J Infect Dis. 2006 Jan 1;193(1):136-45. Epub 2005 Nov 29. Links
Chlamydia pneumoniae Alters Mildly Oxidized Low-Density Lipoprotein-Induced Cell Death in Human Endothelial Cells, Leading to Necrosis Rather Than Apoptosis.
Nazzal D, Cantero AV, Therville N, Segui B, Negre-Salvayre A, Thomsen M, Benoist H.
INSERM U466, Institut Louis Bugnard, Centre Hospitalier Universitaire Rangueil and Universite Paul Sabatier, Toulouse, France.
Background. Atherosclerosis is characterized by oxidative stress that induces lipid and protein oxidation in the vascular wall. Oxidized low-density lipoproteins (oxLDLs) are present in lesions, and one of their actions is to induce apoptosis or necrosis in vascular cells. A role for Chlamydia pneumoniae in atherosclerosis has been proposed, but the mechanisms involved remain largely unknown.Methods. The in vitro effect of C. pneumoniae infection on apoptosis induced by mildly oxidized LDLs (moxLDLs) in human endothelial cells was studied.Results. Infection inhibited apoptosis, as was demonstrated by a decrease in such apoptotic features as cytochrome c release, caspase activity, 89-kilodalton poly(ADP-ribose) polymerase (PARP) fragment formation, nuclear condensation and fragmentation, and DNA fragmentation. However, the inhibition of apoptosis did not favor cell survival, because infection promoted cell death with necrotic features, as was illustrated by an increase in lactate dehydrogenase release, an enhancement of necrotic cellular morphological characteristics, and generation of low-molecular-mass PARP fragments. The increase in occurrence of necrosis-like cell death was correlated with a strong increase in intracellular reactive oxygen species (ROS) concentration. Vitamin E inhibited ROS production and promoted cell survival, underscoring the involvement of ROS in cell death induced by the combination of C. pneumoniae and moxLDLs.Conclusion. C. pneumoniae infection enhances the inflammatory action of oxLDLs in the vascular wall, leading to cell necrosis rather than apoptosis.
PMID: 16323142 [PubMed - in process]
What it means:
This work was on atherosclerosis yet it may have implications for other celluar infection. Why? Because when looking at the effect of CPn infection it reduced apoptosis (programmed cell death) but increased necrotic cell death due to the presence of infection. This was accompanied by MORE oxidative damage. When we talk about why we take our supplements then we are often talking about reducing oxidative damage. It is also well known that MS is positively influenced by antioxidant treatment. Numerous antioxidative approaches have been tried with various results toward a positive effect. It is also well known that a good part of "autoimmune" MS damage is oxidative in nature. There was a study in Russia about 10 years ago in which antioxidants alone were used to treat MS in monthly IV infusions. People had a 44% reduction in leision load (I'm sorry I can't reference this one any more it's not online anymore, so it's hearsay from me) COuld it be that CPn left it's fingerprints al along?
A little off topic but as an interesting side note, LDN is apparently able to inhibit glutamate pathways and thus reduce oxidative damage thus explaining it's effect in MS ("Low dose naltrexone therapy in multiple sclerosis" Medical Hypotheses, 2005;64(4):721-4, Y.P. Agrawal). Circumstantial evidence pointing to the presence of CPn in traditional medical theories, but interesting none the less. Marie