Evaluation of Inteiueukin-1 Receptor Antagonist (Il-1ra) and Tumor Necrosis Factor Binding Protein (TNF-BP) in a Rodent Abscess Model of Host Resistance

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Abstract
Modulation of pro-inflammatory cytokine responses can alter the normal protective mechanisms against invading pathogens. The cytokines interleukin-1β (IL-1β) and tumor necrosis factor-γ (TNF-γ) are crucial in the inflammatory cascade for upregulation of adhesion molecule expression neutrophil recruitment and additional cytokine induction. To determine if the cytokine antagonists interleukin-1 receptor antagonist (IL-lra) and tumor necrosis factor-binding protein (TNF-bp) alter host resistance mechanisms they were evaluated in a rodent abscess model.