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Unregulated uptake of low density lipoprotein (LDL) in macrophages is the hallmark of early atherogenic lesions, and  Chlamydia pneumoniae  infection of macrophages induces this process by an unknown mechanism. It was therefore aimed in this study to investigate (i) the role of  C. pneumoniae  in macrophage expression of the lipoprotein lipase (LpL) gene, (ii) the probable role of Ca[2+] influx signals and (iii) the effect of the process on LDL uptake. Lipoprotein lipase mRNA expression and LpL activity in infected RAW-264.7 cells were significantly upregulated. A biphasic Ca[2+] influx signal was observed in infected cells with a moderate influx (303 nM Ca[2+]) favoring optimal LpL gene expression. Also, the antagonists of Ltype Ca[2+] channel in macrophages significantly downregulated LpL gene expression and the biomolecular content of  C. pneumoniae  responsible for the observed events was in part found to be Chlamydia lipopolysaccharide (cLPS). Investigations aimed at determining the specific relevance of Ca[2+]dependent lipoprotein lipase gene expression in  C. pneumoniae -infected macrophages showed that the condition caused enhanced uptake of LDL which was abrogated by Calphostin-C-mediated downregulation of LpL. This discovery of a specialized Ca[2+] influx signal-mediated LpL upregulation in  C. pneumoniae -infected macrophages provides a mechanistic insight into early events involving C. pneumoniae in macrophage foam cell formation resulting from LDL uptake.

Induction of lipoprotein lipase gene expression in Chlamydia pneumoniae-infected macrophages is dependent on Ca2+ signaling events