Dept. of Cell and Developmental Biology
Oregon Health & Science University
Ricin toxin is a ribotoxic stressor that exhibits well-characterized actions on the ribosomes of cells leading to the inhibition of protein synthesis and the phosphorylation of stress activated protein kinases (SAPKs). In addition, ricin triggers a robust inflammatory response in vivo, but the underlying mechanisms for ricinâs inflammatory effects are incompletely understood. Due to its ease of delivery to human populations by aerosol in the event of bioterrorism, it is important to understand the pathological consequences of ricin exposure in the pulmonary system. In this thesis, I explore the molecular mechanisms of the ricin-mediated inflammatory response in the lungs of mice. Here I report that expression of inflammatory genes, edema, increased microvascular permeability, and in particular, neutrophilia, are important characteristics of ricin-mediated lung damage in mice. I found that depletion of macrophages and genetic deficiency of interleukin-1Î² (IL-1Î²) signaling suppress ricin
School of Medicine
Lindauer, Meghan Lee, "Proinflammatory responses triggerd by ricin toxin require macrophages and IL-1[beta] signaling through the NALP3 inflammasome" (2010). Scholar Archive. 661.