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New research: Chlamyidia pneumoniae in brain cells

A forum for the discussion of antibiotics as a potential therapy for MS

New research: Chlamyidia pneumoniae in brain cells

Postby Jimk » Tue Apr 25, 2006 3:47 pm

This pre-publication abstract looks to be a splendid piece of laboratory work. It strengthens the case for Cpn infection especially in MS and Alzheimer's, and other brain diseases.

I've underlined two findings which seem to me to have particular importance for MS: (1)Neuronal cells: their sensitivity of neuronal cells to infection, as big producers of EB's, and their particular sensitivity to necrosis (tissue death); and (2) the finding in microglial cells that they resist active replicating infection but appear to be potential reservoirs for persistant Cpn.

Neurobiol Aging. 2006 Apr 16; [Epub ahead of print]

Chlamydia pneumoniae infection of brain cells: An in vitro study.

Boelen E, Steinbusch HW, van der Ven AJ, Grauls G, Bruggeman CA, Stassen FR.

Department of Medical Microbiology, CARIM (Cardiovascular Research Institute Maastricht), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Department of Cellular Neuroscience, EURON (European Graduate School of Neurosciences), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.

Inspired by the suggested associations between neurological diseases and infections, we determined the susceptibility of brain cells to Chlamydia pneumoniae (Cpn). Murine astrocyte (C8D1A), neuronal (NB41A3) and microglial (BV-2) cell lines were inoculated with Cpn. Infection was established by immunofluorescence and real-time PCR at various time points. Productive infection was assessed by transferring medium of infected cells to a detection layer. Finally, apoptosis and necrosis post-infection was determined. Our data demonstrate that the neuronal cell line is highly sensitive to Cpn, produces viable progeny and is prone to die after infection by necrosis. Cpn tropism was similar in an astrocyte cell line, apart from the higher production of extracellular Cpn and less pronounced necrosis. In contrast, the microglial cell line is highly resistant to Cpn as the immunohistochemical signs almost completely disappeared after 24h. Nevertheless, significant Cpn DNA amounts could be detected, suggesting Cpn persistence. Low viable progeny and hardly any necrotic microglial cells were observed. Further research is warranted to determine whether these cell types show the same sensitivity to Cpn in an in vivo setting.

PMID: 16621171 [PubMed - as supplied by publisher]
On Wheldon/Stratton protocal since December '04 for non-MS Cpn: CFS/FMS
Ohio, USA
www.CPn Help.org
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