NDLI: CLA-1 and its splicing variant CLA-2 mediate bacterial adhesion and cytosolic bacterial invasion in mammalian cells

Content Provider	PubMed Central
Author	Vishnyakova, Tatyana G. Kurlander, Roger Bocharov, Alexander V. Baranova, Irina N. Chen, Zhigang Abu-asab, Mones S. Maria, Tsokos Daniela, Malide Basso, Federica Remaley, Alan Gyorgy, Csako Eggerman, Thomas L. Patterson, Amy P.
Copyright Year	2006
Abstract	CD36 and LIMPII analog 1, CLA-1, and its splicing variant, CLA-2 (SR-BI and SR-BII in rodents), are human high density lipoprotein receptors with an identical extracellular domain which binds a spectrum of ligands including bacterial cell wall components. In this study, CLA-1- and CLA-2-stably transfected HeLa and HEK293 cells demonstrated several-fold increases in the uptake of various bacteria over mock-transfected cells. All bacteria tested, including both Gram-negatives (Escherichia coli K12, K1 and Salmonella typhimurium) and Gram-positives (Staphylococcus aureus and Listeria monocytogenes), demonstrated various degrees of lower uptake in control cells. This result is consistent with the presence of high-density lipoprotein-receptor-independent bacterial uptake that is enhanced by CLA-1/CLA-2 overexpression. Bacterial lipopolysaccharides, lipoteichoic acid, and synthetic amphipathic helical peptides (L-37pA and D-37pA) competed with E. coli K12 for CLA-1 and CLA-2 binding. Transmission electron microscopy and confocal microscopy revealed cytosolic accumulation of bacteria in CLA-1/CLA-2-overexpressing HeLa cells. The antibiotic protection assay confirmed that E. coli K12 was able to survive and replicate intracellularly in CLA-1- and CLA-2-overexpressing HeLa, but both L-37pA and D-37pA prevented E. coli K12 invasion. Peritoneal macrophages isolated from SR-BI/BII-knockout mice demonstrated a 30% decrease in bacterial uptake when compared with macrophages from normal mice. Knockout macrophages were also characterized by decreased bacterial cytosolic invasion, ubiquitination, and proteasome mobilization while retaining bacterial lysosomal accumulation. These results indicate that, by facilitating bacterial adhesion and cytosolic invasion, CLA-1 and CLA-2 may play an important role in infection and sepsis.
Related Links	http://dx.doi.org/10.1073/pnas.0602126103
Starting Page	16888
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	45
Volume Number	103
Language	English
Publisher	National Academy of Sciences
Publisher Date	2006-11-07
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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