Chlamydia is caused by infection with Chlamydia trachomatis bacteria. It can affect both the urogenital tract and the eyes. If untreated, the outcome of both ocular and genital infections can be severe. Ocular Chlamydia infections are the leading cause of infectious blindness, and genital infections can lead to infertility. The health of infants born vaginally to infected mothers is also often severely compromised.
Chlamydia trachomatis bacteria need the essential amino acid, tryptophan, to survive. They are dependent upon their host cells, or the microbiome, to provide it. Genital Chlamydia strains have a unique mechanism to avoid tryptophan starvation. By conditionally making an enzyme called tryptophan synthase, they can use a molecule called indole, which is sometimes made by the genital microbiome, to make tryptophan. Ocular strains make an inactive version of tryptophan synthase or have lost the gene for the enzyme entirely. The goal of this research was to discover why ocular Chlamydia no longer make an active tryptophan synthase.Previous studies have shown that trp de-repressors also kill other pathogenic bacteria, such as Legionella pneumophila and Mycobacterium tuberculosis, via unknown mechanisms.
“It is possible that the mechanism we have described for Chlamydia extends to these other bacteria as well,” notes Aiyar.Next steps include research on the mechanisms to restrict the availability of indole in cells in the genital area, thereby creating conditions under which trp de-repressors will effectively kill genital Chlamydia by forcing the production of ammonia.
The research team also included Dr. Shardulendra Sherchand, a fellow in the Department of Microbiology, Immunology and Parasitology at LSU Health New Orleans School of Medicine.The research was supported by a grant from the National Institutes of Health.