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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Brain Behav Immun. 2011 Nov 12;26(3):371–382. doi: 10.1016/j.bbi.2011.11.002

Figure 2.

Figure 2

Intestinal microbiota are necessary for SDR stressor-induced enhancement in bacterial killing and peroxynitrite production. Fig 2A–C: Spleen mass, the number of splenic monocytes/macrophages, and number of splenic neutrophils were increased in both germfree and conventionalized mice exposed to the SDR stressor (*p<0.05 vs. HCC Control). Fig. 2D: Stressor exposure did not affect the number of splenic lymphocytes. Fig. 2E: Splenic macrophages from SDR stressor-exposed germfree mice that lack any endogenous microbiota failed to kill more E. coli than cells from nonstressed HCC Control germfree mice. Conventionalizing the Germfree mice with stool from conventionally-housed mice recapitulated the SDR stressor-enhanced bacterial killing. Splenic macrophages from conventionalized mice exposed to the SDR Stressor killed significantly more E. coli than did cells from nonstressed HCC Control conventionalized mice (*p<0.05). Fig 2F: Splenic macrophages from conventionalized mice exposed to SDR produced significantly more peroxynitrite at 45, 60, 75, 90 min compared to macrophages from mice in all other groups (*p<0.05). Values are means ± SE [n=9(HCC Control Germfree), n=8(SDR Stressor Germfree), n=9(HCC Control Conventionalized), n=8(SDR Stressor Conventionalized), *p<0.05)].