Fig. 3
From: PI3Kδ inhibition prevents IL33, ILC2s and inflammatory eosinophils in persistent airway inflammation
Re-exposure to HDM after resolution on day 33 re-initiated pulmonary inflammation, which was characterised by rapid cytokine production and by leukocyte infiltration. A The dose of HDM required to elicit a submaximal (ED80) response in BAL IL5 and KC was 100 µg/50 µl and this dose was used for all subsequent re-challenge experiments (n = 4–11 per dose group). B All BAL and C serum cytokine responses peaked between 2 and 4 h post HDM re-challenge, with the exception of BAL IL5, which peaked at 24 h. Mice sensitised with HDM but challenged with saline did not exhibit cytokine responses in either BAL or serum, (n = 3–5 per time-point in saline controls and 4–11 mice per time-point for the HDM re-challenged group). D After re-challenge with HDM, the earliest leukocyte response was that of neutrophils which peaked at 6 h and remained in higher numbers 7 days post re-challenge compared to saline controls. BAL macrophage numbers peaked at 3 days and returned to saline control levels by day 7. Eosinophils were present in the BAL of HDM re-challenged mice at 24 h, whereas lymphocytes were evident from 2 days post HDM re-challenge (n = 3–5 mice per time-point in saline controls and 8–10 mice per time-point for the HDM re-challenged group). E Exemplar dot plot graph demonstrating difference between resident (Siglec-Fint) eosinophil population and the infiltrating inflammatory eosinophil (Siglec-Fhi) population. F Infiltrating lung inflammatory eosinophils, absent in HDM sensitised and saline challenged controls peaked at day 3 post re-challenge, but were present in numbers from 24 h after re-challenge and were differentiated from resident populations based on Siglec-F expression, (n = 4–10 per time-point for saline controls and 6–17 for HDM re-challenged group). *p < 0.05, **p < 0.01, ***p < 0.001 compared to saline