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. Author manuscript; available in PMC: 2018 Sep 15.
Published in final edited form as: J Immunol. 2017 Aug 7;199(6):2140–2148. doi: 10.4049/jimmunol.1602186

Figure 6. Increased IL-1R signaling is not the mechanism associated with enhanced PGE2 and IL-22 in Il1rl1−/− mice after A. fumigatus exposure.

Figure 6

C57BL/6 wild-type (WT) and Il1r1−/− (IL-1R1 deficient) mice were challenged intratracheally with A. fumigatus conidia and 48 h after exposure, the right lungs were collected, enzymatically digested and unfractionated lung cells cultured in triplicate for 24 h. (A) PGE2 levels were quantified in clarified co-culture supernatants by EIA and (B) IL-22 levels were quantified in clarified co-culture supernatants by ELISA. The Figures illustrates cumulative data from four independent studies (n = 1–2 mice per group, per study). (C) C57BL/6 wild-type mice were challenged with A. fumigatus and 6 and 24 h thereafter, administered IL-33 (1 µg in 50 µl) or PBS intratracheally. Forty-eight h after exposure, the right lungs were collected, enzymatically digested and unfractionated lung cells cultured in triplicate for 24 h. IL-1α and IL-1β levels were quantified in clarified co-culture supernatants by Bio-Plex. The Figure illustrates cumulative data from two independent studies (n = 1–2 mice per group, per study). For all graphs, *** represents a P value of < 0.001, respectively (Unpaired two-tailed Student’s t test).