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. 2015 Oct 28;65(4):575–583. doi: 10.1136/gutjnl-2015-309728

Figure 4.

Figure 4

The gut microbiota enhances primary alveolar macrophage function. (A) Capacity of alveolar macrophages derived from gut microbiota-depleted (white) mice and control (black) mice to phagocytose Streptococcus pneumoniae ex vivo for 30 min. (B) Capacity of whole-blood neutrophils derived from gut microbiota-depleted (white) mice and control (black) mice to phagocytose S. pneumoniae ex vivo for 30 min. (C) Capacity of peritoneal macrophages derived from gut microbiota-depleted (white) mice and control (black) mice to phagocytose S. pneumoniae ex vivo for 10 and 30 min. (D and E) Responsiveness of alveolar macrophages derived from gut microbiota-depleted (white) mice and control (black) mice towards lipoteichoic acid (LTA) and (F and G) lipopolysaccharide (LPS) in terms of interleukin (IL)-6 and tumour necrosis factor (TNF)-α production. (H) TNF-α production of whole blood derived from gut microbiota-depleted (white) mice and control (black) mice upon stimulated with LPS. (I and J) LTA-stimulated peritoneal macrophages derived from gut microbiota-depleted mice (white) and controls (black). (K and L) LPS-stimulated peritoneal macrophages derived from gut microbiota-depleted mice (white) and controls (black). Group size is 8 per group; results are shown as means±SEM; n.s. denotes not significant; *p<0.05, **p<0.01 and ***p<0.001.