Transplanted mice were kept in individual ventilation cages and supplemented with 0.001% enrofloxacin (Bayer HealthCare, Berlin, Germany) in sterile drinking water. Engraftment was evaluated at 6-9 weeks by determining the presence of human CD45+ populations Selleck Talazoparib in mouse blood and BM. The percentage of human CD45+ cells was calculated as the proportion of labeled human CD45+ over isotype antibody control. For multilineage engraftment, human CD45+CD33+ and CD45+CD71+ cells were measured in mouse BM; human CD45+CD19+ and

CD45+CD4+ cells were measured in mouse peripheral blood by flow cytometry. Anti-CD45-FITC and anti-CD4-APC antibodies were from BD Pharmingen; anti-CD19-PE, anti-CD33-APC, and anti-CD71-APC antibodies were from BioLegend. Data are presented as the percentage and the mean ± standard deviation (SD). Fisher’s exact test and the Student t test were performed using SPSS software (v. 16.0; SPSS, Inc., Chicago, IL). P < 0.05 was regarded as statistically significant. Although blood chimerism development is not uncommon in LT patients, the related reports have presented only a single or a few cases. There has not been any study on hematopoietic chimerism in a large cohort and in long-term LT patients. We investigated hematopoietic chimerism of donor origin

in 249 LT survival patients; the shortest time after LT was 1 day, and the longest time Osimertinib after LT was 8 years. The overall incidence of blood chimerism was 6.43% (16 of 249; Table 1). The incidence of chimerism was 11.11% (10 of 90) among patients evaluated a short time after LT (1 day to <6 months), whereas the incidence was 3.77% (6 of 159) among long-term LT survival patients (6 months to 8 years; Table 2). There were 6 patients with chimerism lasting more than 7 months, with the longest lasting 4.0-4.5 years (case 351; Fig. 1A). Thus, the short time after LT group had a significantly

higher blood chimerism (P = 0.03; Table 2). Blood chimerism of donor origin could result from resident leukocytes/lymphocytes in the liver graft6, 16, 17; it could also result from HSPCs present in the liver. If the chimerism results from donor HSPCs, then the type of donor liver, the sex of the donor, and the age of the donor may have an effect on the development of blood chimerism. We found that there were selleck no statistically significant associations between donor liver type (i.e., cadaveric and living), donor sex (male and female), or donor age (<50 and ≥50 years old), and chimerism formation (Table 2). Thus, liver graft type and sex and age of the donor had no significant effects on the development of chimerism. Interestingly, chimerism-positive cases were 7.57% (14 of 185) in non–hepatocellular carcinoma (non-HCC) LT patients. These non-HCC LT patients included those with cirrhosis or cirrhosis with acute complication, chronic or acute hepatitis; and congenital or heritable diseases. By comparison, there were 3.13% (2 of 64) positive cases in HCC patients.