Decreased bacterial burden in mice with T-cell targeted deletion of HIF-1 α.

Abstract

<p><u>A: </u><i>T cell lineage specific HIF-1</i> α <i>deficient mice have much less bacterial burden in liver and spleen 72 hrs after CLP</i> *:p<0.05 vs. WT, means±SEM, N = 3 per group. <u>B: </u><i>Growth of gas-forming bacteria and tissue destruction during CLP-induced sepsis in mice with HIF-1</i> α<i>-expressing T cells, but not in mice with HIF-1</i> α <i>gene–deleted T cells.</i> Masses of bacteria form rings around gas bubbles in spleens of mice with HIF-1 α expressing T cells. Much less bacteria could be seen in the spleen taken 72 h after CLP from mice with HIF-1 α deficiency in T cells.<u> C: </u><i>T-cell specific deficiency in HIF-1 α enhances effector functions of bactericidal granulocytes. </i><u>Left Panel:</u> Much stronger upregulation of activation marker CD11b on tissue granulocytes (CD11b⁺/Gr-1^bright cells) isolated from HIF-1 α-deleted mice compared to HIF-1 α -expressing control mice. *:p<0.05 vs. WT, N = 3. <u>Right Panel:</u> Higher spontaneous production of hydrogen peroxide by tissue granulocytes (CD11b⁺/Gr-1^bright cells) in HIF-1 α-deleted mice than in HIF-1 α-expressing control mice. *:p<0.05 vs. WT, N = 3.</p