Thrombospondin-1 Restricts Interleukin-36γ-Mediated Neutrophilic Inflammation during Pseudomonas aeruginosa Pulmonary Infection
Hernán F. Peñaloza, Tolani F. Olonisakin, William Bain, Yanyan Qu, Rick van der Geest, Jill Zupetic, Mei Hulver, Zeyu Xiong, Michael W. Newstead, Chunbin Zou, Jonathan K. Alder, Joel A. Ybe, Theodore J. Standiford, Janet Lee
Abstract
Pseudomonas aeruginosa pulmonary infection can lead to exaggerated neutrophilic inflammation and tissue destruction, yet host factors that regulate the neutrophilic response is not fully known. IL-36γ is a proinflammatory cytokine that dramatically increases in bioactivity following N-terminal processing by proteases.
Topics & Concepts
Proinflammatory cytokinePseudomonas aeruginosaInflammationProteasesMicrobiologyImmunologyImmune systemCytokineInterleukinBiologyBacteriaEnzymeBiochemistryGeneticsS100 Proteins and AnnexinsImmune Response and InflammationInflammation biomarkers and pathways