Vascular cell adhesion molecule-l expression in the renal interstitium of diabetic KKAy mice

Ina, Keisuke; Kitamura, Hirokazu; Okeda, Toshimitsu; Nagai, Kaoruko; Liu, Zhong Y; Matsuda, Midori; Fujikura, Yoshihisa

doi:10.1016/s0168-8227(99)00011-x

Cited by 34 publications

(23 citation statements)

References 28 publications

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“…Of interest, we observed expression of VCAM-1 in inflammatory cells infiltrating the lung interstitium of OVAtreated mice. Prior reports have noted VCAM-1 expression in vascular dendritic cells present in human atherosclerotic plaques (35) and in lymphocytes and monocytes invading the renal interstitium of diabetic KKAy mice (36).…”

Section: Discussionmentioning

confidence: 89%

Soluble IL-4 Receptor Inhibits Airway Inflammation Following Allergen Challenge in a Mouse Model of Asthma

Henderson¹,

Emil

Maliszewski³

2000

The Journal of Immunology

149

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In vitro and in vivo studies, in both animal models and human asthmatics, have implicated IL-4 as an important inflammatory mediator in asthma. In a murine asthma model, we examined the anti-inflammatory activities of soluble IL-4R (sIL-4R). In this model, mice sensitized to OVA by i.p. and intranasal (i.n.) routes are challenged with the allergen by i.n. administration. The OVA challenge elicits an eosinophil infiltration into the lungs, with widespread mucus occlusion of the airways, and results in bronchial hyperreactivity. sIL-4R (0.1–100 μg) was administered by either i.n. or i.p. routes before OVA challenge in OVA-sensitized mice. Both blood and bronchoalveolar lavage fluid levels of sIL-4R were significantly elevated compared with controls by i.n. delivery of 100 μg sIL-4R; i.p. delivery of 100 μg sIL-4R only raised blood levels of sIL-4R. The i.n. administration of 100 μg sIL-4R before allergen challenge significantly reduced late phase pulmonary inflammation, blocking airway eosinophil infiltration, VCAM-1 expression, and mucus hypersecretion. In contrast, i.p. delivery of 100 μg sIL-4R inhibited only the influx of eosinophils into the lungs, but not airway mucus release. Furthermore, sIL-4R treatment by either i.n. or i.p. routes did not reduce airway hyperreactivity in response to methacholine challenge. Thus, elevating airway levels of sIL-4R through the administration of exogenous sIL-4R is effective in blocking the late phase pulmonary inflammation that occurs in this murine allergen-challenge asthma model. These results suggest that sIL-4R may have beneficial anti-inflammatory effects in asthmatic patients.

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Section: Discussionmentioning

confidence: 89%

Soluble IL-4 Receptor Inhibits Airway Inflammation Following Allergen Challenge in a Mouse Model of Asthma

Henderson¹,

Emil

Maliszewski³

2000

The Journal of Immunology

149

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“…These results suggest a general role for these chemokines in the inflammatory tubulointerstitial infiltrate of progressive DN. Soluble vascular adhesion model-1 has been reported to be correlated with the degree of microvascular complications in diabetes (27) and interstitial inflammation in DN (28). Finally, upregulation of HLA-A and -B and of ␤2-microglobulin is consistent with an inflammatory state and increased cell turnover in kidneys with progressive DN.…”

Section: Discussionmentioning

confidence: 91%

Modular Activation of Nuclear Factor-κB Transcriptional Programs in Human Diabetic Nephropathy

et al. 2006

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“…Experimental works in diabetic mice demonstrated an increased expression of VCAM-1 by endothelial as well as by infiltrating cells in the renal interstitium [103] . Studies in subjects with DN have shown elevated circulating concentrations of VCAM-1 [104,105] .…”

Section: Intercellular Adhesion Molecule-1mentioning

confidence: 97%

Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy

Luis-Rodríguez¹,

Martínez‐Castelao²,

Górriz³

et al. 2012

WJD

115

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Diabetes mellitus and its complications are becoming one of the most important health problems in the world. Diabetic nephropathy is now the main cause of end-stage renal disease. The mechanisms leading to the development and progression of renal injury are not well known. Therefore, it is very important to find new pathogenic pathways to provide opportunities for early diagnosis and targets for novel treatments. At the present time, we know that activation of innate immunity with development of a chronic low grade inflammatory response is a recognized factor in the pathogenesis of diabetic nephropathy. Numerous experimental and clinical studies have shown the participation of different inflammatory molecules and pathways in the pathophysiology of this complication.

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Vascular cell adhesion molecule-l expression in the renal interstitium of diabetic KKAy mice

Cited by 34 publications

References 28 publications

Soluble IL-4 Receptor Inhibits Airway Inflammation Following Allergen Challenge in a Mouse Model of Asthma

Soluble IL-4 Receptor Inhibits Airway Inflammation Following Allergen Challenge in a Mouse Model of Asthma

Modular Activation of Nuclear Factor-κB Transcriptional Programs in Human Diabetic Nephropathy

Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy

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