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

Guo, Ling; Zheng, Zhong; Ai, Junting; Huang, Bin; Li, Xiang-An

doi:10.1074/jbc.m113.537258

Cited by 37 publications

(37 citation statements)

References 76 publications

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“…As expected, lipopolysaccharide resulted in a significant increase in tissue uptake for all tissues and organs studied, with liver showing the largest uptake overall across time points. These data are consistent with prior reports implicating liver as a primary route of lipopolysaccharide clearance during bacterial sepsis (27,28). Moreover, hepatic myeloid interstitial dendritic cell ectonucleoside triphosphate diphosphohydrolase-1 (CD39) hyporesponsiveness has been reported in mice (29).…”

Section: Discussionsupporting

confidence: 82%

Characterization of ¹¹C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

et al. 2016

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Section: Discussionsupporting

confidence: 82%

Characterization of ¹¹C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

et al. 2016

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“…Recent studies in our laboratory and others demonstrated that SR-BI is a critical protective factor in sepsis (24)(25)(26)(27)(28)(29)(30)(31). SR-BI is most abundantly expressed in adrenal glands, mediating intracellular cholesterol uptake from HDL for corticosteroid synthesis (22,32).…”

mentioning

confidence: 98%

Corticosteroid Therapy Benefits Septic Mice With Adrenal Insufficiency But Harms Septic Mice Without Adrenal Insufficiency*

Guo

Zheng

et al. 2015

Critical Care Medicine

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This study demonstrates that corticosteroid treatment benefits mice with adrenal insufficiency but harms mice without adrenal insufficiency. This study also reveals that inducible corticosteroid has both immunosuppressive and immunopermissive properties, suppressing interleukin-6 production, promoting phagocytosis of immune effector cells, but not inducing peripheral lymphocyte apoptosis. These findings support our hypothesis that corticosteroid is an effective therapy for a subgroup of septic patients with adrenal insufficiency but harms septic patients without adrenal insufficiency and encourage further efforts to test this hypothesis in clinic.

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“…A third mechanism of SR-B1 to promote tumor growth is by the inhibition of acute inflammation [73,74]. SR-B1 has been implicated in several biological processes such as apoptosis [86,87], sepsis [88], binding and internalization of endogenous proteins and pathogens and, in most cases, its signaling pathway is associated with an anti-inflammatory response [73,74]. In the steady state, HDL interaction with SR-B1 inhibits the expression of adhesion molecules on endothelial cells activating the nitric oxide synthase [87].…”

Section: Sr-b1 Promotes Cancer Progression: Sr-b1 Antagonist As Anti-mentioning

confidence: 99%

“…Moreover, microbial by-products are removed via SR-B1. For instance, SR-B1 can bind and internalize LPS without triggering an inflammatory signaling cascade, thus limiting the bioavailability of LPS and dampening the inflammatory response triggered via TLR4 [88]. A similar situation applies to the role of SR-B1 in modulating the response of B cells to CpG oligonucleotides; CpG binding to SR-B1 on the B-cell surface was shown to trigger Ca 2+ entry through TRPC3 channels, leading to dampened cytokine production in response to CpG via TLR9 activation [90].…”

Section: Sr-b1 Promotes Cancer Progression: Sr-b1 Antagonist As Anti-mentioning

confidence: 99%

Exploiting scavenger receptors in cancer immunotherapy: Lessons from CD5 and SR‐B1

et al. 2017

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Scavenger receptors (SRs) are structurally heterogeneous cell surface receptors characterized by their capacity to remove extraneous or modified self-macromolecules from circulation, thus avoiding the accumulation of noxious agents in the extracellular space. This scavenging activity makes SRs important molecules for host defense and homeostasis. In turn, SRs keep the activation of the steady-state immune response in check, and participate as co-receptors in the priming of the effector immune responses when the macromolecules are associated with a threat that might compromise host homeostasis. Therefore, SRs built up sophisticated sensor mechanisms controlling the immune system, which may be exploited to develop novel drugs for cancer immunotherapy. In this review, we focus on the regulation of the anti-tumor immune response by two paradigmatic SRs: the lymphocyte receptor CD5 and the more broadly distributed scavenger receptor class B type 1 (SR-B1). Cancer immunity can be boosted by blockade of SRs working as immune checkpoint inhibitors (CD5) and/or by proper engagement of SRs working as innate danger receptor (SR-B1). Thus, these receptors illustrate both the complexity of targeting SRs in cancer immunotherapy and also the opportunities offered by such an approach. Keywords:Cancer immunotherapy r CD5 r Danger signal r Immune-checkpoint r Scavenger receptor r Scavenger receptor class B type 1 r Toll-like receptors IntroductionThe cancer-immunity cycle can be subverted by tumors at many steps, thus novel therapeutic interventions should be considered for all these possibilities [1]. This cycle starts with the release of tumor antigens and their subsequent capture by professional antigen-presenting cells (mainly, dendritic cells; DCs) for the activation of effector cells of the innate and adaptive immune Correspondence: Dr. Pedro Berraondo e-mail: pberraondol@unav.es system. This is a highly regulated process aimed at maintaining the integrity of the host without inducing significant side effects (e.g., inflammation or autoimmunity) [2]. Tissue homeostasis involves phagocytic processes to remove the excess of native or modified molecules from unviable or stressed cells, as well as from invading microbial agents [3]. Such molecules include lipids, whose intracellular levels should be carefully controlled to sustain proper cell metabolism; endogenous glyco-and lipo-proteins, damaged or * These authors contributed equally to this work. * * These authors are senior co-authors of this work. [4,5]. This phagocytic activity should be coupled to an alarm signal system that awakens other effector mechanisms of the immune system when the tissue damage cannot be controlled by the removal of the endogenous or exogenous molecules. To this end, the immune system has a myriad of specialized soluble or membrane-bound receptors called pattern recognition receptors (PRRs). These PRRs are non-polymorphic, nonclonally distributed, and germ-line encoded receptors recognizing microorganism-associated molecular patterns (MAMPs) -tha...

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

Cited by 37 publications

References 76 publications

Characterization of ¹¹C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

Characterization of ¹¹C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

Corticosteroid Therapy Benefits Septic Mice With Adrenal Insufficiency But Harms Septic Mice Without Adrenal Insufficiency*

Exploiting scavenger receptors in cancer immunotherapy: Lessons from CD5 and SR‐B1

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

Cited by 37 publications

References 76 publications

Characterization of 11C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

Characterization of 11C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

Corticosteroid Therapy Benefits Septic Mice With Adrenal Insufficiency But Harms Septic Mice Without Adrenal Insufficiency*

Exploiting scavenger receptors in cancer immunotherapy: Lessons from CD5 and SR‐B1

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Characterization of ¹¹C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation

Characterization of ¹¹C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation