This Is MS Multiple Sclerosis Knowledge & Support Community

NHE wrote:Anyways, if consuming Chlorella really does increase the activity of T and B cells thereby strengthening the immune system, then this effect does not seem desirable in MS patients and consuming Chlorella would appear to be contraindicated.

Anecdote wrote:Since I am on abx I take it primarily for detoxification, but it is supposed to be beneficial for MS in any case.

Cojack wrote:isn't this essentially the up regulate or down regulate the immune system argument? Jack

1: Vascul Pharmacol. 2007 Feb;46(2):77-84. Epub 2006 Jul 14. Links
Sulforaphane suppresses angiogenesis and disrupts endothelial mitotic progression and microtubule polymerization.Jackson SJ, Singletary KW, Venema RC.
Medical College of Georgia, Vascular Biology Center, CB 3330, 1459 Laney Walker Boulevard Augusta, GA 30912, USA.

Sulforaphane (SUL), an isothiocyanate derived from broccoli and other cruciferous vegetables, is known to induce phase II detoxification enzymes, disrupt cancer cell microtubule polymerization, and trigger cell cycle arrest in breast and colon cancer cells. Here, we provide the first evidence that SUL also acts to inhibit angiogenesis via suppression of endothelial cell proliferation. Bovine aortic endothelial (BAE) cells were exposed to concentrations of up to 15 microM SUL prior to cell cycle analysis and mitotic index quantification. Within 24 h, 15 microM SUL clearly induced G(2)/M accumulation and pre-metaphase arrest in BAE cells. Moreover, immunofluorescence tubulin staining indicated that this same SUL concentration was efficacious in not only disrupting mitotic progression, but also in perturbing normal polymerization of mitotic (and cytoplasmic) microtubules. Furthermore, daily administration of SUL (100 nmol/day, i.v. for 7 days) to female Balb/c mice bearing VEGF-impregnated Matrigel plugs strongly and significantly (P<0.05) suppressed angiogenesis progression as measured by hemoglobin concentration. Taken together, these findings suggest that the endothelial cell population is a novel target of SUL action both in vitro and in vivo. This mechanism of SUL-induced endothelial microtubule disruption and early mitotic arrest may further discern a potential role of SUL as a chemopreventive agent.

PMID: 16938492 [PubMed - indexed for MEDLINE]

1: J Immunol. 2006 Sep 1;177(5):3477-83. Links
Phase II enzymes induction blocks the enhanced IgE production in B cells by diesel exhaust particles.Wan J, Diaz-Sanchez D.
Hart and Louise Lyon Laboratory, Division of Clinical Immunology and Allergy, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

Oxidant pollutants such as diesel exhaust particles (DEPs) can initiate and exacerbate airway allergic responses through enhanced IgE production. These effects are especially pronounced in individuals in whom phase II antioxidant enzyme responses are impaired. We confirmed that DEPs and DEP extracts (DEPX) can act directly on B lymphocytes and showed that DEPX could enhance IgH epsilon germline transcription in a B cell line and in PBMCs. We therefore studied the regulation in B cells of NAD(P)H: quinone oxidoreductase (NQO1) as a typical model phase II enzyme and its role in modulating DEPX-enhanced IgE responses. DEPX increased NQO1 mRNA expression in a dose-dependent manner. NQO1 protein induction by DEPX was confirmed by Western blot. DEPs induced activity of the antioxidant response element located in the NQO1 gene promoter. Induction of both NQO1 mRNA and protein expression could be blocked by coculture with an antioxidant and partly repressed by inhibitors of PI3K and p38 MAPK, but not by inhibitors of MAPK/ERK kinase (MEK/ERK) or protein kinase C. The ability of DEPX to enhance IgE production was blocked by the induction of phase II enzymes, including NQO1 in B cells by the chemical sulforaphane. These findings suggest that a natural protective mechanism in B cells from oxidant pollutants such as diesel particles is the expression of phase II enzymes through induction of antioxidant response elements and support the approach of overexpression of these enzymes as a potential future chemopreventative strategy.

PMID: 16920990 [PubMed - indexed for MEDLINE]

1: Free Radic Biol Med. 2006 Jul 15;41(2):311-7. Epub 2006 Apr 26. Links
NAD(P)H:quinone oxidoreductase 1 expression in multiple sclerosis lesions.van Horssen J, Schreibelt G, Bö L, Montagne L, Drukarch B, van Muiswinkel FL, de Vries HE.
Department of Molecular Cell Biology and Immunology, VU University Medical Center Amsterdam, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands. j.vanhorssen@vumc.nl

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), marked by infiltration of monocyte-derived macrophages in the brain parenchyma. Macrophages contribute to disease pathology by secretion of inflammatory mediators, such as reactive oxygen species (ROS). ROS are involved in various processes underlying MS pathology, including monocyte migration across the blood-brain barrier, phagocytosis and degradation of myelin, axonal degeneration, and oligodendrocyte damage. High concentrations of ROS cause oxidative stress, which induces transcriptional activation of phase II detoxification enzymes, such as the antioxidant protein NAD(P)H:quinone oxidoreductase 1 (NQO1). Since NQO1 expression may act as an indicator of oxidative stress and knowledge about the cellular distribution pattern of NQO1 in MS brains is lacking, we examined the expression of NQO1 in various well-characterized MS lesions. Here, we show for the first time that NQO1 is highly upregulated in active and chronic active MS lesions, particularly in hypertrophic astrocytes and myelin-laden macrophages. We hypothesize that increased NQO1 expression may reflect an endogenous defense response against ROS-mediated cellular toxicity. Compounds that induce the production of endogenous antioxidant enzymes, such as NQO1, may be potential targets for future treatment strategies in MS.
PMID: 16814112 [PubMed - indexed for MEDLINE]