IL-37 Inhibits Inflammasome Activation and Disease Severity in Murine Aspergillosis

• DOI: 10.1371/journal.ppat.1004462
• Publication Date: 2014-11-06T19:39:11Z
• Authors: Silvia Moretti; Silvia Bozza; Vasilis Oikonomou; Giorgia Renga; Andrea Casagrande; Rossana G. Iannitti; Matteo Puccetti; Cecilia Garlanda; Soohyun Kim; Suzhao Li; Frank L. van de V...; Charles A. Dinarello; Luigina Romani
• Keywords: Radboudumc 4: lnfectious Diseases and Global Health RIMLS: Radboud Institute for Molecular Life Sciences; Inflammation; Mice, Knockout; 0301 basic medicine; QH301-705.5; Inflammasomes; Interleukin-1beta; Receptors, Interleukin-1; Animals; Carrier Proteins; Disease Models, Animal; Female; Inflammasomes; Inflammation; Interleukin-1; Interleukin-1beta; Mice; Mice, Knockout; Pulmonary Aspergillosis; Receptors, Interleukin-1; RC581-607; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; NLR Family, Pyrin Domain-Containing 3 Protein; Animals; Female; Pulmonary Aspergillosis; Immunologic diseases. Allergy; Biology (General); Carrier Proteins; Research Article; Interleukin-1

Since IL-37 transgenic mice possesses broad anti-inflammatory properties, we assessed whether recombinant affects inflammation in a murine model of invasive pulmonary aspergillosis. Recombinant human was injected intraperitoneally into prior to infection and the effects on lung inflammasome activation were evaluated. markedly reduced NLRP3-dependent neutrophil recruitment steady state mRNA levels IL-1β production mitigated damage relevant clinical model, namely aspergillosis with cystic fibrosis. The activity requires IL-1 family decoy receptor TIR-8/SIGIRR. Thus, by preventing NLRP3 reducing secretion, functions as spectrum inhibitor innate response infection-mediated inflammation, could be considered therapeutic due non-resolving Aspergillus disease.