Date

November 2010

Document Type

Dissertation

Degree Name

Ph.D.

Department

Dept. of Cell and Developmental Biology

Institution

Oregon Health & Science University

Abstract

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 ricin’s 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-1β (IL-1β) signaling suppress ricin

Identifier

doi:10.6083/M4KK98S0

School

School of Medicine

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