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We previously reported that massive infiltration of neutrophils in C3H/HeN (C3H) mice could not efficiently control Chlamydia muridarum (Cm) infection and might contribute to the high susceptibility of these mice to lung infection. To further define the nature of neutrophil responses in C3H mice during chlamydial infection, we examine the expression of adhesion molecules and CD11b related to neutrophils infiltration and activation, respectively, following intranasal Cm infection. The results showed that the expression of selectins (E-selectin, P-selectin and L-selectin), and intercellular cell adhesion molecule-1 (ICAM-1) in the lung of C3H mice increased more significantly than in C57BL/6 (B6) mice, the more resistant strain. These results correlated well with the massive neutrophils infiltration in C3H mice. In contrast, CD11b expression on peripheral blood and lung neutrophils in C3H mice exhibited a significant reduction compared with B6 mice during the late phage of infection (day 14). These findings suggest that the high-level expression of adhesion molecules in C3H mice may enhance neutrophils recruitment to the lung, but the decline of CD11b expression on neutrophils may attenuate neutrophil function. Therefore, CD11b down-regulation on neutrophils may contribute to the failure of C3H mice to control chlamydial lung infection. Cellular & Molecular Immunology. 2009;6(4):253-260.

Methods: nt-mESCs were cultured using a bioreactor system to develop embryoid bodies, which were induced with 1% ascorbic acid to differentiate into cardiomyocytes. nt-mESC-derived cardiomyocytes (nt-mESCs-CMs) were enriched by Percoll density gradient separation to generate nt-mESCs-PE-CMs. Ischemia was induced by ligating the left anterior descending coronary artery in female Sprague-Dawley rats. Immunosuppressed rats were randomly assigned to received an injection containing 5Â10 6 cells of mESCs, nt-mESCs, nt-mESC-CMs, or nt-mESC-PE-CMs. Results: Analysis performed 8 weeks after transplantation revealed teratoma formation in 80%, 87%, and 33%* of rats administered mESCs, nt-mESCs, and nt-mESC-CMs, respectively, (*P< 0.05 nt-mESC-CMs vs. mESCs). Mean tumor volumes were 82.72AE6.52, 83.17AE3.58, and 50.50AE5.98* mm 3 , respectively, (*P< 0.05 nt-mESC-CMs vs. mESCs). In contrast, no teratoma was detected in rats that received nt-mESC-PE-CMs. Octamer-binding transcription factor 4, a specific marker of undifferentiated nt-ESCs, was detected by polymerase chain reaction in rats that received nt-mESCs and nt-mESC-CMs, but not in rats that received nt-mESC-PE-CMs. Conclusions: nt-mESCs have the same pluripotency as mESCs and teratoma formation with nt-mESC transplantation could be induced by cell differentiation and enrichment.

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