Inflammatory factors

HIV-infected glia secrete inflammatory factors that can indirectly contribute to excitotoxicity (Giulian et al. 1996). The HIV envelope protein induces the secretion... 

Other pro-inflammatory factors produced and secreted by these cell populations snch as interlenkins (IL) -1, -6, -12, and tumor necrosis factor alpha (TNF-a) are instrnmental in the resolution of bacterial clearance (Daley et al. 2005 Ishikawa and Miyazak 2005 Kudo et al. 2005 Man et al. 2007 Wang et al. 2005 Warner and Srinivasan 2004). 

Douglas SD (2001) Methadone may promote HIV replication study. AIDS Alert 16 120 Dreyer EB, Kaiser PK, Offermann IT, Lipton SA (1990) HIV-1 coat protein neurotoxicity prevented by calcium channel antagonists. Science 248 364-367 Dunn S, Vohra RS, Murphy JE, Homer-Vanniasinkam S, Walker JH, Ponnambalam S (2008) The lectin-like oxidized low-density-lipoprotein receptor a pro-inflammatory factor in vascular disease. Biochem J 409 349-355... 

Thus, inflammatory factors play a role at all stages of atherosclerosis in its initiation, progression, and final clinical manifestations. This new understanding of the pathophysiology of atherosclerosis has partly resulted from the study of chemokines and their receptors (4). 

The effect of MAPK activation on cellular processes that affect cell function and the resulting pharmacology has been delineated using modem techniques such as knock-out cells and animals [1,3,6]. Activation of MAPK in inflammatory cells such as T-cells, B-cells, macrophages and eosinophils leads to expression and/or activation of pro-inflammatory genes and mediators such as interleukin-1(3 (IL-1(3), TNFa, IL-6, chemokines [e.g., IL-8, macrophage inflammatory factor-1 a, (3 (MIP-la,[3)J, MMPs and toxic molecules such as free radicals and nitric oxide [1,3]. These pro-inflammatory mediators induce cellular proliferation, differentiation, survival, apoptosis and tissue degradation/destruction and help induce chronic inflammation. Inhibition of any one or more of the MAPK family... 

Kitawaki T, Kadowaki N, Sugimoto N, et al IgE-activated mast cells in combination with pro-inflammatory factors induce Th2-promoting dendritic cells. Int Immunol 2006 18 1789-1799. 

Monraats PS, Pires NM, Agema WR, et al. Genetic inflammatory factors predict restenosis after percutaneous coronary interventions. Circulation. Oct 18 2005 112(16) 2417-2425. 

Garofalo, R. P., and Goldman, A. S. (1999). Expression of functional immunomodulatory and anti-inflammatory factors in human milk. Clin. Perinatal. 26, 361-377. 

Xu, . X., Jin, H, Chung, Y. S., Shin, J. Y., Lee, . H., Beck, G. R., Palmos, G. N., Choi, B. D., and Cho, M. H. (2008a). Chondroitin sulfate extracted from ascidian tunic inhibits phorbol ester-induced expression of inflammatory factors VCAM-1 and COX-2 by blocking NF- activation in mouse skin. J. Agric. Food Chem. 56, 9667-9675. 

Twenty-five percent ofthrombophilic patients develop thrombosis at unusual sites resulting in cerebral venous thrombosis, mesenteric vein thrombosis, hepatic venous thrombosis, retinal vein thrombosis, purpura fulminans, splenic vein thrombosis, portal vein thrombosis, renal vein thrombosis, or axillary vein thrombosis. The thrombotic disorders may involve inflammatory factors that contribute to the vascular deficit. In addition, embolic events also play a role in the development of these thrombotic complications. 

Inflammatory factors platelet factor 4 CD 154 (CD40L) PDGF... 

Increases in plasma S-AA levels have previously been reported in patients with coronary disease (57). S-AA and plasma intracellular adhesion molecule-1 were elevated in patients with CAD and hyperhomocysteinemia, but only S-AA decreased after vitamin supplementation (35). Homocysteine activates nuclear factor- in endothelial cells, possibly via oxidative stress (58), and increases monocyte chemoattractant protein-1 expression in vascular smooth muscle cells (59). Additionally, it stimulates interleukin-8 expression in human endothelial cultures (60). These inflammatory factors are known to participate in the development of atherosclerosis. Taken together, these reports suggest an association of elevated tHcy and low-grade inflammation in CAD. 

Microglia are phagocytic cells with the capability of antigen presentation. They rapidly respond to a wide variety of stimuli including inflammation and hypoxia/ischemia (Block et al., 2007 del Zoppo et al., 2007). Activated microglia release several inflammatory factors, which modulate the permeability properties of the neurovascular unit (Stoll and lander, 1999 Block et al., 2007). 

Squamous cell metaplasia was the predominant aberrant cell type found in many of these cases. Squamous cell metaplasia is found in the young and old and does not always represent a benign-to-malignant process. More frequently, a nonspecific bronchial epithehal reaction develops, and this reaction is readily reversible with the disappearance of the toxic, infectious, or inflammatory factors that caused it. Although, squamous cell metaplasia may develop into neoplasia, patients with neoplasia also... 

This section provides an overview of several potential mechanisms involved in the development of asbestos-induced health effects (direct interaction with macromolecules, active oxygen mechanisms, and other cell-mediated mechanisms). An expert panel convened by lARC concluded in 1996, Overall, the available evidence in favor or against any of these mechanisms leading to the development of lung cancer and mesothelioma in either animals or humans is evaluated as weak (lARC Expert Panel 1996). Pulmonary inflammatory factors (a subset of other cell-mediated mechanisms) were considered by the lARC panel as having the most support among the potential mechanisms involved. For additional information on the molecular mechanisms of asbestos-induced pulmonary disease discussed below, including potential interactions between a number of the mechanisms, see recent reviews (Kamp and Weitzman 1999 Kinnula 1999 Lee and Testa 1999 Murthy and Testa 1999 Robledo and Mossman 1999). 

The limitations of the primate or cat models of human HIV-1 CNS infection include the costs, special facility requirements, the necessity of using mixtures of viral strains (in order to develop reproducible CNS infection), and the relatively small numbers of animals studied that preclude meaningful statistical analyses. These obstacles have urged researchers to develop small animal models. Several rodent models were established including transgenic mice (expressing viral proteins or relevant inflammatory factors seen in HAD), mice infected primarily with murine retroviruses, or severe combined immunodeficient (SCID) mice inoculated intracerebrally with human HIV-1 infected macrophages and reconstituted with human peripheral blood lymphocytes (PBL). 

Grammas P, Ovase R (2001) Inflammatory factors ar e elevated in brain micro vessels in Alzheimer s disease. Neui obiol Aging 22 837-842. 

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