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. 2020 Feb 26;318(5):L864–L872. doi: 10.1152/ajplung.00455.2019

Fig. 4.

Fig. 4.

Neutralization of TNFα signaling partially blocks production of macrophage-derived C-C motif chemokine ligand 22 (CCL22/MDC) by alveolar macrophages in vitro and prevents elevation of serum CCL22/MDC levels after hemorrhage and resuscitation (H/R) in vivo. A: alveolar macrophages were treated with antibodies against TNFα (α-TNFα), TNFα receptor subtype 1 or 2 (α-TNFR1 or α-TNFR2), or a combination of the anti-TNFα receptor antibodies (α-TNFR1 + R2) in vitro in the presence of 1 ng/mL IFNγ, and CCL22/MDC levels in the supernatant were quantified by ELISA after 24 h (n = 4 replicates/group). *P < 0.05 vs. IFNγ only (by ANOVA with Tukey’s post test). B: male C57BL/6 mice were injected intraperitoneally with antibodies against IFNγ and/or TNFα. After 2 h, mice were subjected to a pressure-clamped model of H/R with Ringer’s lactate (LR) or a sham procedure. CCL22/MDC levels were quantified by ELISA in the serum 4 h after the hypotensive episode (n = 5 mice/group). *P < 0.05 vs. H/R only (by ANOVA with Tukey’s post test).