Fig 2: Innate signals regulate the neutrophilia, IL-6 and TNF-α in stingray venom inflammation. Stingray venom (300 μg/ml) in 500 μl or sterile saline were injected i.p. into C57BL/6 WT or mast cell-deficient Kit Wsh/Wsh, ST2−/−, and AHR−/−; or in TLR2/4−/−, MyD88−/− and TRIF−/−; or in NLRP3−/−, ICE−/− and IL-1β−/−; or in P2RX7−/− and CD39−/−; or in IL-17A−/− and IL-17RA−/−, or in TBX21−/− and IL-18R−/−. Two hours later, peritoneal cells were harvested and aliquots applied on glass slides were stained and neutrophils (A) were counted in a proportion of total cells. IL-6 (B) and TNF-α (C) were analyzed by CBA in the peritoneal exudates of C57BL/6 WT or deficient mice. Results represent mean ± SEM. Pooled results of two independent experiments are shown. *p < 0.05 compared with the control-group (dotted line) and # p < 0.05 compared to WT mice injected with ray venom.

Fig 3: Blocking ST2 partially abrogates dectin-1-induced inhibition of osteoclastogenesis(A) Mouse BMCs cells were cultured with M-CSF for 2 days and with M-CSF plus RANKL for 3 days. At day 2, cells were treated with or without (control) curdlan in the presence of a ST2 blocking antibody (αST2) or a control IgG (IgG). Cells were stained for TRAP+ cells. (B and C) The cell number (B) and mean cell circumference (C) of OCs as obtained in (A). (D and E) qPCR assessed Nfatc1 (D) and Ctsk (E) expression in the cells as obtained in (A). (F) ELISA assessed TRAP5b secretion in the cultures. Data are representative of three (A) independent experiments or presented as mean ± SD of three (B-F) independent experiments. *P < 0.05; **P < 0.01.