Figure 5.

Increased mortality in streptomycin-treated mice is IFNγ dependent. (A) Mice were given streptomycin for 2 weeks before infection with Sendai virus (SeV). At day 5 and 9 PI SeV, 100 µg of an IFNγ blocking or control IgG monoclonal antibody was given SQ and mortality measured (n = 5/group). (B) Mice were treated as in panel (A) but with the indicated doses of anti-IFNγ antibodies being administered (n = 5/group). p < 0.04 for dose–response (χ²). (C) No difference was noted in the number of SeV-specific CD8⁺ T cells, total CD8⁺ T cells, total CD4⁺ T cells, NK cells (CD3⁻NK1.1⁺ lymphocytes), NKT cells (CD3⁺NK1.1⁺ lymphocytes), innate lymphoid cells (Lin⁻ CD4⁺ lymphocytes), and macrophages (Mac3⁺) at 8 days PI SeV in the lungs of mice treated with reverse osmosis (RO) or RO + streptomycin (n = 3–5 mice/group). (D) IFNγ from NK1.1, CD4, CD8-expressing lymphocytes, CD4⁺Lin⁻ cells, or lung Mac3⁺ macrophages was determined by intracellular flow cytometry on day 8 PI SeV. Mean ± SEM percent of given cell type expressing IFNγ is shown (n = 4–10 mice/treatment/group). See Figure S1 in Supplementary Material for gating strategy.