Here is ariticle co authored by M Hammerschlag on CPn in ashthma and atherosclerosis discussing the culturing of it

the above is clickable abstract :

Persistent infections with Chlamydia pneumoniae have been implicated in the development of chronic diseases, such as atherosclerosis and asthma. Although azithromycin, clarithromycin, and levofloxacin are frequently used for the treatment of respiratory C. pneumoniae infections, little is known about the dose and duration of therapy needed to treat a putative chronic C. pneumoniae infection. In this study, we investigated the effect of prolonged treatment with azithromycin, clarithromycin, or levofloxacin on the viability of C. pneumoniae and cytokineⁱ production in an in vitro model of continuous infection. We found that a 30-day treatment with azithromycin, clarithromycin, and levofloxacin at concentrations comparable to those achieved in the pulmonary epithelial lining fluid reduced but did not eliminate C. pneumoniae in continuously infected HEp-2 cells. All three antibiotics decreased levels of interleukin-6 (IL-6) and IL-8 in HEp-2 cells, but this effect appeared to be secondary to the antichlamydial activity, as the cytokine levels correlated with the concentrations of microorganisms. The levels of IL-1β, IL-4, IL-10, tumor necrosis factor alphaⁱ, and gamma interferon were too low to assess the effect of antibiotics. These data suggest that the dosage and duration of antibiotic therapy currently being used may not be sufficient to eradicate a putative chronic C. pneumoniae infection.

I have culled from Mitchell & Stratton patent #6,884,784 an exhaustive list of diseasesⁱ where Cpnⁱ has been implicated as a possible cause or co-factor (reference: Mitchell & Stratton patent #6,884,784):

Editorial comment: Strong findings from their research. If you have any of these it suggests to me that at least an empirical course of the combination antibiotic therapy is strongly indicated, with or without serologyⁱ.

Multiple Sclerosis (MSⁱ)
Rheumatoid Arthritis (RA)
Inflammatory Bowel Diseaseⁱ (IBD)
Interstitial Cystitisⁱ (IC)
Fibromyalgiaⁱ (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndromeⁱ (CFSⁱ).

It has been noted that most users of the combination antibiotic protocolsⁱ commenting here have not been on the treatment long enough to give a big enough pool of reports to feel assured of the efficacy of this approach. I had asked Drs. Stratton, Wheldon, and Powell to perhaps tally up at least some basic numbers from their case experience to help us out with this problem, but this would involve problems of confidentiality and use of private data, etc.  

Then, I suddenly realized that we already have a good list of anecdotal reports of response to treatment reported data available to us... right in the Stratton/Mitchell patent materials! (Sheepish, embarrassed grin). So I took it as a project to summarize this data by disease treated. Occasionally I have used the exact wording from the patent materials as they were brief and descriptive. We have the full text referenced in our treatment and links if you want to see more detail.

All reported had with positive serologyⁱ for Cpnⁱ using the highly sensitive tests developed by Stratton/Mitchell. I left out a few whose diagnosis was not clear to me, you can see them in the patent materials #6,884,784
All on some form of the combination antibiotic therapy protocol.

David Wheldonⁱ offered this citation as another good reason to use alpha-lipoic acid as a supplement on the protocolsⁱ here. This study notes it's anti-inflammatory effect through T-cell inhibition. Although this study is orienting from the autoimmune model of MS, David notes " I read this as positive, if you are taking antibioticsⁱ. While killing the organisms you want as little inflammationⁱ as possible."

Alpha lipoic acid inhibits human T-cell migration: implications for multiple sclerosis.

Ann Neurol. 2003 Dec;54(6):828-31.
Chlamydia pneumoniae and the risk for exacerbation in multiple sclerosis patients.

Buljevac D, Verkooyen RP, Jacobs BC, Hop W, van der Zwaan LA, van Doorn PA, Hintzen RQ.

Department of Neurology, Erasmus MC, 3000 CA Rotterdam, The Netherlands.

In this prospective study of 73 relapsing remitting multiple sclerosis patients followed up for a mean of 1.7 years, the relation was tested between serologically defined Chlamydia pneumoniae (CP) infection periods and exacerbation rate. Episodes of serologically defined CP infections were observed in a subgroup, and these episodes were associated with increased risk for exacerbation. CP polymerase chain reaction was positive in most of the CP seropositive patients. No correlation was found between the anti-CP antibody increase and titers of control antibodies.

Epidemiology. 2003 Mar;14(2):141-7. Related Articles, Links

Comment in:
Epidemiology. 2003 Mar;14(2):133-4.

Infection with Chlamydia pneumoniae and risk of multiple sclerosis.

Munger KL, Peeling RW, Hernan MA, Chasan-Taber L, Olek MJ, Hankinson SE, Hunter D, Ascherio A.

Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA.

