Simvastatin and fluvastatin reduce interleukin-6 and interleukin-8 lipopolysaccharide (LPS) stimulated production by isolated human monocytes from chronic kidney disease patients

Mantuano, Emanuela; Santi, Samuele; Filippi, C.; Manca-Rizza, Giovanni; Paoletti, Sabrina; Consani, Cristina; Giovannini, Luca; Tramonti, Gianfranco; Carpi, Angelo; Panichi, Vincenzo

doi:10.1016/j.biopha.2007.03.002

Cited by 22 publications

(12 citation statements)

References 33 publications

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“…Numerous studies suggest that statin can lead to a reduction in pro-inflammatory cytokines in monocytes, dendritic cells and macrophages, a result of NF-κB activation [5,24,39,40]. In concordance with these studies, previous work done by our group also showed that atorvastatin attenuates TLR4-mediated NF-κB activation in murine pro-B cells transfected with TLR4 [16].…”

Section: Discussionsupporting

confidence: 76%

“…Possible mechanisms by which statins reduce CVD risk independent of their lipid regulation include anti-thrombotic and anti-inflammatory effects [4,5,24], plaque stabilization [25][26][27][28], and endothelial wall relaxation resulting in lower intra-arterial pressure and increased blood flow [29][30][31]. Recently, numerous studies have pointed out that statins have immunomodulating effects which can influence various immunological disorders including atherosclerosis [3,[32][33][34].…”

Section: Discussionmentioning

confidence: 98%

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Atorvastatin affects TLR4 clustering via lipid raft modulation

Chansrichavala

Chantharaksri

Sritara

et al. 2010

International Immunopharmacology

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 98%

Atorvastatin affects TLR4 clustering via lipid raft modulation

Chansrichavala

Chantharaksri

Sritara

et al. 2010

International Immunopharmacology

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“…After washing with phosphate-buffered saline (PBS), the cells were suspended in RPMI 1640 medium (Gibco) supplemented with 2 mM L-glutamine, 100 U/ml penicillin, 100 mg/ ml streptomycin, and 10% heat-inactivated FBS (Biological Industries). Human monocytes were isolated from PBMC by collecting the attached cells [Mantuano et al, 2007], which were differentiated into macrophages by treatment with IL-4 (Peprotech EC LTD) (10 ng/ml) for 3 days . This study was approved by the Ethical Review Board of the National Taiwan University Hospital.…”

Section: Cell Preparation and Culturementioning

confidence: 99%

Rosiglitazone inhibits monocyte/macrophage adhesion through de novo adiponectin production in human monocytes

Tsai

Chen

et al. 2010

J of Cellular Biochemistry

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Rosiglitazone (RSG) has a variety of actions on both insulin sensitization and anti-atherogenic effects. The molecular effect of RSG on monocyte/macrophage function in terms of de novo synthesis of adiponectin is not fully understood. Here, we examined the regulation of adiponectin expression in human monocytes/macrophages by RSG and its function on monocyte adhesion during initiation of atherosclerosis. Adiponectin expression in monocytes and macrophages was studied by RT-PCR, quantitative real-time PCR, Western blot, and immunocytochemistry. Signal transduction and adhesion molecules were studied in order to describe the function of de novo synthesized adiponectin in monocyte adhesion. Adiponectin was expressed and upregulated during monocyte differentiation. The expression of adiponectin was enhanced, albeit at a much lesser degree, by a peroxisome proliferator-activated receptor gamma (PPAR gamma) agonist RSG, which was similar to what was found in adipocytes. Monocyte adhesion was remarkably reduced when the cells were treated with RSG for 12 h. This inhibitory effect of RSG was abolished by specific anti-adiponectin antibodies but not by non-immune immunoglobulin G in a serum-free condition. Adiponectin-induced suppression on monocyte adhesion was inhibited by a selective AMP-activated protein kinase (AMPK) inhibitor compound C. The reduced expression and/or function of adhesion molecule integrins may underlie the mechanism contributing to reduced monocyte adhesion upon AMPK activation. Our data suggest that the inhibitory effect of RSG on monocyte adhesion might be at least in part through de novo adiponectin expression and activation of an AMPK-dependent pathway, which might play an important role in atherogenesis.

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“…However, conflicting results exist to date, on whether a single HD session increases or decreases the concentration of IL-8 [50,51] . Of interest, increasing doses of simvastatin to PBMC cultures from CKD patients induced a dose-dependent inhibition of both IL-6 and IL-8 [52,53] .…”

Section: Interleukin-8mentioning

confidence: 99%

Cytokine Dysregulation in Chronic Kidney Disease: How Can We Treat It?

et al. 2008

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As the kidney is the major site for elimination of many cytokines, the delicate equilibrium of pro-inflammatory cytokines and their inhibitors is clearly dysregulated in chronic kidney disease (CKD) patients. The consequences of the altered immune response in uremia lead to a state of persistent inflammation which is highly prevalent among CKD patients and is linked to complications such as the development of protein-energy wasting and atherosclerotic vascular disease. The present review aims at reviewing this complex orchestration of uremic cytokines beyond the well-studied interleukin-6 and tumor necrosis factor-α. Finally, we update our current understanding on anti-inflammatory treatment strategies in CKD patients, including nutritional and lifestyle measurements, pharmacological intervention and specific anticytokine strategies targeting the dialytic procedure.

show abstract

Simvastatin and fluvastatin reduce interleukin-6 and interleukin-8 lipopolysaccharide (LPS) stimulated production by isolated human monocytes from chronic kidney disease patients

Cited by 22 publications

References 33 publications

Atorvastatin affects TLR4 clustering via lipid raft modulation

Atorvastatin affects TLR4 clustering via lipid raft modulation

Rosiglitazone inhibits monocyte/macrophage adhesion through de novo adiponectin production in human monocytes

Cytokine Dysregulation in Chronic Kidney Disease: How Can We Treat It?

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