Pulmonary epithelial CCR3 promotes LPS‐induced lung inflammation by mediating release of IL‐8

Li, Bo; Dong, Chunling; Wang, Guifang; Zheng, Huiru; Wang, Xiangdong; Bai, Chunxue

doi:10.1002/jcp.22577

Cited by 34 publications

(29 citation statements)

References 27 publications

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“…Similar observations have been reported by several other groups of defective eosinophil recruitment in ovalbumin (OVA)-induced skin inflammation and an OVA-induced experimental asthma model (Pope et al, 2005). More recently, an in vivo study examined the role of epithelial CCR3 in an LPS-induced model of lung inflammation (Li et al, 2011). A specific CCR3 inhibitor [SB-328437, methyl (2S)-2-(naphthalene-1-carbonylamino)-3-(4-nitrophenyl)propanoate] at 5 mg/kg was given via intratracheal instillation to mice with LPS-induced acute lung injury.…”

Section: Ccr3supporting

confidence: 83%

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CC Chemokine Receptors and Chronic Inflammation—Therapeutic Opportunities and Pharmacological Challenges

2013

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Section: Ccr3supporting

confidence: 83%

“…Improved histologic scores were also observed in mice treated with SB-328437 inhibitor. Collectively these findings revealed for the first time a potential role for epithelial expressed CCR3 in promoting LPS-induced lung inflammation through mediating the release of IL-8 (Li et al, 2011).…”

Section: Ccr3mentioning

confidence: 72%

CC Chemokine Receptors and Chronic Inflammation—Therapeutic Opportunities and Pharmacological Challenges

2013

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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: 77%

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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“…2B). Our data are consistent with recent studies, which have shown increased levels of IL-8 in lung epithelia as a potent chemoattractant for recruiting inflammatory cells (30,31).…”

Section: Cse Triggers Il-8 Release In Pulmonary Epithelial Cellssupporting

confidence: 93%

Shp2 Plays an Important Role in Acute Cigarette Smoke-Mediated Lung Inflammation

Shen

et al. 2012

The Journal of Immunology

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Cigarette smoke (CS), the major cause of chronic obstructive pulmonary disease, contains a variety of oxidative components that were implicated in the regulation of Src homology domain 2-containing protein tyrosine phosphatase 2 (Shp2) activity. However, the contribution of Shp2 enzyme to chronic obstructive pulmonary disease pathogenesis remains unclear. We investigated the role of Shp2 enzyme in blockading CS-induced pulmonary inflammation. Shp2 levels were assessed in vivo and in vitro. Mice (C57BL/6) or pulmonary epithelial cells (NCI-H292) were exposed to CS or cigarette smoke extract (CSE) to induce acute injury and inflammation. Lungs of smoking mice showed increased levels of Shp2, compared with those of controls. Treatment of lung epithelial cells with CSE showed elevated levels of Shp2 associated with the increased release of IL-8. Selective inhibition or knockdown of Shp2 resulted in decreased IL-8 release in response to CSE treatment in pulmonary epithelial cells. In comparison with CS-exposed wild-type mice, selective inhibition or conditional knockout of Shp2 in lung epithelia reduced IL-8 release and pulmonary inflammation in CS-exposed mice. In vitro biochemical data correlate CSE-mediated IL-8 release with Shp2-regulated epidermal growth factor receptor/Grb-2–associated binders/MAPK signaling. Our data suggest an important role for Shp2 in the pathological alteration associated with CS-mediated inflammation. Shp2 may be a potential target for therapeutic intervention for inflammation in CS-induced pulmonary diseases.

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Pulmonary epithelial CCR3 promotes LPS‐induced lung inflammation by mediating release of IL‐8

Cited by 34 publications

References 27 publications

CC Chemokine Receptors and Chronic Inflammation—Therapeutic Opportunities and Pharmacological Challenges

CC Chemokine Receptors and Chronic Inflammation—Therapeutic Opportunities and Pharmacological Challenges

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

Shp2 Plays an Important Role in Acute Cigarette Smoke-Mediated Lung Inflammation

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