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. 2019 Feb 14;9(5):1369–1384. doi: 10.7150/thno.32451

Figure 1.

Figure 1

GdX deletion attenuates LPS-induced inflammatory responses in vivo. (A) GdX-deficient mice (GdX-/Y) were resistant to LPS challenge. Survival rates of GdX-/Y and their wildtype (GdX+/Y) littermates (n=15) were observed after challenged with a lethal dosage of LPS (30 mg/kg body weight, ip). (B) A number of NF-κB target genes had significantly lower expressions in GdX-/Y mice than control mice after LPS injection. The heat map of downregulated NF-κB target genes (list of 32 genes, absolute log2 >1, false discovery rate <0.05, p<0.05) in GdX-/Y mice (n=2) and wildtype littermates (n=2) injected with LPS. The mice were injected with LPS (20 mg/kg body weight, ip), and 6 hrs after injection, RNA was extracted from their splenocytes and performed the RNA-Seq analysis. (C-D) GdX deletion decreased the serum concentrations of pro-inflammatory cytokines under acute inflammation. Levels of IL-6 and TNF-α in serum from GdX+/Y and GdX-/Y mice (n≥6) were examined by ELISA after LPS challenge (20 mg/kg body weight; ip). (E) GdX is abundantly expressed in myeloid cells. mRNA levels of GdX were measured by real-time PCR in different immune cells. (F) GdX is highly expressed in RAW264.7 and DC2.4 cell lines. (G-I) Different subtypes of FLDCs from GdX+/Y and GdX-/Y mice were used to measure the productions of IL-6 in response to indicated TLR ligand stimulation. Results were presented as mean ± SEM from at least two repeats *, p < 0.05; **, p < 0.01; ***, p < 0.001.