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Biota Announces Positive Phase IIb Data for Asthmatic Patients With Human …
MarketWatch (press release) "While the clinical link between HRV infection and loss of asthma control is now widely accepted, Biota is the first company to evaluate the use of an antiviral to treat the infection in asthmatics. This has the potential to be of considerable benefit … |
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1?,25-Dihydroxyvitamin D3 promotes CD200 expression by human peripheral and airway-resident T cells.
Thorax. 2012 Feb 14;
Authors: Dimeloe S, Richards DF, Urry ZL, Gupta A, Stratigou V, Farooque S, Saglani S, Bush A, Hawrylowicz CM
Abstract
BackgroundCD200, a cell-surface immunoglobulin-like molecule expressed by immune and stromal cells, dampens the pro-inflammatory activity of tissue-resident innate cells via its receptor, CD200R. This interaction appears critical for peripheral immune tolerance, particularly in the airways where excessive inflammation is undesirable. Vitamin D contributes to pulmonary health and promotes regulatory immune pathways, therefore its influence on CD200 and CD200R was investigated.MethodsCD200 and CD200R expression were assessed by qPCR and immunoreactivity of human lymphoid, myeloid and epithelial cells following 1?,25-dihydroxyvitamin D3 (1?,25VitD3) exposure in vitro and in peripheral T cells following 1?,25VitD3 oral ingestion in vivo. The effect of 1?25VitD3 was also assessed in human airway-resident cells.Results1?25VitD3 potently upregulated CD200 on peripheral human CD4+ T cells in vitro, and in vivo there was a trend towards upregulation in healthy, but not asthmatic individuals. CD200R expression was not modulated in any cells studied. CD200 induction was observed to a lesser extent in CD8+ T cells and not in B cells or airway epithelium. T cells isolated from the human airway also responded strongly to 1?25VitD3 to upregulate CD200.ConclusionsThe capacity of 1?,25-dihydroxyvitamin D3 to induce CD200 expression by peripheral and respiratory tract T cells identifies an additional pathway via which vitamin D can restrain inflammation in the airways to maintain respiratory health.
PMID: 22334534 [PubMed – as supplied by publisher]
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Chlamydophila pneumonia inhibits the corticosteroid-induced suppressions of metalloproteinase-9 and tissue inhibitor metalloproteinase-1 secretion by human peripheral blood mononuclear cells.
J Med Microbiol. 2012 Jan 26;
Authors: Park CS, Lee YS, Kwon HS, Lee TH, Kim TB, Moon KA, Yoo B, Moon HB, Cho YS
Abstract
Chlamydophila pneumoniae infection has been suggested to be associated with severe asthma characterized by persistent airway limitation, which may be related to airway remodeling. We investigated whether C. pneumoniae infection affected the secretion of metalloproteinase-9 (MMP9) and tissue inhibitor metalloproteinase-1 (TIMP1), and altered the responsiveness of inflammatory cells to corticosteroids. Human peripheral blood mononuclear cells (PBMC) were cultured in vitro in the presence or absence of C. pneumoniae. Secretion of both MMP9 and TIMP1 was strongly suppressed by dexamethasone treatment in uninfected cells. MMP9 secretion was also significantly inhibited by dexamethasone in C. pneumoniae-infected cells, but TIMP1 secretion was not; hence the MMP9 to TIMP1 ratio decreased. Interestingly, expression of human glucocorticoid receptor (GR)?, which is believed to confer resistance to corticosteroids, was enhanced by dexamethasone treatment in C. pneumoniae-infected PBMC. We conclude that C. pneumoniae infection may promote airway remodeling by decreasing the ratio of MMP9 to TIMP1 secreted by inflammatory cells, and by altering cellular responsiveness to corticosteroids.
PMID: 22282461 [PubMed – as supplied by publisher]
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Surrey couple claims human rights violated by smoking neighbour
The Province A Surrey woman who says her neighbour's cigarette smoke wafts into her condo and triggers her asthma has won the right to launch a human rights complaint. Kathryn Arndt and her husband Douglas filed … Smoking neighbour human-rights case moves forward in BC |
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 Moneycontrol.com |
Glenmark starts phase IIb human trials of molecule
mydigitalfc.com Glenmark is positioning Revlimast as a treatment for chronic inflammatory disorders such as asthma and rheumatoid arthritis. Rheumatoid arthritis and asthma drugs are estimated to have a market in excess of $20 billion each. … Glenmark starts Phase-IIb human trials of Revamilast molecule Glenmark Initiates Phase IIb Human Trials Globally for its Novel Molecule … |
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Glenmark starts Phase-IIb human trials of Revamilast molecule
Economic Times NEW DELHI: Glenmark Pharmaceuticals on Wednesday said it has started Phase-IIb human trials of its 'Revamilast' molecule, which is being developed for treatment of inflammatory disorders like asthma and rheumatoid arthritis. The Phase-IIb studies of … Glenmark initiates Phase IIb human trials globally for its novel molecule … |
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S-Nitrosoglutathione reductase in human lung cancer.
