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Pathogenic Intestinal Bacteria Enhance Prostate Cancer Development via Systemic Activation of Immune Cells in Mice

Figure 2

Intestinal H. hepaticus infection triggers systemic elevations in pro-inflammatory cytokines.

A) Serum levels of pro-inflammatory cytokines were increased in ApcMin/+ mice after H. hepaticus infection. Eotaxin, IL-3, TNF-α and IL-1α were significantly elevated in comparison with age-matched uninfected ApcMin/+ controls. When compared with H. hepaticus infected wt mice, infected ApcMin/+ mice had significantly higher IL-17, IL-1α, IL-3, eotaxin and IL-9 concentration in their blood serum. Bio-Plex Cytokine Assay used sera of n=5 mice per group. ***p<0.001; *p<0.05. B) Paracortical areas in mesenteric lymph nodes. H. hepaticus infected ApcMin/+ mice at high risk of prostate cancer had large amounts of cytoplasmic and extracellular IL-17 that significantly decreased after depletion of TNF-α. IL-17-specific immunohistochemistry; Hematoxylin counterstain, DAB chromogen. Bars=25 μm. C) Morphometric assessment of IL-17 in immunohistochemically stained sections of mesenteric lymph nodes. Both ApcMin/+ genetic status and intestinal infection by H. hepaticus significantly correlate with a TNF-α-mediated increase of IL-17 expression in the mesenteric lymph nodes. ***p<0.001; **p<0.01; *p<0.05.

Figure 2