Browsing by Subject "Pro-oxidative stressors"

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    Platelet-Activating Factor-Receptor and Tumor Immunity
    (JSciMed Central, 2014) Sahu, Ravi P.; Konger, Raymond L.; Travers, Jeffrey B.; Department of Pathology and Laboratory Medicine, IU School of Medicine
    First described in 1972 by Benveniste and colleagues, platelet-activating factor (PAF) remains one of the potent phospholipid known to date. The role of PAF produced enzymatically in mediating diverse biological and pathophysiological processes including inflammatory and allergic diseases and cancers in response to various stimuli has been extensively studied. However, little is known about the role of non-enzymatically-generated PAF-like lipids produced in response to pro-oxidative stressors, particularly in modulating the host immune responses to tumor immunity, which is the focus of this review.
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    Systemic Platelet-activating Factor Receptor Activation Augments Experimental Lung Tumor Growth and Metastasis
    (Sage, 2014-06-19) Hackler, Patrick C.; Reuss, Sarah; Konger, Raymond L.; Travers, Jeffrey B.; Sahu, Ravi P.; Dermatology, School of Medicine
    Pro-oxidative stressors including cigarette smoke (CS) generate novel lipids with platelet-activated factor-receptor (PAF-R) agonistic activity mediate systemic immunosuppression, one of the most recognized events in promoting carcinogenesis. Our previous studies have established that these oxidized-PAF-R-agonists augment murine B16F10 melanoma tumor growth in a PAF-R-dependent manner because of its effects on host immunity. As CS generates PAF-R agonists, the current studies sought to determine the impact of PAF-R agonists on lung cancer growth and metastasis. Using the murine Lewis Lung Carcinoma (LLC1) model, we demonstrate that treatment of C57BL/6 mice with a PAF-R agonist augments tumor growth and lung metastasis in a PAF-R-dependent manner as these findings were not seen in PAF-R-deficient mice. Importantly, this effect was because of host rather than tumor cells PAF-R dependent as LLC1 cells do not express functional PAF-R. These findings indicate that experimental lung cancer progression can be modulated by the PAF system.