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Chlamydia pneumoniae and MS

Posted: Fri Mar 16, 2007 4:20 am
by milica

Posted: Sat Mar 17, 2007 4:33 pm
by SarahLonglands
Milica, if you type CPn, cytokine and multiple sclerosis into PubMed or even just Google, you now get so much more than just a couple of years ago, including the piece you posted above:
Abstract
Continuous cultures of human lymphocyte- and monocyte-derived cell lines were examined for levels of immunoregulatory cytokines important in resistance to the intracellular opportunistic bacterium Chlamydia pneumoniae (Cp), a ubiquitous pathogen widely disseminated in the population and hypothesized to be involved in chronic inflammatory diseases such as atherosclerosis and neurological diseases like multiple sclerosis and Alzheimer's disease. The results of this study showed that the continuous human T lymphocyte cell line MOLT-4 and the continuous monocytic cell line THP-1 were readily infected by Cp in vitro as shown by immunofluorescence microscopy for Cp lipopolysaccharide (LPS). The 16S rRNA expression determined by real-time RT-PCR increased rapidly after infection of either cell line with these bacteria. The THP-1 cells infected with Cp showed increased levels of the immunoregulatory cytokine IL-12 and also of TNFα and IL-10 compared to cultures stimulated with heat-killed Cp (KCp) or Escherichia coli LPS as a control. Stimulation of MOLT-4 cells with KCp or E. coli LPS also induced the Th1 cytokines IFNγ and IL-12 and the Th2 cytokine IL-10, but infection with viable Cp induced higher Th1 cytokine levels. These results suggest that Cp infection induces a predominant Th1 cytokine profile by T cells, in addition to induction of TNFα by monocytes/macrophages. Such effects are likely involved in antibacterial immunity against Cp infection
and this one:


http://iai.asm.org/cgi/content/abstract/64/11/4872
Chlamydia pneumoniae was able to survive and to multiply in the human monocytic cell line Mono Mac 6. Growth of C. pneumoniae induced production of tumor necrosis factor alpha, interleukin 1beta, and interleukin 6, as well as up-regulation of the CD14 molecule in a time- dependent manner. Infection of monocytic cells and a proinflammatory cytokine response may be important in C. pneumoniae pathogenesis.
Since I have made very great recoveries from multiple sclerosis and my husband, David Wheldon, has from severe arterial disease, just by treatimg for chlamydia pneumoniae, it tends to show that the CPn thing is more than just hot air!

Sarah

Posted: Mon May 21, 2007 10:31 am
by notasperfectasyou
Since I have made very great recoveries from multiple sclerosis and my husband, David Wheldon, has from severe arterial disease, just by treatimg for chlamydia pneumoniae, it tends to show that the CPn thing is more than just hot air!

Sarah
Sarah, this is very interesting. On what basis did you present this to your doctor and did you seek treatment from your neuro or family physician? Meaning, I'm doubtful that we could just walk in to the neuro and ask him to test for this. napay

Posted: Tue May 22, 2007 2:48 am
by SarahLonglands
No, it wasn't my neurologist, he's disowned me. It was my husband who started to treat me, since he is a prescribing doctor. He told my GP to carry on with the repeat prescriptions, because he is the person at the hospital to whom all the GPs come for advice about abx.

A family physician is probably a better person to approach than a neurologist, although there are a few on both sides of the Atlantic now willing to look outside the shackles of autoimmunity. David started to treat me, though, without knowing if I had a CPn infection, since it is a very difficult pathogen to test for. It won't show positive if you are negative but it could well show negative when you are positive. He just thought I looked like I had some sort of chronic infection and the Vanderbilt research indicated CPn as the culprit. When I was tested a few weeks later, I was only marginally positive at a time when the antibodies might well have risen rather than fallen.

Sarah