Duke University immunologist Jörn Coers has warned that chlamydia might become a global epidemic that goes unnoticed. The bacterial illness is the most frequently diagnosed STD in the United States, with the Centers for Disease Control and Prevention (CDC) estimating that 4 million individuals caught it in 2018. Nonetheless, he warns that infections may linger for months even after they haven’t been properly detected. Inflammation brought on by a chlamydia infection may develop fibrosis in the reproductive system. The symptoms are minimal in males, but they may cause ectopic pregnancies and infertility in women.
Coers has spent years studying the resistance mechanisms of Chlamydia trachomatis, the human chlamydia-causing bacteria, in an attempt to accelerate the development of a vaccine against the disease. Coers and his colleagues have recently uncovered a crucial protein that facilitates C. trachomatis’s ability to evade the host immune system.
Chlamydia enters a host cell by slicing off a portion of the host cell’s membrane, creating a vacuole or inclusion in which it may grow and divide without being attacked by the host cell’s immune system. Because of the short time that Chlamydia spends outside of the cell, T cells are able to recognize it and respond by secreting gamma interferon (IFN-), an inflammatory cytokine that causes the infection to be destroyed. Chlamydia is able to evade the immune system for months or even years because to the inclusion.
Coers and his team of researchers have known for a long that C. trachomatis is very adept at avoiding the human immune system, in contrast to the closely related rodent pathogen C. muridarum. Coers found in a 2016 research that C. muridarum inclusions in human cells are destroyed once the protein ubiquitin attaches to them, whereas C. trachomatis inclusions are resistant to ubiquitin binding. They wanted to know how in the latest study, so they did that.
Researchers screened for genetic differences between C. trachomatis strains with and without IFN- while cultivating the bacteria in human epithelial cells. Mutations in the gene encoding a protein called GarD (previously CTL0390) were found in the C. trachomatis strains that were most sensitive to IFN—mediated destruction, suggesting that GarD is essential for C. trachomatis survival. Imaging tests on IFN-γ-resistant C. trachomatis strains demonstrated that GarD prevents ubiquitin binding by inserting itself into the inclusion membrane. When GarD was inactivated, ubiquitin binding was enabled, leaving the bacterium open to attack. Mice, on the other hand, prevent infection from the rodent-infecting C. muridarum by preventing ubiquitin via an other method.
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