Role of CD14 in a Mouse Model of Acute Lung Inflammation Induced by Different Lipopolysaccharide Chemotypes

Anas, Adam A.; Hovius, Joppe W.; Veer, Cornelis van ’t; Poll, Tom van der; Vos, Alex F. de

doi:10.1371/journal.pone.0010183

Cited by 14 publications

(20 citation statements)

References 32 publications

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“…The concentration of lipopolysaccharide chosen was consistent with previous work. 37,38 As expected, a basal concentration of cytokines in the supernatant was detected in control cells. 39 Remarkably, no effect of treatment with nanoparticles, regardless of their physicochemical surface properties, was observed, with IL-8 and IL-6 concentrations in the supernatant not being different between the treatment groups.…”

supporting

confidence: 79%

Influence of surface charge on the potential toxicity of PLGA nanoparticles towards Calu-3 cells

Mura¹,

Hillaireau²,

Nicolas³

et al. 2011

IJN

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Background Because of the described hazards related to inhalation of manufactured nanoparticles, we investigated the lung toxicity of biodegradable poly (lactide-co-glycolide) (PLGA) nanoparticles displaying various surface properties on human bronchial Calu-3 cells. Methods Positively and negatively charged as well as neutral nanoparticles were tailored by coating their surface with chitosan, Poloxamer, or poly (vinyl alcohol), respectively. Nanoparticles were characterized in terms of size, zeta potential, and surface chemical composition, confirming modifications provided by hydrophilic polymers. Results Although nanoparticle internalization by lung cells was clearly demonstrated, the cytotoxicity of the nanoparticles was very limited, with an absence of inflammatory response, regardless of the surface properties of the PLGA nanoparticles. Conclusion These in vitro results highlight the safety of biodegradable PLGA nanoparticles in the bronchial epithelium and provide initial data on their potential effects and the risks associated with their use as nanomedicines.

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supporting

confidence: 79%

Influence of surface charge on the potential toxicity of PLGA nanoparticles towards Calu-3 cells

Mura¹,

Hillaireau²,

Nicolas³

et al. 2011

IJN

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“…Lung inflammation was induced in mice as described previously [ 31 ]. In short, mice were lightly anesthetized by inhalation of isoflurane, after which 50 μl of LPS of B .…”

Section: Methodsmentioning

confidence: 99%

Differential Toll-Like Receptor-Signalling of Burkholderia pseudomallei Lipopolysaccharide in Murine and Human Models

et al. 2015

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The Gram-negative bacterium Burkholderia pseudomallei causes melioidosis and is a CDC category B bioterrorism agent. Toll-like receptor (TLR)-2 impairs host defense during pulmonary B.pseudomallei infection while TLR4 only has limited impact. We investigated the role of TLRs in B.pseudomallei-lipopolysaccharide (LPS) induced inflammation. Purified B.pseudomallei-LPS activated only TLR2-transfected-HEK-cells during short stimulation but both HEK-TLR2 and HEK-TLR4-cells after 24 h. In human blood, an additive effect of TLR2 on TLR4-mediated signalling induced by B.pseudomallei-LPS was observed. In contrast, murine peritoneal macrophages recognized B.pseudomallei-LPS solely through TLR4. Intranasal inoculation of B.pseudomallei-LPS showed that both TLR4-knockout(-/-) and TLR2x4-/-, but not TLR2-/- mice, displayed diminished cytokine responses and neutrophil influx compared to wild-type controls. These data suggest that B.pseudomallei-LPS signalling occurs solely through murine TLR4, while in human models TLR2 plays an additional role, highlighting important differences between specificity of human and murine models that may have important consequences for B.pseudomallei-LPS sensing by TLRs and subsequent susceptibility to melioidosis.

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“…By interacting with host cell receptors, such as monocyte/macrophage CD14 and toll-like receptor 4 (TLR4), LPS induces proinflammatory mediators e.g. eicosanoids and cytokines, such as tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), IL-6 [10]. Cytokines are produced by several cell types, including neutrophils, monocytes, macrophages, lymphocytes, and endothelial cells [7].…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways

Holloway

Gillespie

Becker

et al. 2016

Vascular Pharmacology

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Sepsis is often characterized by an acute brain inflammation and dysfunction, which is associated with increased morbidity and mortality worldwide. Preventing cerebral leukocyte recruitment may provide the key to halt progression of systemic inflammation to the brain. Here we investigated the influence of the anti-inflammatory and anti-oxidant compound, sulforaphane (SFN) on lipopolysachharide (LPS)-induced cellular interactions in the brain. The inflammatory response elicited by LPS was blunted by SFN administration (5 and 50 mg/Kg i.p.) 24 h prior to LPS treatment in WT animals, as visualized and quantified using intravital microscopy. This protective effect of SFN was lost in Nrf2-KO mice at the lower dose tested, however 50 mg/Kg SFN revealed a partial effect, suggesting SFN works in part independently of Nrf2 activity. In vitro, SFN reduced neutrophil recruitment to human brain endothelial cells via a down regulation of E-selectin and vascular cell adhesion molecule 1 (VCAM-1). Our data confirm a fundamental dose-dependent role of SFN in limiting cerebral inflammation. Furthermore, our data demonstrate that not only is Nrf2 in part essential in mediating these neuroprotective effects, but they occur via down-regulation of E-selectin and VCAM-1. In conclusion, SFN may provide a useful therapeutic drug to reduce cerebral inflammation in sepsis.

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Role of CD14 in a Mouse Model of Acute Lung Inflammation Induced by Different Lipopolysaccharide Chemotypes

Cited by 14 publications

References 32 publications

Influence of surface charge on the potential toxicity of PLGA nanoparticles towards Calu-3 cells

Influence of surface charge on the potential toxicity of PLGA nanoparticles towards Calu-3 cells

Differential Toll-Like Receptor-Signalling of Burkholderia pseudomallei Lipopolysaccharide in Murine and Human Models

Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways

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