The obligate intracellular bacteria Chlamydia trachomatis causes serious diseases in both humans and animals. Understanding the mechanisms of its interactions with host cells is essential for controlling infections. C. trachomatis can alter the stability of intracellular host proteins in the cells it infects and the consequences for the host and bacterium are not fully understood. We have determined that infection destabilizes and degrades a model host protein independently of mRNA transcript levels and as a result increases the levels of peptides derived from the host protein. These peptides can bind to MHC class I molecules and be presented to CD8+ T cells at the cell surface. We will determine how C. trachomatis alters the host protein stability by determining which chlamydial genes are responsible for this phenotype. We will also determine if enhancing host peptide presentation decreases the efficiency of the host cell to present peptides derived from chlamydial antigens.
There is a need to understand how cells infected with intracellular bacterial pathogens are eliminated from the body. We will determine how the bacteria Chlamydia trachomatis alters the host cell protein levels and how the immune response changes as a result. This information is necessary to understand and combat Chlamydial infections as well as determine how infected cells can be destroyed to prevent the spread of intracellular pathogens.