mRNA levels were measured using reverse transcription‑quantitative PCR. Cell viability was examined using Cell Counting Kit‑8 assays. Protein expression levels were measured using western blot analysis. Following APAP challenge, the mice were administered 5 mg/kg FTY720 for 30 min. AILI was induced using intraperitoneal injection of 300 mg/kg APAP in male C57BL/6J mice. The aim of the present study was to determine whether FTY720 has a protective effect on AILI. However, the role of FTY720 in AILI remains unclear. Fingolimod (FTY720) is an immunosuppressive drug developed in recent years that has been shown to have a protective effect against ischemia/reperfusion liver injury. doi:10.1371/002Īs the current clinical treatment of acetaminophen (APAP)‑induced liver injury (AILI) has its limitations, new and effective treatment methods are required. Statistical analysis was performed with Kruskal-Wallis test followed by Dunn´s post-test comparing samples from infected mice with samples from control animals (day 0) (C). Graphs show the total numbers of CD11b + GR1 low MΦ/ monocytes and CD11b + GR1 hi neutrophils (y-axis) at the indicated point in time (x-axis). Total numbers of CD11b + GR1 low MΦ/monocytes and CD11b + GR1 hi neutrophils among spleen cells (y-axis) were assessed by flow cytometric staining as described above during the course of infection. with 2×10 6 sfu into the base of the tail. BALB/c (n = 5–7) and CB17 SCID mice (n = 5–7) were infected s.c. Asterisks indicate statistically significant differences (** p<0.01) (B). Statistical analysis was performed with student`s t-test after D´Agostino and Pearson normality test. Each dot in the graphs represents a single mouse (n = 10–11). Graphs show combined results from two independent experiments. Numbers indicate the percentage of the CD11b + GR1 hi neutrophils and CD11b + GR1 low MΦ/monocytes. A representative staining for CD11b and GR1 and gating of cells is shown for a control mouse and a R. typhi-infected CB17 SCID mice (black circles) was assessed at the time of death of the animals by flow cytometry. The percentage of CD11b + GR1 low MΦ/monocytes and CD11b + GR1 hi neutrophils among spleen cells (y-axis) in CB17 SCID control animals (open circles) and R. Asterisks indicate statistically significant differences (***p<0.001) (A). Each dot represents a single mouse (n = 10–11). The graph shows combined results from two independent experiments. typhiinfected CB17 SCID mice at the time of death (middle and right). The photograph shows a representative spleen of a control mouse (left) and two R. The results of this study indicate that scid specifically impairs the differentiation of stem cells into mature lymphocytes myeloid cell differentiation is not affected.CB17 SCID mice develop splenomegaly which is largely due to the accumulation of MΦ and neutrophils. The microenvironment of the C.B-17 scid mouse is conducive to lymphocyte differentiation, because functional B and T cells are easily detectable in mice reconstituted with normal bone marrow cells. B lymphocyte colony-forming units are absent, as are cytotoxic lymphocyte precursors and cells that can generate T cell colonies with cytotoxic progenitors. C.B-17 scid splenocytes fail to proliferate in response to T and B cell mitogens or to allogeneic lymphocytes in a one-way MLR C.B-17 scid cells do serve as stimulators in MLR. Cells from C.B-17 scid spleen are consistently negative in all tests of B and T cell function. The absolute number of bone marrow colony-forming units in C.B-17 scid and C.B-17 mice is comparable. The frequency of in vitro myeloid colony-forming units in C.B-17 scid spleen is elevated, but the absolute number of colony-forming units in C.B-17 scid and C.B-17 spleen is similar. Results showed that C.B-17 scid and their normal counterparts (C.B-17) have similar levels of spleen colony-forming units. Cells from mice with severe combined immunodeficiency disease (SCID) were tested in assays that measure myeloid and lymphoid function.
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