Thanks for asking. I am mildly uncomfortable with the abx apologist role, but will offer the information from the best understanding I have accepting that the connection to MS is more circumstantial than proven and stating that to you up front. IT is not proven of course but it is an interesting theory becasue on many levels it answers the conundrums of MS. The difficulty some researchers have culturing it in MS brains is a problem for the acceptance of this idea as "proven" though there are some serious questions about how the cultures ought to be done in the brain. I speculate here with the caveat that this is not medical advice, but a theoretical model.
Well, since we know that MS whatever it is causes loss of neural tissue I have always assumed it eventually adds up to a noticable atrophy. ie nerves die, the brain is made up of nerves, ergo the brain shrinks (atrophies).
I'll go this way, I'll make the case for CPn infection of neural cells, then make the case for cell death in any CPn affected cells.
Does CPn infect neural tissue:
this reference in in regards to alzheimers disease and it's connection to CPn. I qoute
identified C. pneumoniae within pericytes, microglia, and astroglia. Further immunolabelling studies confirmed the organisms' intracellular presence primarily in areas of neuropathology in the AD brain. Thus, C. pneumoniae is present, viable, and transcriptionally active in areas of neuropathology in the AD brain.
So here is evidence by this author that the cells of the AD brain were infected with CPn I could of course have offered the Vanderbilt University work suggesting it is found in MS brains also, but wanted to use different refs showing the specific neural cells
here <shortened url
> is a reference in relation to mice that shows that intranasal infection with CPn established a persistent (low level but active) infection still present 3 months later, and that with this infection the mice developed CPn in the brain also.
I offer that these suggest that CPn has an affinity for brain cells as well as the blood vessel cells and respiratory cells that EVERYONE accepts everyhwere ( this is just not a debatable thing it's well accepted. the CDC considers CPn an emerging pathogen in atherosclerosis- in other words there's enough evidence it is considered a matter of time until it's proven) The links to asthma are very well established also. We KNOW this pathogen goes into the lungs and can establish a persistent inflammatory infection (it's not acute pneumonia, it is a low level infection that results in permanent colonization and what we call "asthma". Completely proven? not yet, there are still some people producing "no we did not find it papers" but not too many, and mainly 'Gee we treated asthma with abx but did not get better asthma outcomes' sugggesting not that the CPn was not there but that the abx were inadequate) So why not the brain? The above references suggest it can
be the brain. In fact the perivascular nature (near blood vessels) of MS plaques taken along with the affinity CPn has for blood vessels makes one even more suspicious. Here we have a known respiratory pathogen that in SOME people (not everyone has athersclerosis) colonizes the blood vessels resulting in scarring and plaques there. Why not the brain also?
So what happens to a cell infected by CPn?
This easy reference to read enlightens us on the basics of CPn function in
I'll quote from it now;
The chlamydiae are a small group of nonmotile coccoid bacteria that are obligate intracellular parasites of eukaryotic cells. Chlamydial cells are unable to carry out energy metabolism and lack many biosynthetic pathways; therefore they are entirely dependent on the host cell to supply them with ATP and other intermediates. Because of their dependence on host biosynthetic machinery, the chlamydiae were originally thought to be viruses; however, they have a cell wall and contain DNA, RNA, and ribosomes and therefore are now classified as bacteria.
I think it's interesting they were thought to be viruses in the beginning.
Notice that these bugs hide inside the cell and take it over like viruses do.
The cell cannot function as it should then. IT uses all it's energy to do the work of the CPn, not what it is assigned to do (make myelin perhaps? who knows, if a myelin making cell had CPn in it it would not be able to do that, would it?) and it enventually dies- see the table on the quoted reference cell death is at the end.
additionally it would have inflammation
Chlamydial infections are characterized by chronic inflammation
sound like any disease you know?
All chlamydial infections induce IgM, IgG, IgA, and IgE antibodies, but these antibodies do not prevent reinfection. Although secretions from trachomatous eyes contain specific antitrachoma IgG and IgA antibodies, these antibodies do not impede the infection. Moreover, antibodies that bind to C trachomatis elementary bodies do not impair their infectivity in cell cultures
(but there is inflammation as we've already established)
The initial infection usually occurs in childhood, and the active disease eventually appears (mostly by 10 to 15 years of age (and else where in tha article it says that people may develop symptoms years after leaving a CT endemic area .MR)
SO chlamydiae are very slow insidious infections, not one that is a dramatic 'get sick get over it' in a giant reactive frenzy of illness. Nope, this is a quiet slow and stealthy infection in which antibodies do not impair infectivity and which may take years to show scarring and permanent damage.
Cultured chlamydiae are sensitive to interferon, which is produced by cultured cells infected with chlamydiae
hmmmm. how about that. I just threw that in for fun cause it was there.
this reference is a easy to read for the lay person's paper on CPn. If you are interested there is much more in depth material to be read on the subject, this paper is the easy not too deep version/overview.
So, if the cell dies eventually then is not replaced (clearly the infection should this be a factor in MS woud impact other cells nearby and eventually the repairative ability would be impacted as fewer healthy cells are available to do repair.) thus atrophy would occur it seems to me, as well as scarring and inflammation and chronic activation of the immune system. IL-15, gamma interferon, nitric oxide, potnetially glutamate as above on and on. These alterations in the immune system are plausibly nothing more than reactions to CPn as it is known that they are upregulated in CPn infection-----dang I cant get the quote to work mid paper so heres a quote:------------------------------------------------------
C. pneumoniae has also been shown to induce cytokines such as IL-1ß, IL-6, IL-8, IL-12, TNF-, IFN-, and intercellular adhesion molecule-1 in various systems such as human peripheral blood mononuclear cells, alveolar macrophages, and various mouse cell models (11, 16, 19, 22, 39). The possible relationship between C. pneumoniae and atherosclerosis led to many studies of the cytokine effects of infection on human endothelial cells and smooth muscle cells in which IL-6, IL-8, and monocyte chemotactic protein-1 were shown to be readily induced by infection and activation of NF-B was shown to be a requirement for monocyte chemotactic protein-1 gene expression (6, 32, 33, 37, 40). C. pneumoniae infection can also stimulate the production of anti-inflammatory cytokines such as IL-10, which can down regulate the expression of major histocompatibility complex class I molecules (5, 16). Interestingly, C. pneumoniae-infected epithelial cells and peripheral blood mononuclear cells are resistant to apoptosis induced by chemicals or death receptors, and this resistance is at least partially due to IL-10 induction (12, 38). Thus, the overall effect of cytokine release by host cells following C. pneumoniae infection is likely to be determined by complex interactions between beneficial and detrimental cytokine actions End quote----------------------------------------------------------------------
Wow, look at that immune system wide alterations and abnormalities, and note the similarity to MS observed cytokine upregulation Found here http://iai.asm.org/cgi/content/full/71/2/614
You might bring up the notion that older people then should be the ones diagnosed with ms IF CPn plays a role, but not really. Notice that kids are the ones with the trachoma age 10-15 for average, yet while enedemic in those areas, not everyone gets trachoma (the CT eye disease); some people resist it somehow even though as quoted above the presence of antigens does not impair infectivity
this suggest there is some other resistive factor in the individual that is as yet undefined. MS is less common but all that means to me is that this is a less common complication of this illness depending on many factors for everything to fall into place "just right" for it to happen. 95% of polio victims were so mildly ill they did not know they had it. 5% had what we think of as "Polio" A very rare few died.
It is an interesting possibility in the arena of MS though not proven
Thank you for asking