MediTest
Submitted by Jim K on Sun, 2006-04-23 09:10

This pre-publication abstract is a remarkable piece of laboratory work. It strengthens the case for Cpn infection especially in MS and Alzheimer's, and other brain diseases. The two findings I've underlined which seem to have espeical importance is (1) the 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]

Holy cow! finally! Thank you for htis we have ot get it in the research pages of course.....
marie

On CAP since Sept '05 for MS, RA, Asthma, sciatica. EDSS at start 5.5.(early cane) Now 6 (cane full time) Originally on: Doxy 200, Azith 3x week, Tini cont. over summer '07, Revamp of protocol in Summer '08 by Stratton due to functional loss; clarithro

I'm not sure I understand all the detail, but it's great that more research is being carried out on Cpn and brain cells and showing what we know is true.  Michele: Spokesperson for Ella on Wheldon protocol since 17th March 2006 from Sussex, UK

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

Evidence.  I just LOVE evidence.  Thanks for posting this!The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems.  Mohandas Gandhi

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi