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Bacterial LPS Influences Receptor Activator NF Kappa B and Fractalkine Receptors Expression In Arterial Smooth Muscle Cells Derived From Limbs Amputated For Peripheral Arterial Disease
Author(s) -
Zamin Rasheeda,
Norman Paul,
Filgueira Luis
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.526.4
Subject(s) - cx3cr1 , receptor , lipopolysaccharide , flow cytometry , biology , pathology , medicine , immunology , chemokine , chemokine receptor
Bacterial infections may trigger peripheral arterial disease (PAD) through their lipopolysaccharide (LPS) molecules by changing expression of CX3CR1 and RANK, which are associated with atherosclerosis and arterial calcification. Arterial samples were harvested from 9 patients undergoing lower limb amputation for PAD. We initially identified the presence of bacterial (chlamydia and mycoplasm) antigens/LPS and inflammatory markers (CX3CR1 and RANK) in tissue samples using immunofluorescence staining. Secondly, the effect of LPS was tested in vitro (10ng/ml) using proliferating primary human arterial smooth muscle cells (pASMC). The expression of CX3CR1 and RANK post‐activation, with or without LPS, was assessed on 2 different pASMC cell lines using flow cytometry. All samples showed evidence of infection. RANK and CX3CR1 were expressed in all arterial samples. Flow data showed that LPS down‐regulated RANK expression on pASMC (0.52–0.62 reduction in standardized mean intensity), while CX3CR1 expression was up regulated (1.27–1.75 increment) compared to non‐activated pASMC. Our studies suggest that LPS may induce inflammatory changes seen in PAD lesions. Down‐regulation of RANK may play a role in calcification of infected arteries, while up regulation of CX3CR1 may contribute to the atherosclerotic changes.