A recent article in PNAS indicates that Chlamydophila pneumoniae phospholipase D (CpPLD) is a major C. pneumoniae factor able to induce Th17 immune response in atherosclerosis.
It is known that atherosclerosis/carotid disease pathology and symptomatology might be causally related to the presence of Chlamydophila pneumoniae.
Phospholipases (PLs), a heterogeneous group of proteins with enzymatic activity, able to hydrolize phospholipids, are likely to be involved in membrane disruption occurring in host cell invasion, and bacterial and fungal virulence.
In the PNAS study, Marisa Benagiano and colleagues from the Azienda Ospedaliero-Universitaria Careggi Firenze, Florence, Italy report that CpPLD-specific T cells are present within the atherosclerotic lesion that exhibit a Th17 cytokine pattern. Furthermore, they show that CpPLD-specific T cells promote the production of tissue factor (TF) and metalloproteinase-9 (MMP-9), factors known to be involved in plaque rupture and athero-trombotic events.
The authors also demonstrate that CpPLD was able to activate monocytes by binding Toll-like receptor 4, leading to the production of IL-23, IL-6, IL-1β, TGF-β, and CCL-20, molecules critical for the generation, differentiation, and maintenance of Th17 cells.
Thus, the study is perhaps the first to suggest that the CpPLD-related Th17 pathway may represent a new therapeutic target for the prevention/treatment of atherosclerosis.
Source: Proc Natl Acad Sci U S A, 2012; 109:1222-7. doi: 10.1073/pnas.1111833109. Epub 2012 Jan 9.