BACKGROUND: Chlamydia pneumoniae (Cpnⁱ) has been proposed as a possible etiologic agent for multiple sclerosis (MSⁱ), but results of previous studies are conflicting. METHODS: Using a nested case-control design, we examined the association between Cpn infection and MS in the Nurses' Health Study (NHS) and Nurses' Health Study II (NHS II) cohorts. Among 32,826 women in the NHS and 29,722 women in the NHS II with blood samples, 141 incident cases of definite or probable MS were documented. Each case was matched to two healthy controls on year of birth and NHS cohort. Serum samples were tested for the presence of Cpn-specific immunoglobin G antibodies using microimmunofluorescence. RESULTS: Cpn immunoglobin G seropositivity was positively associated with risk of MS (odds ratio [OR] = 1.7; 95% confidence interval [CI] = 1.1-2.7). This association did not change after adjusting for age at blood collection, ancestry, latitude of residence at birth, and smoking (OR = 1.9; CI = 1.1-3.1). Seropositivity for Cpn was only moderately associated with risk of relapsing-remitting MS (OR = 1.7; CI = 0.9-3.2), but it was strongly associated with risk of progressive MS (OR = 7.3; CI = 1.4-37.2). Geometric mean titers of Cpn-specific immunoglobin G antibody were similar in women with relapsing-remitting MS as compared with matched controls (44 vs 39), but they were elevated in women with progressive MS (99 vs 40). CONCLUSIONS: These results support a positive association between Cpn infection and progressive MS.

What follows is a study sent to us by Dr Wheldon. Below I have pasted his comment about it...Marie
Med Microbiol Immunol (Berl). 2004 Nov;193(4):163-71. Epub 2003 Oct 31.

Expression and localization of type III secretion-related proteins of Chlamydia pneumoniae.

Lugert R, Kuhns M, Polch T, Gross U.

Department of Bacteriology, University of Gottingen, Kreuzbergring 57, 37075 Gottingen, Germany.

The entire developmental cycle of the obligate intracellularⁱ bacteria Chlamydia pneumoniae takes place within the inclusion body. As many gram negative bacteria, Chlamydia possess a type III-secretion system (TTSS), which allows them to target effector molecules into the host cell. The expression and localization of several proteins constituting the TTSS apparatus and of proteins supposed to be secreted by the TTSS have been investigated. For the TTSS-constituting proteins, we selected representatives such as YscN (ATPase), LcrE (putative "lid" of the TTSS) and LcrH1 (postulated to be a chaperone). Furthermore, we focused on the putative effector proteins IncA, IncB, IncC, Cpn0809 and Cpn1020. Expression of these proteins was detected by reverse transcriptase-PCRⁱ followed by immunoblot analysis using antisera that were generated against the corresponding recombinant proteins. Thereby, expression could be detected on the RNA and/or protein level. Intracellular localization of proteins under investigation was determined by immunofluorescence assays using the respective antisera. YscN was shown to be distributed equally throughout the inclusion body, whereas LcrE gave a more prominent staining of the inclusion membrane. IncA was detected mainly on the membrane of the inclusion body, whereas IncB and IncC were shown to be located within the inclusion. Immunofluorescence assays with antisera raised against Cpn0809 and Cpn1020 showed completely different labeling. Signals corresponding to Cpn0809 and Cpn1020 were distributed within the host cell rather than inside the inclusions. Taken together, the different localization patterns of the effector proteins indicate differences in function and interplay with the host cell.

Am J Respir Cell Mol Biol. 2005 Dec 9; [Epub ahead of print]

Mechanisms of Chlamydophila pneumoniae Mediated GM-CSF Release in Human Bronchial Epithelial Cells.

Krull M, Bockstaller P, Wuppermann FN, Klucken AC, Muhling J, Schmeck B, Seybold J, Walter C, Maass M, Rosseau S, Hegemann JH, Suttorp N, Hippenstiel S.

Department of Internal Medicine/Infectious Diseasesⁱ, Charite, Universitatsmedizin, Berlin, Germany.

Chlamydophila pneumoniae is an important respiratory pathogen. In this study we characterized C. pneumoniae strain TW183-mediated activation of human small airway epithelial cells (SAEC) and the bronchial epithelial cell line BEAS-2B and demonstrated time-dependent secretion of granulocyte macrophage colony-stimulating factor (GM-CSF) upon stimulation. TW183 activated p38 mitogen activated protein kinase (MAPK) in epithelial cells. Kinase inhibition by SB202190 blocked chlamydia mediated GM-CSF release on mRNA- and protein-level. In addition, the chemical inhibitor as well as dominant negative mutants of p38 MAPK isoforms p38alpha, beta2, and gamma inhibited C. pneumoniae-related NF-kappaB activation. In contrast, blocking of MAPK ERK, c-Jun kinase/JNK or PI-3 Kinase showed no effect on Chlamydia related epithelial cell GM-CSF release. UV-inactivated pathogens as compared to viable bacteria induced a smaller GM-CSF -release suggesting that viable Chlamydia were only partly required for a full effect. Presence of an anti-chlamydial outer membrane protein-A (Omp-A) antibody reduced and addition of recombinant heat-shock protein 60 from C. pneumoniae (cHsp60, GroEL-1) enhanced GM-CSF -release suggesting a role of these proteins in epithelial cell activation. Our data demonstrate that C. pneumoniae triggers an early proinflammatory signaling cascade involving p38 MAPK dependent NF-kappaB activation resulting in subsequent GM-CSF release. C. pneumoniae-induced epithelial cytokineⁱ liberation may contribute significantly to inflammatory airway diseases like chronic obstructive pulmonary disease (COPD) or bronchial asthma.