%0 Journal Article
%T Mannan-binding lectin in cerebrospinal fluid: a leptomeningeal protein
%A Hansotto Reiber
%A Barbara Padilla-Docal
%A Jens Jensenius
%A Alberto Dorta-Contreras
%J Fluids and Barriers of the CNS
%D 2012
%I BioMed Central
%R 10.1186/2045-8118-9-17
%X MBL was assayed in samples of CSF and serum with an ELISA, coated with anti MBL antibodies. Routine parameters such as albumin-, immunoglobulin- CSF/serum quotients, oligoclonal IgG and cell count were used to characterize the patient groups. Groups comprised firstly, control patients without organic brain disease with normal CSF and normal barrier function and secondly, patients without inflammatory diseases but with increased QAlb, i.e. with a blood CSF barrier dysfunction.MBL concentration in CSF was at least five-fold higher than expected for a molecular-size-dependent passage from blood. Secondly, in a QIgM/QAlb quotient diagram (Reibergram) 9/13 cases showed an intrathecal fraction in some cases over 80% of total CSF MBL concentration 3) The smaller inter-individual variation of MBL concentrations in CSF of the control group (CV£¿=£¿66%) compared to the MBL concentrations in serum (CV£¿=£¿146%) indicate an independent source of MBL in CSF. 4) The absolute MBL concentration in CSF increases with increasing QAlb. Among brain-derived proteins in CSF only the leptomeningeal proteins showed a (linear) increase with decreasing CSF flow rate, neuronal and glial proteins are invariant to changes of QAlb.MBL in CSF is predominantly brain-derived and all results pointed to the leptomeningeal cells as the source of the protein. The evaluation of this protein requires the interpretation of its absolute concentrations in CSF as a function of the albumin quotient, QAlb. This recognition of MBL in brain cells opens a new field of discussion about the function of the innate immune response in CNS in cases of acute and chronic neurological diseases.Increased protein concentrations in the cerebrospinal fluid (CSF) of patients with neurological diseases, frequently ascribed to a blood-CSF barrier dysfunction, are due to pathologically-reduced CSF flow rates [1]. This view is based on the molecular diffusion/CSF flow theory [1] which shows that the concentration of a blood-derived pr
%K CSF
%K CSF Flow
%K Protein dynamics
%K Blood-derived proteins
%K Brain-derived proteins
%K Leptomeninges
%K Mannan binding lectin
%K Innate immune system in CNS
%K Blood- CSF barrier function
%U http://www.fluidsbarrierscns.com/content/9/1/17