Ligands of Macrophage Scavenger Receptor Induce Cytokine Expression via Differential Modulation of Protein Kinase Signaling Pathways

Hsu, Han‐Shui; Chiu, Show-Lan; Wen, Meng-Hsuan; Chen, Kuo-Yen; Hua, Kuo-Feng

doi:10.1074/jbc.m011117200

Cited by 160 publications

(144 citation statements)

References 63 publications

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“…Consistent with this possibility are studies that implicated CD204 involvement in the regulation of IL-12 release from AM (7,30). CD204 ligands such as fucoidan are known to induce TNF-␣ and IL-1␤ production in macrophage cell lines (11,24). Furthermore, following endotoxin exposure, CD204Ϫ/Ϫ mice exhibited significantly higher plasma levels of IL-6 and TNF-␣, whereas IL-10 showed no change relative to wild-type mice at 14 days (22).…”

Section: Discussionsupporting

confidence: 56%

“…Class A SR are believed to play a role in multiple pathophysiological processes, including atherosclerosis and host defense through ligand internalization and promotion of cell adhesion (43). Furthermore, studies have begun to explore the role of CD204 activation and its intracellular signaling ability to modulate these diverse functions in macrophages (11,24,32,41,43).…”

mentioning

confidence: 99%

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Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Beamer¹,

Holian²

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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Alveolar macrophages express the class A scavenger receptor (CD204) (Babaev VR, Gleaves LA, Carter KJ, Suzuki H, Kodama T, Fazio S, and Linton MF. Arterioscler Thromb Vasc Biol 20: 2593–2599, 2000); yet its role in vivo in lung defense against environmental particles has not been clearly defined. In the current study, CD204 null mice (129Sv background) were used to investigate the link between CD204 and downstream events of inflammation and fibrosis following silica exposure in vivo. CD204−/− macrophages were shown to recognize and uptake silica in vitro, although this response was attenuated compared with 129Sv wild-type mice. The production of tumor necrosis factor-α in lavage fluid was significantly enhanced in CD204 null mice compared with wild-type mice following silica exposure. Moreover, after exposure to environmental particles, CD204−/− macrophages exhibited improved cell viability in a dose-dependent manner compared with wild-type macrophages. Finally, histopathology from a murine model of chronic silicosis in 129Sv wild-type mice displayed typical focal lesions, interstitial thickening with increased connective tissue matrix, and cellular infiltrate into air space. In contrast, CD204−/− mice exhibited little to no deposition of collagen, yet they demonstrated enhanced accumulation of inflammatory cells largely composed of neutrophils. Our findings point to an important role of CD204 in mounting an efficient and appropriately regulated immune response against inhaled particles. Furthermore, these results indicate that the functions of CD204 are critical to the development of fibrosis and the resolution of inflammation.

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Section: Discussionsupporting

confidence: 56%

mentioning

confidence: 99%

Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Beamer¹,

Holian²

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Post-transcriptional regulation and processing of the pro-IL-1 protein into a mature IL-1 secretion via ICE has been well reported in various cells, including macrophages, as in our previous reports (22,23,34,51). Because incubation of macrophages with LPS-induced pro-IL-1 protein simultaneously increased IL-1 secretion in a time-dependent fashion (Fig.…”

Section: Lps Induction and The Role Of Lps-induced Ros In Regulation mentioning

confidence: 97%

“…Previous studies have shown that the p38 pathway is critical for LPS-stimulated cytokines release (25,33), including IL-1 and TNF induction in monocytes (17). Moreover, previous findings (34,35) indicated that p38 activity could be regulated via Rho GTPase (Rac1) and PAK.…”

mentioning

confidence: 99%

Lipopolysaccharide-mediated Reactive Oxygen Species and Signal Transduction in the Regulation of Interleukin-1 Gene Expression

Hsu

Wen

2002

Journal of Biological Chemistry

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463

354

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“…Indeed, increased levels of TNF-α and TGF-β1 have been detected in the serum or glomeruli of diabetic rodents [16,17] and serum levels of these cytokines are increased in diabetic patients [18]. Furthermore, advanced glycation, glycoxidation and lipoxidation end-products can stimulate IL-1 and TNF-α production by macrophages [19,20]. IL-1 and TNF-α are potent inducers of p38 MAPK in renal parenchymal cells [6,21] and TGF-β1 stimulates p38 MAPK phosphorylation in mesangial cells and fibroblasts [7,8].…”

Section: Introductionmentioning

confidence: 99%

Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy

et al. 2004

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Aims/hypothesis. Inflammation and fibrosis are pathological mechanisms that are partially regulated by cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway. Elements of the diabetic milieu such as high glucose and advanced glycation endproducts induce activation of this pathway in renal cells. Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy. Methods. Immunostaining identified phosphorylated (active) p38 MAPK in human biopsies with no abnormality (n=6) and with Type 2 diabetic nephropathy (n=12). Changes in kidney levels of phosphorylated p38 were assessed by immunostaining and western blotting in mice with streptozotocin-induced Type 1 diabetes that had been killed after 0.5, 2, 3, 4 and 8 months, and in Type 2 diabetic db/db mice at 2, 4, 6 and 8 months of age. Results. Phosphorylated p38 was detected in some intrinsic cells in normal human kidney, including podocytes, cortical tubules and occasional interstitial cells. Greater numbers of these phosphorylated p38+ cells were observed in diabetic patients, and phosphorylated p38 was identified in accumulating interstitial macrophages and myofibroblasts. A similar pattern of p38 activation was observed in both mouse models of diabetes. In mice, kidney levels of phosphorylated p38 increased (2-6 fold) following the onset of Type 1 and Type 2 diabetes. In both mouse models, interstitial phosphorylated p38+ cells were associated with hyperglycaemia, increased HbA 1 c levels and albuminuria. Further assessment of streptozotocin-induced diabetic nephropathy showed that interstitial phosphorylated p38+ cells correlated with interstitial fibrosis (myofibroblasts, collagen). Conclusions/interpretation. Increased p38 MAPK signalling is a feature of human and experimental diabetic nephropathy. Time course studies in mouse models suggest that phosphorylation of p38 plays a pathological role, particularly in the development of interstitial fibrosis.

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Ligands of Macrophage Scavenger Receptor Induce Cytokine Expression via Differential Modulation of Protein Kinase Signaling Pathways

Cited by 160 publications

References 63 publications

Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Scavenger receptor class A type I/II (CD204) null mice fail to develop fibrosis following silica exposure

Lipopolysaccharide-mediated Reactive Oxygen Species and Signal Transduction in the Regulation of Interleukin-1 Gene Expression

Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy

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