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Reactivation of Chlamydia pneumoniae infection in mice by cortisone treatment.
K Laitinen, A L Laurila, M Leinonen, and P Saikku
National Public Health Institute, Helsinki, Finland.

Infect Immun. 1996 April; 64(4): 1488–1490

Reactivation of Chlamydia pneumoniae infection was studied by inducing immunosuppression by cortisone acetate treatment given every other day for 14 days in intranasally infected NIH/s mice. The treatment started 2 or 4 weeks after primary infection, when no C. pneumoniae was detected. C. pneumoniae could be recovered from the lung cultures on days 7 and 9 in 10 and 60% of the mice, respectively, when cortisone treatment was begun 30 days after infection. These results confirm the persistent nature of C. pneumoniae infection.

Med Hypotheses. 2007;68(2):278-80. Epub 2006 Oct 11.
Role of Tryptophan supplementation in the treatment of Chlamydia.Singla M.
Department of Pediatrics, University of Illinois, 840 S. Wood St., CSB Chicago, IL 60612, USA. msingla@uic.edu

In some recent correspondance with Dr. Stratton at Vanderbilt University, he kindly answered some of the questions which had formed as I've understood more about the combination antibiotic protocol and about Cpn. From the patient's perspective I wanted to correlate some observations about treatment reactions with his deeper understanding about the biology of the Cpn. I'll list the questions I put to him, and then his generous response below.1.  In an earlier correspondance you had mentioned pulsing the INH band metronidazole together.         * Why do that rather than take it continuously?        * My understanding is that INH is one of the anti-replicatives, and the point is to use these continuously to drive the bug into the cryptic phase where it will be obliterated by the flagyl/tini. Does INH act differently than the other antireplicatives?        * I also understood that we use a dual abx to prevent developing resistance. Why can we use INH alone without developing resistance? 

Vestn Ross Akad Med Nauk. 2005;(2):17-22. Related Articles, Links

[The immune system, atherosclerosis and persisting infection]

[Article in Russian]

Pigarevskii PV, Mal'tseva SV, Seliverstova VG.

The paper demonstrates that lymph nodes situated in the vicinity of magistral blood vessels are the source of immune and inflammatory response to LDL as the main pathogenetic factor in atherosclerosis. The activation of T-cell-mediated immunity takes place in them at the very early stages of the disease, resulting in forming of CD4+T-lymphocytes, activated mononuclear cells and immunostabilizing B-lymphocytes. The cell changes in lymph nodes correlate with the severity of atherosclerotic lesions in the vessel intima and closely reflect the peculiarities of immune inflammation development in fatty streaks and atherosclerotic plaques in human atherogenesis. A paradoxical reaction was observed in cases with Chlamydia pneumoniae found in the wall of aorta and paraaortal lymph nodes. No evident immune response on the part of immunocompetent cells took place, but, on the contrary, the function of mononuclear cells, including T-lymphocytes, was suppressed. This phenomenon may be explained by the fact that intracellular localization of Chlamydia pneumoniae hides it from immune system control or by the possible microorganism capability of direct immunosuppressive influence on lymphoid cells both in the blood vessel wall and in regional lymph nodes.