Cytokines in relapsing experimental autoimmune encephalomyelitis in DA rats: persistent mRNA expression of proinflammatory cytokines and absent expression of interleukin-10 and transforming growth factor-β

1996 ◽  
Vol 69 (1-2) ◽  
pp. 103-115 ◽  
Author(s):  
Shohreh Issazadeh ◽  
Johnny C. Lorentzen ◽  
Maha I. Mustafa ◽  
Bo Höjeberg ◽  
Åsa Miissener ◽  
...  
Keyword(s):  
Growth Factor ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Mrna Expression ◽  
Proinflammatory Cytokines ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interleukin 10 ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

The Regulatory Effect of Liuwei Dihuang Pills on Cytokines in Mice with Experimental Autoimmune Encephalomyelitis

2012 ◽  
Vol 40 (02) ◽  
pp. 295-308 ◽  
Author(s):  
Yan Liu ◽  
Hui Zhao ◽  
Jie Zhang ◽  
Ping Zhang ◽  
Ming Li ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Mrna Expression ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Demyelinating Diseases ◽  
Regulatory Effect ◽  
Autoimmune Encephalomyelitis ◽  
Tnf Α ◽  
Liuwei Dihuang Pills ◽  
Experimental Autoimmune

The regulatory effect of Liuwei Dihuang Pills (LDP) was studied on cytokines in mice with experimental autoimmune encephalomyelitis (EAE), a model for human multiple sclerosis (MS), induced by immunization with MOG35-55 and complete Freund's adjuvant (CFA) supplemented with pertussis toxin (PTX). LDP was administrated orally for 40 days, and prednisone acetate (PA) was used as a control. The pathological changes in the spinal cords of mice were observed by light microscope with hematoxylin-eosin (HE) staining and transmission electron microscope (TEM). The protein and mRNA expression of tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) in the spinal cords were assessed by immunohistochemistry and RT-PCR assay, and the cyclic adenosine monophosphate (cAMP) in mice plasma was measured by radioimmunoassay (RIA) on days 12, 25 and 40 post-immunization (PI). The results showed that inflammatory cells, demyelination and axonal loss were reduced, and that the protein and mRNA expression of TNF-α and the ratio of TNF-α/TGF-β were obviously decreased, to different extents. However, the levels of cAMP were enhanced in LDP-treated groups. These findings suggested that LDP regulates the cytokine balance in favor of T helper 1 (Th1)/regulatory T (Treg) cells, which depend on enhancement of cAMP levels. LDP has a potential role in the treatment of MS and other demyelinating diseases of the central nervous system.

Intracisternal administration of transforming growth factor-β evokes fever through the induction of cyclooxygenase-2 in brain endothelial cells

2008 ◽  
Vol 294 (1) ◽  
pp. R266-R275 ◽  
Author(s):  
Shigenobu Matsumura ◽  
Tetsuro Shibakusa ◽  
Teppei Fujikawa ◽  
Hiroyuki Yamada ◽  
Kiyoshi Matsumura ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Proinflammatory Cytokines ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cyclooxygenase 2 ◽  
Dependent Manner ◽  
Cox 2 ◽  
Β Receptor

Transforming growth factor-β (TGF-β), a pleiotropic cytokine, regulates cell proliferation, differentiation, and apoptosis, and plays a key role in development and tissue homeostasis. TGF-β functions as an anti-inflammatory cytokine because it suppresses microglia and B-lymphocyte functions, as well as the production of proinflammatory cytokines. However, we previously demonstrated that the intracisternal administration of TGF-β induces fever like that produced by proinflammatory cytokines. In this study, we investigated the mechanism of TGF-β-induced fever. The intracisternal administration of TGF-β increased body temperature in a dose-dependent manner. Pretreatment with cyclooxygenase-2 (COX-2)-selective inhibitor significantly suppressed TGF-β-induced fever. COX-2 is known as one of the rate-limiting enzymes of the PGE2 synthesis pathway, suggesting that fever induced by TGF-β is COX-2 and PGE2 dependent. TGF-β increased PGE2 levels in cerebrospinal fluid and increased the expression of COX-2 in the brain. Double immunostaining of COX-2 and von Willebrand factor (vWF, an endothelial cell marker) revealed that COX-2-expressing cells were mainly endothelial cells. Although not all COX-2-immunoreactive cells express TGF-β receptor, some COX-2-immunoreactive cells express activin receptor-like kinase-1 (ALK-1, an endothelial cell-specific TGF-β receptor), suggesting that TGF-β directly or indirectly acts on endothelial cells to induce COX-2 expression. These findings suggest a novel function of TGF-β as a proinflammatory cytokine in the central nervous system.

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