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

Vishnyakova, Tatyana G.; Kurlander, Roger; Bocharov, Alexander V.; Baranova, Irina N.; Chen, Zhigang; Abu‐Asab, Mones; Tsokos, Maria; Malide, Daniela; Basso, Federica; Remaley, Alan T.; Csákó, György; Eggerman, Thomas L.; Patterson, Amy P.

doi:10.1073/pnas.0602126103

Cited by 60 publications

(72 citation statements)

References 25 publications

(38 reference statements)

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“…SR-BI is capable of binding Gram-negative bacteria and facilitating the uptake of Gram-negative bacteria in vitro (54,68). This raises a possibility that SR-BI might play a role in bacterial clearance in sepsis.…”

Section: Figure 2 Exacerbated Inflammatory Cytokine Production Inmentioning

confidence: 99%

Hepatic Scavenger Receptor BI Protects Against Polymicrobial-induced Sepsis through Promoting LPS Clearance in Mice

Guo

Zheng

Ai³

et al. 2014

Journal of Biological Chemistry

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Background: We utilized Scarb1I179N mice, a model deficient in hepatic SR-BI, to determine the role of hepatic SR-BI in sepsis. Results: Upon cecal ligation and puncture (CLP), Scarb1 I179N mice had a 3.5-fold increase in fatality associated with an impaired LPS clearance. Conclusion: Hepatic SR-BI protects against sepsis through promoting LPS clearance. Significance: Promoting hepatic SR-BI-mediated LPS clearance may provide a therapeutic approach for sepsis.

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Section: Figure 2 Exacerbated Inflammatory Cytokine Production Inmentioning

confidence: 99%

Hepatic Scavenger Receptor BI Protects Against Polymicrobial-induced Sepsis through Promoting LPS Clearance in Mice

Guo

Zheng

Ai³

et al. 2014

Journal of Biological Chemistry

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“…In mice, it is suggested to protect against endotoxemia through its roles in facilitating glucocorticoid production as well as hepatic clearance of LPS. In this respect, SR-BI has been suggested to mediate the binding and uptake of LPS as well as LTA (Vishnyakova et al 2006). Additionally, an alternatively spliced variant, SR-BII, has been shown to bind directly a variety of bacteria suggesting a conserved role of these receptors in pattern recognition and innate immunity (Webb et al 1998).…”

Section: Bacterial Pathogensmentioning

confidence: 99%

Functionality of HDL: Antioxidation and Detoxifying Effects

Karlsson

Kontush

James

2014

High Density Lipoproteins

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“…showed that SR-BI facilitates the uptake of Gram-negative bacteria (27,43), suggesting that SR-BI may play a role in bacteria clearance in sepsis. We collected blood and quantified the Gram-negative bacteria using blood agar culture.…”

Section: Effect Of Sr-bi On Bacteremia During Sepsis-previous In Vitrmentioning

confidence: 99%

“…Effect of SR-BI on LPS Clearance during Sepsis-SR-BI has been shown to bind LPS and enhance LPS intracellular uptake in vitro (27,43), which raises the possibility that SR-BI might facilitate LPS clearance during sepsis. We measured plasma LPS levels in CLP-challenged mice.…”

Section: Effect Of Sr-bi On Bacteremia During Sepsis-previous In Vitrmentioning

confidence: 99%

“…These studies suggest that SR-BI might play a role in sepsis. Interestingly, using in vitro cell culture, Vishnyakova et al (27) reported recently that SR-BI enhances the uptake of Gram-negative bacteria, which raises a possibility that this SR-BI-mediated bacterial uptake may facilitate bacterial infection and therefore play a deleterious role in sepsis. Given the limitations of endotoxemia animal model (28), it is of importance to determine whether and how SR-BI plays a protective role in sepsis.…”

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confidence: 99%

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Scavenger Receptor BI Protects against Septic Death through Its Role in Modulating Inflammatory Response

Guo

Song

et al. 2009

Journal of Biological Chemistry

126

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Sepsis is a leading cause of death that is characterized by uncontrolled inflammatory response. In this study, we report that scavenger receptor BI (SR-BI), a high density lipoprotein receptor, is a critical survival factor of sepsis. We induced sepsis using an established septic animal model, cecal ligation and puncture (CLP). CLP induced 100% fatality in SR-BI-null mice but only 21% fatality in wild type littermates. SR-BI-null mice exhibited aberrant inflammatory responses with delayed inflammatory cytokine generation at the early stage of sepsis and highly elevated inflammatory cytokine production 20 h after CLP treatment. To understand the mechanisms underlying SR-BI protection, we elucidated the effect of macrophage SR-BI on inflammatory cytokine generation. Macrophages from SR-BI-null mice produced significantly higher levels of inflammatory cytokines than those of wild type controls in response to LPS. Importantly, transgenic mice overexpressing SR-BI were more resistant to CLP-induced septic death. Using an HEKBlue TM cell system, we demonstrated that expression of SR-BI suppressed TLR4-mediated NF-B activation. To understand why SR-BI-null mice had a delayed inflammatory response, we elucidated the effect of SR-BI on LPS clearance during sepsis. Compared with wild type controls, SR-BI-null mice had lower plasma LPS levels in the early stage of sepsis and elevated plasma LPS levels 20 h following CLP treatment. In conclusion, our findings demonstrate that SR-BI is a critical protective modulator of sepsis in mice. SR-BI exerts its protective function through its role in modulating inflammatory response in macrophages and facilitating LPS recruitment and clearance.Sepsis is one of the major causes of death that claims over 215,000 lives and costs $16.7 billion per year in America alone (1-4). The death rate from sepsis is high, exceeding 50%, due to poor understanding of the disease (5). Identifying molecules involved in sepsis, especially endogenous protective modulators, is of great importance not only in understanding the mechanisms but also in providing new insights for efficient therapies.Scavenger receptor BI (SR-BI 2 or Scarb1) is a 75-kDa membrane protein expressed in the liver, endothelial cells, macrophages, and steroidogenic tissues (6, 7). It is a well established high density lipoprotein (HDL) receptor. It mediates intracellular uptake of cholesterol ester from HDL, which plays a key role in regulating plasma cholesterol levels and steroidogenesis (8 -11). Mice deficient in SR-BI have a 2-fold increase in plasma cholesterol levels and develop cardiovascular diseases (10,(12)(13)(14)(15)(16). Recent studies reveal that SR-BI is a multifunctional protein. It activates endothelial nitric-oxide synthase in endothelial cells in the presence of HDL (17-20), induces apoptosis in the absence of HDL/endothelial nitric-oxide synthase (21), and protects against nitric oxide (NO)-induced oxidative damage (22). Emerging evidence indicates that specific expression of SR-BI in macrophages provides protecti...

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

Cited by 60 publications

References 25 publications

Hepatic Scavenger Receptor BI Protects Against Polymicrobial-induced Sepsis through Promoting LPS Clearance in Mice

Hepatic Scavenger Receptor BI Protects Against Polymicrobial-induced Sepsis through Promoting LPS Clearance in Mice

Functionality of HDL: Antioxidation and Detoxifying Effects

Scavenger Receptor BI Protects against Septic Death through Its Role in Modulating Inflammatory Response

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