Coronary Artery Disease (CAD), a major cause of death worldwide, arises due to the interference in blood supply by the deposition of foam cell (fat laden macrophages) in the form of waxy plaque. Chlamydia pneumoniae is the microorganism associated with the respiratory infection and also its role in enhanced inflammation during atherosclerosis has been revealed significantly. Heat Shock Protein 60 (HSP 60) produced by this microorganism is contributing to the inflammation by increasing the expression of inflammatory mediators. Computational study may provide us the insight into the functional significance of this protein in CAD. So, homology based 3D model of chlamydial heat shock protein 60 (cHSP 60) was constructed via Modeller (version 9.12) followed by validation through PROCHECK, Verify 3D, WHAT-IF, ERRAT and PROVE for reliability. Interacting partners of cHSP 60 was identified using STRING server for elucidating possible role of this protein along with interacting partners in plaque formation. Molecular level analysis of the residues involved in the active enzymatic role was identified to study the non-canonical protein-protein interactions. Identification of the B and T cell epitopes provided the base to study the possible immune-modulatory effect of cHSP60. This structure can be utilized for the future drug designing in order to minimize the effect of inflammation.
