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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Crit Care Med. 2016 Jul;44(7):e530–e543. doi: 10.1097/CCM.0000000000001562

Figure 5. Spred-2 in nonimmune cells plays critical role against influenza virus infection.

Figure 5

The following bone marrow chimeras were created (donor → host): WT → WT, Spred-2 KO → WT, Spred-2 KO → Spred-2 KO, and WT → Spred-2 KO. 8 weeks after reconstitution, bone marrow chimeras were intranasally infected with influenza virus (1 × 102 pfu), and then sacrificed at 5 days post-infection. (A) Representative photomicrographs of hematoxylin-stained lung sections of WT → WT, KO → WT, KO → KO, and WT → KO chimeras at day 5 post-H1N1 infection. Original magnification, ×40; ×200. (B) Quantitative analysis of histopathologic changes using a scoring system detailed in the methods. (C) Viral load in BM-chimera mice measured by TCID50. (D) Absolute numbers of inflammatory leukocytes in the BAL fluid of BM-chimera mice. SP2KO = Spred-2 KO. *p < 0.05, **p < 0.01 compared with when both donors and recipients were from WT mice. Data shown indicate mean ± SEM and are from a representative experiment of 2 independent experiments. Each group had 4–6 mice per group.