Tenenbaum, T., Adam, R., Eggelnp?hler, I., Matalon, D., Seibt, A., Novotny, G. E.K., Galla, H.-J. and Schroten, H. (2005), Strain-dependent disruption of blood?cerebrospinal fluid barrier by Streptoccocus suis in vitro. FEMS Immunology & Medical Microbiology, 44: 25?34. doi: 10.1016/j.femsim.2004.12.006
Abstract
Streptococcus suis capsular type 2 is an important agent of diseases including meningitis among pigs worldwide, and is also a zoonotic agent. The barrier function of the choroid plexus epithelium that constitutes the structural basis for the blood-cerebrospinal fluid (CSF) barrier has not been elucidated yet in bacterial meningitis. We investigated the influence of various S. suis isolates on the barrier function of cultured porcine choroid plexus epithelial cells with respect to the transepithelial resistance and paracellular [3H]-mannitol flux. Preferentially apical application of S. suis isolates significantly decreased transepithelial resistance and significantly increased paracellular [3H]-mannitol flux in a time-, dose- and strain-dependent manner. Viable S. suis isolates caused cytotoxicity determined by lactate dehydrogenase assay and electron microscopy, whereas S. suis sonicates and UV-inactivated S. suis did not cause cytotoxicity. The observed effects on porcine choroid plexus epithelial cells barrier function could not exclusively be ascribed to known virulence factors of S. suis such as suilysin. In conclusion, S. suis isolates induce loss of blood?cerebrospinal fluid barrier function in an in vitro model. Thus, S. suis may facilitate trafficking of bacteria and leucocytes across the blood?cerebrospinal fluid barrier. The underlying mechanisms for the barrier breakdown have yet to be determined.
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Moreover, monocyte-associated bacteria may enter the CNS via the ?Trojan horse? (bacteria inside cells) [15,16] or ?modified? Trojan horse (bacteria adhered to cells and not phagocytosed) mechanism [12,17], thus being responsible for persistent bacteraemia and disseminated infection. S. suis is likely to survive once it reaches the CSF, because immunoglobulin concentrations in the CSF are low and complement compounds are virtually absent. Thus, S. suis may be responsible for barrier disruption, causing persistent bacteraemia and disseminated infection. Furthermore, autolysis of S. suis (as well as antibiotic treatment) may lead to release of bacterial products that stimulate proinflammatory host factors, thus altering CNS barrier function....
