Figure 3.

The absence of CX3CR1 signaling results in increased neutrophil infiltration and associated responses during fungal-associated allergic airway inflammation. A: C57BL/6 [wild-type (WT)] and CX3CR1-deficient (Cx3cr1-/-) mice were chronically exposed to Aspergillus fumigatus as described in materials and methods. Twenty-four hours after the last organism challenge, lung cells were isolated by bronchoalveolar lavage, enumerated, Fc-blocked, stained with a live/dead staining kit, and stained for neutrophils (CD45⁺, CD11b⁺, Ly-6G⁺, Siglec F⁻). A illustrates cumulative data from 2–3 independent studies (n = 3–4 mice per group per study). B–E: 24 h after last challenge, right lungs were collected and enzymatically digested and unfractionated lung cells were cocultured with A. fumigatus conidia for 24 h at a cell to organism ratio of 1:1. IL-17A (B), granulocyte colony-stimulating factor (G-CSF; C); CXCL1, CCL3, and CCL4 (D); and TNF-α, IL-1α, and IL-1β (E) levels were quantified in lung digest cell culture supernatants by MilliPlex. B–E illustrate cumulative data from 3 independent studies (n = 3–5 mice per group per study). *P < 0.05, **P < 0.01, and ***P < 0.001, respectively (two-tailed Student’s t test).