There is good reason to believe that chronic chlamydial infection may facilitate the growth of cancers in that chlamydiae prevent host cells from killing themselves (apoptosisi). A cell that ‘feels’ itself undergoing malignant change kills itself using the caspase pathway.
Although this news item is not specifically about Cpn, it certainly is in the ball park. Most of us are focused on getting help via the antibiotic protocol for one disease or another, but it may turn out that we are nipping some other problems in the bud...
This is an important paper as it shows that genetic differences influence susceptibility to disease in mycoplasma which is related to CPn in that it also has a cryptic form. This is the perfect counter to t hose w ho would say "CPn can't cause MS because if it did then everyone would have it" While that sounds logical it is dead wrong.
Repeated respiratory Mycoplasma pneumoniae infections in mice: effect of host genetic background.Chu HW, Breed R, Rino JG, Harbeck RJ, Sills MR, Martin RJ.
Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, CO 80206, USA. email@example.com
Respiratory Mycoplasma pneumoniae (Mp) infection is involved in several acute and chronic lung diseases including community-acquired pneumonia, asthma and chronic obstructive pulmonary disease. In the chronic disease process, recurrent respiratory bacterial infections could occur, which may result in varying degrees of symptoms and lung inflammation among patients. However, the lung immunologic differences of host responses to repeated bacterial (i.e., Mp) infections remain to be determined. In the present study, we examined cellular and humoral responses to multiple (up to 3) Mp infections in two genetically different strains of mice (BALB/c and C57BL/6). Mice were intranasally inoculated with one Mp infection, two or three Mp infections (4 weeks apart), and sacrificed on days 3, 7 and 14 after the last Mp infection. Overall, compared to C57BL/6 mice, BALB/c mice demonstrated a significantly higher degree of lung tissue inflammatory cell infiltrate, BAL cellularity, and release of pro-inflammatory cytokines (TNF-alpha, keratinocyte-derived chemokine (KC, a mouse homolog of human chemokine Gro-alpha [CXCL1], and IFN-gamma). In addition, BALB/c mice presented higher levels of serum Mp-specific IgG and IgM, but not IgA. Consistently with lung and serum data, Mp load in BAL and lung specimens was significantly higher in BALB/c mice than C57BL/6 mice. Moreover, repeated Mp infections in BALB/c, but not C57BL/6 mice, produced a greater inflammatory response than did a single Mp infection. Our results suggest that hosts with different genetic background may have different susceptibility to repeated respiratory Mp infections along with inflammatory responses.
I am very excited to present the following article that summarizes Dr. Stratton's recent observations on Chlamydia pneumoniae infection. Putting it together has contributed greatly to my own understanding of Cpn as well as to my appreciation of Dr. Stratton's generosity with his time, and his great depth of knowledge of this area. Thanks to him for his contribution. Jim K Recent observations by Dr Recent observations by Dr. Charles Stratton on Chlamydia Pneumoniae (Cpn) Infection
Cypriane, Your doctor's interest in 'henchman' viruses has prompted me to make an update on my page. Here's the link: http://www.davidwheldon.co.uk/hhv6.html with regards, David
Microb Pathog. 2005 Jul-Aug;39(1-2):19-26.
The load of Chlamydia pneumoniae in the Alzheimer's brain varies with APOE genotype.
Gerard HC, Wildt KL, Whittum-Hudson JA, Lai Z, Ager J, Hudson AP.
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Studies from this laboratory have indicated that the intracellular eubacterial respiratory pathogen Chlamydophila (Chlamydia) pneumoniae is commonly found in brain regions displaying characteristic neuropathology in patients with late-onset Alzheimer's disease (AD) but not in congruent samples from non-AD control individuals. In later work, we provided evidence suggesting that some relationship exists between the APOE epsilon4 gene product and the pathobiology of this organism. In the present report, in situ hybridization analyses indicated that the number of C. pneumoniae-infected cells in affected brain regions of epsilon4-bearing AD patients was higher overall than that in congruent brain regions from AD patients lacking that allele. Quantitative real-time PCR analyses of AD brain tissue samples demonstrated that actual bacterial burden in those samples varied over several orders of magnitude, but that samples from epsilon4-bearing patients did have significantly higher bacterial loads than did congruent samples from patients without the allele (ANOVA, p<0.05). These results may explain in part the observations that epsilon4-bearing individuals have a higher risk of developing AD, and that such patients progress more rapidly to cognitive dysfunction than do individuals lacking this allele.