More research is desperately needed to address the issue of intracellular infections like Chlamydia pneumoniae. Much of the work done in Arthritis, Alzheimers, Heart Disease and MS was done nearly a decade ago (or more in some cases). It is exceedingly difficult to procure research funding in general, but even more-so when a condition is treatable with a generic medication. The antibiotics which address these infections are in fact generic, which precludes pharmaceutical company involvement in studies.
The challenges of eradicating infections like C. pneuomoniae or even C. trachomatis undeniably point in the direction of a vaccine. To date there has been progress made, but a truly effective vaccine is not yet available. There are scientists working on this, like Dr. Wilmore Webley at UMASS, but the research funding is extremely difficult to come by. As seen in the cardiovascular studies on this site, it is likely important to catch the infection before disease progression is too advanced. What better way to address this than to prevent the infection from ever entering our cells?
Human Vaccines and Immunotherapeutics, 2017.
Absrtact- “Chlamydia trachomatis is the leading cause of preventable blindness and the most common bacterial sexually transmitted infection. Remarkable progress in vaccine research over the past six decades has led to the advancement of novel C. trachomatis vaccine candidates into clinical trials. However, many questions regarding the role of specific cellular populations and molecular mechanisms in protective immunity against human C. trachomatis genital tract infections remain unanswered. Biomarkers of vaccine induced protective immunity are elusive in humans, while a cautionary message on the translatability of data obtained from current animal models has emanated from vaccine research and development efforts against other important human pathogens. In this commentary, we highlight recent advances in Chlamydia vaccine development and discuss their implications in the context of a rational approach to the design of a human C. trachomatis vaccine.”
Clinical and Vaccine Immunology, 2017.
Abstract- “Attempts to produce a vaccine to protect against Chlamydia trachomatis-induced trachoma were initiated more than 100 years ago and continued for several decades. Using whole organisms, protective responses were obtained. However, upon exposure to C. trachomatis, disease exacerbation developed in some immunized individuals, precluding the implementation of the vaccine. Evidence of the role of C. trachomatis as a sexually transmitted pathogen started to emerge in the 1960s, and it soon became evident that it can cause acute infections and long-term sequelae in women, men, and newborns. The main focus of this minireview is to summarize recent findings and discuss formulations, including antigens, adjuvants, routes, and delivery systems for immunization, primarily explored in the female mouse model, with the goal of implementing a vaccine against C. trachomatis genital infections.”
Chlamydia trachomatis: The persistent pathogen
Clinical and Vaccine Immunology, 2017.
Abstract- Chlamydia trachomatis is an obligate intracellular bacterium whose only natural host is man. Although asymptomatic in most women, genital tract chlamydial infections are a leading cause of pelvic inflammatory disease, tubal factor infertility and ectopic pregnancy. C. trachomatis has evolved successful mechanisms to avoid destruction by autophagy and the host immune system and persist within host epithelial cells. The intracellular form of this organism, the reticulate body, can enter into a persistent non-replicative but viable state under unfavorable conditions. The infectious form of the organism, the elementary body, is again generated when the immune attack subsides. In its persistent form C. trachomatis ceases to produce its major structural and membrane components, but synthesis of its 60kDa heat shock protein (hsp60) is greatly up-regulated and released from the cell. The immune response to hsp60, perhaps exacerbated by repeated cycles of productive infection and persistence, may promote damage to fallopian tube epithelial cells, scar formation and tubal occlusion. The chlamydial and human hsp60 proteins are very similar, and hsp60 is one of the first proteins produced by newly formed embryos. Thus, development of immunity to epitopes in the chlamydial hsp60 that are also present in the corresponding human hsp60 may increase susceptibility to pregnancy failure in infected women. Delineation of host factors that increase the likelihood that C. trachomatis will avoid immune destruction and survive within host epithelial cells and utilization of this knowledge to design individualized preventative and treatment protocols are needed to more effectively combat infections by this persistent pathogen.