Usenet Newsgroups Inflammatory Asthma From: teamtanner@hotmail.com (ironjustice) "Suppresses NF-?B activity" Experimental nonsteroidal treatment of asthma shows promise July 1, 2010 A new nonsteroidal, anti-inflammatory therapy made from a human protein significantly decreases disease signs of asthma in mice, opening the possibility of a new asthma therapy for patients who do not respond to current steroid treatments. Results of this therapy in an Pictures of Animals">animal model were presented at The Endocrine Society's 92nd Annual Meeting in San Diego. The protein, insulin-like growth factor binding protein-3 (IGFBP-3), uniquely inhibits specific physiological consequences of asthma examined in asthmatic mice, said Youngman Oh, PhD, a study co-author and a professor of pathology at Virginia Commonwealth University, Richmond, Virginia. IGFBP-3 reportedly targets a key cellular pathway called nuclear factor kappa B, or NF-?B that plays a role in inflammation. The IGFBP-3 protein interferes with its cellular signaling and suppresses NF-?B activity. "This novel mechanism has never been identified before. Our findings could have major implications not only for asthma but also other inflammatory diseases that NF-?B plays a role in, such as atherosclerosis and rheumatoid arthritis," Oh said. In asthma, when the airways become inflamed, they become hyperreactive, or overly sensitive, to "triggers," such as dust, smoke and pet dander. This leads to a chain of reactions that elicit an asthma "attack". According to the American Lung Association nearly 23 million people have asthma, of which 9 million are children. "Anti-inflammatory corticosteroid medicines are an important part of asthma management for many people, but an estimated 20 percent of patients with asthma are resistant to existing steroid medications and there is a critical need for alternate therapies," Oh said. Using a mouse model, Oh and his colleagues showed that IGFBP-3 production is suppressed in asthma. They measured NF-?B inflammatory activity, using molecular and cellular techniques, and found that treatment with IGFBP-3 blocked NF-?B activity. The researchers administered IGFBP-3 to the mice by spraying a synthetic form of the protein into their opened trachea. The treatment "reduced all physiological manifestations of asthma," including airway inflammation and hyperreactivity, Oh said. His research team plans to study IGFBP-3 treatment in asthmatic canine models next. ---------------- "Iron overload activates NF-kappaB" Involvement of the nuclear factor-kappaB pathway in the pathogenesis of endometriosis. González-Ramos R, Van Langendonckt A, Defrère S, Lousse JC, Colette S, Devoto L, Donnez J. Fertil Steril. 2010 Feb 24. Instituto de Investigaciones Materno Infantil, Departamento de Obstetricia y Ginecología, Hospital Clínico San Borja-Arriarán, Facultad de Medicina, Universidad de Chile, Santiago, Chile. OBJECTIVE: To evaluate the role of nuclear factor-kappaB (NF-kappaB) in the pathogenesis of endometriosis. DESIGN: A literature search was conducted in PubMed to identify all relevant citations. RESULT(S): Our findings highlight the important role of NF-kappaB in the pathophysiology of endometriosis. In vitro and in vivo studies show that NF-kappaB-mediated gene transcription promotes inflammation, invasion, angiogenesis, and cell proliferation and inhibits apoptosis of endometriotic cells. Constitutive activation of NF-kappaB has been demonstrated in endometriotic lesions and peritoneal macrophages of endometriosis patients. Agents blocking NF-kappaB are effective inhibitors of endometriosis development and some drugs with known NF-kappaB inhibitory properties have proved efficient at reducing endometriosis-associated symptoms in women. Iron overload activates NF-kappaB in macrophages. NF-kappaB activation in macrophages and ectopic endometrial cells stimulates synthesis of proinflammatory cytokines, generating a positive feedback loop in the NF-kappaB pathway and promoting endometriotic lesion establishment, maintenance and development. CONCLUSION(S): NF-kappaB transcriptional activity modulates key cell processes contributing to the initiation and progression of endometriosis. Because endometriosis is a multifactorial disease, inhibiting NF-kappaB appears to be a promising strategy for future therapies targeting different cell functions involved in endometriosis development, such as cell adhesion, invasion, angiogenesis, inflammation, proliferation, and apoptosis. Upcoming research will elucidate these hypotheses. Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved. PMID: 20188363 Who loves ya. Tom Jesus Was A Vegetarian! Man Is A Herbivore! DEAD PEOPLE WALKING Subject  Inflammatory Asthma  Re: SPAM