (lymphocytic meningitis with cranial nerve invoIvement) there was no essential difference with control group. It was stated in group of forestry workers with serological features of infection B. burgdorferi lasting for years. CONCLUSIONS: Results of the study do not support the thesis of participation of IgG autoantibodies against gangliosides in pathogenesis early disseminated Lyme borreliosis in form of lymphocytic meningitis with cranial nerves paresis. Antibodies against endogenous glicosfingolipides in Lyme borreliosis probably can lead to affecting nervous system (demielinisation and polineuropathy) but probably require long-term immunization, what is suggested by results of examined group of patients with the multi-annual serological features of infection.

[Fractalkine--structure, functions and biological activity]. / Fraktalkina--budowa, wlasnosci i biologiczna rola.

Although chemokines, as chemotactic factors, were already known in 70's of the past century, it was only the progress in molecular biology, genetics and immunology which occurred in the past few years that opened the way to discover new molecules, their chemical structure and biological functions. Fkn (fractalkine, CX3CL1) is a unique chemokine and the only representative of CX3C group. It exists as a membrane-bound and soluble form. It interacts with cells expressing CX3CR1, a G-coupled protein receptor. The polymorphism of CX3CR1 gene modulates Fkn affinity to its receptror, which influences the risk of development and progression of various diseases. Its unique character is determined by its functions. Fkn is not only a chemotactic factor, but it also participates in leukocyte trafficking, adhesion and cytotoxic activities, modulates expression of cytokines, adhesion molecules, free oxygen radicals, iNOS and influences apoptosis. Its elucidation should not only help understanding of molecular events occurring in many autoimmune inflammatory, neoplasmatic diseases, but would allow to use Fkn, its receptor, or anti-Fkn antibodies in treatment of those diseases.