Fig 1: Knockdown of neutrophil recruitment in the SDME model decreased NET formation in peritoneal fluid and developing lesions.(A–D) ELISA for ELA2 in peritoneal fluid from I:I (n = 4), I:α (n = 11), α:I (n = 5), and α:α (n = 5); ELA2 in lesions from I:I (n = 7), I:α (n = 8), α:I (n = 6), and α:α (n = 11); MPO in peritoneal fluid from I:I (n = 4), I:α (n = 4), α:I (n = 5), and α:α (n = 5); and MPO in lesions from I:I (n = 11), I:α (n = 6), α:I (n = 7), and α:α (n = 15). Each graph contains biological replicates from 2 independent experiments. Data for each graph represent ± SEM. Statistical significance for each graph was determined by nonparametric, Kruskal-Wallis followed with 1-tailed Mann-Whitney U tests. Letters different from each other are statistically significant. P ≤ 0.05.
Fig 2: Schematic representation of a proposed mechanism for neutrophil-mediated lesion adhesion and survival.The early development of lesions consists of concurrent neutrophil-dependent and endometrial-dependent phases. Neutrophils recruited to the peritoneal cavity are polarized or activated toward an aged or proangiogenic phenotype (black arrows). Aged neutrophils release NETs (and their byproducts: MPO, ELA2), which respond to fibrinogen to initiate adhesion of minced endometrial pieces and subsequent survival to develop lesions. Proangiogenic neutrophils that may produce NETs and drive survival of minced endometrial pieces through angiogenesis are shown by the dotted pink line. Minced endometrial pieces express survival and adhesive factors to further establish lesion development through attachment, survival, and angiogenesis.
Fig 3: Effect of eGFP K181 infection on the NF-κB signaling pathway in allogeneic skin transplantation mice. 1 × 105 PFU eGFP K181 were inoculated intranasally into allogeneic skin transplantation BALB/c mice on day 14 posttransplantation. The serum levels of (A) TNF-α, (B) IL-1β, (C) IL-6, (D) IL-8, and (E) IL-12 were measured by ELISA; (F) The expression levels of IKKα, IKKβ, p65, p52, TRIF, MyD88, TRAF6, and TAK1 in colon tissues were measured by Western blot at 5, 9, 14, or 21 d postinfection. (G) The levels of anti-flagellin IgG and anti-LPS IgG in serum and MPO in colon tissues were measured at 28 d postinfection. Data are shown as the mean ± SD of six mice per group. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. control
Fig 4: Effect of eGFP K181 infection on colon inflammation and the NF-κB signaling pathway in allogeneic skin transplantation mice. 1 × 105 PFU eGFP K181 were inoculated intranasally into allogeneic skin transplantation MyD88(−/−) and MyD88(+/+) BALB/c mice on day 14 posttransplantation. The serum levels of (A) TNF-α, (B) IL-1β, (C) IL-6, (D) IL-8, and (E) IL-12 were measured by ELISA; (F) The expression levels of IKKα, IKKβ, p65, p52, TRIF, MyD88, TRAF6, and TAK1 in colon tissues were measured by Western blot at 5, 9, 14, or 21 d postinfection. (G) The levels of anti-flagellin IgG and anti-LPS IgG in serum and MPO in colon tissues were measured at 28 d postinfection. Data are shown as the mean ± SD of six mice per group. ** P < 0.01, *** P < 0.001 vs. Myd88(+/+)
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