Am J Respir Cell Mol Biol. 2011 Aug 4;
Authors: Marozkina NV, Yemen S, Wei C, Wallrabe H, Nagji AS, Liu L, Morozkina T, Jones DR, Gaston B
S-Nitrosoglutathione (GSNO) reductase regulates cell signaling pathways relevant to asthma and protects cells from nitrosative stress. Recent evidence suggests that this enzyme may prevent human hepatocellular carcinoma arising in the setting of chronic hepatitis. We hypothesized that GSNO reductase could also protect the lung against potentially carcinogenic reactions of associated with nitrosative stress. We report that wild-type Ras is S-nitrosylated and activated by nitrosative stress; and that it is denitrosylated by GSNO reductase. In human lung cancer, GSNO reductase activity and expression are decreased. Further, distribution of the enzyme – including its colocalization with wild-type Ras – is abnormal. We conclude that decreased GSNO reductase activity could leave the human lung vulnerable to the oncogenic effects of nitrosative stress, as is the case in the liver. This potential should be considered when developing therapies that inhibit pulmonary GSNO reductase to treat asthma and other conditions.
PMID: 21816964 [PubMed – as supplied by publisher]
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VT Researches Study Horses to Help Treat Human Asthma
WSET AP National/International News Entertainment News from AP Blacksburg, VA – 1-in-15 Americans suffer from the respiratory disease asthma. In fact, asthma accounts for 25% of all emergency room visits here in the United States. The millions of Americans … |
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Cinryze® (C1 Esterase Inhibitor [Human]) Data Presented at 2011 American …
PR Newswire (press release) There can be no assurance that that the data presented during the 2011 American Academy of Allergy Asthma & Immunology (AAAAI) Annual Meeting regarding Cinryze is predictive of how Cinryze will perform in commercial usage. … |
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Flagellin Induces the Expression of Thymic Stromal Lymphopoietin in Human Keratinocytes via Toll-Like Receptor 5.
Int Arch Allergy Immunol. 2010 Nov 25;155(1):31-37
Authors: Le TA, Takai T, Vu AT, Kinoshita H, Chen X, Ikeda S, Ogawa H, Okumura K
Background: Thymic stromal lymphopoietin (TSLP), highly expressed by keratinocytes in skin lesions of atopic dermatitis patients and bronchial epithelial cells in asthma, plays a key role in allergic diseases. Information on triggers for the release of TSLP in keratinocytes is still limited. Keratinocytes express Toll-like receptor (TLR) 5, the ligand for which is flagellin, the major structural protein of the flagella of Gram-negative bacteria. IL-4, IL-13 and TNF-? (Th2/TNF) are associated with allergic diseases. TGF-?, one of the ligands for the epidermal growth factor receptor, is overexpressed in keratinocytes in atopic dermatitis. We investigated the induction of TSLP expression in keratinocytes stimulated with flagellin and its modulation by the Th2/TNF cytokines and TGF-?. Methods: Primary human keratinocytes were stimulated with flagellin with or without cytokines. The TSLP released was measured by ELISA. Gene expression was analyzed by quantitative real-time PCR. Results: Stimulation of keratinocytes with flagellin induced the release of TSLP protein and upregulation of the gene expression of TSLP and other pro-inflammatory molecules. The flagellin-induced release of TSLP was enhanced by the Th2/TNF cytokines or TGF-?. Small interfering RNA-mediated knockdown of TLR5 expression suppressed the flagellin-induced TSLP gene expression. Conclusions: Flagellin induces TSLP expression in keratinocytes via TLR5 and the expression can be upregulated by a cytokine milieu with Th2/TNF or TGF-?, suggesting that exposure of barrier-defective skin to Gram-negative bacteria or environmental flagellin contributes to the initiation and/or amplification of Th2-type skin inflammation including atopic dermatitis through the induction of TSLP expression in keratinocytes.
PMID: 21109746 [PubMed – as supplied by publisher]
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