Objective:To investigate the risk factors for retrograde type A dissection (RTAD) associated with thoracic endovascular aortic repair (TEVAR) which provided the basis for clinical risk stratification and treatment decision.Methods:The clinical data of 1 688 patients with thoracic aortic disease who underwent TEVAR in our center from January 2004 to December 2019 were retrospectively analyzed. The pathological classification included aortic dissection (1 592 cases) and other thoracic aortic diseases (96 cases). Univariate analysis and categorical multiple logistic regression analysis were used to explore the risk factors for the development of RTAD during or after TEVAR.Results:A total of 18 cases of RTAD were found, with an overall incidence of 1.1% (18/1 688), all of which occurred in aortic dissection group. After adjusting for confounding factors, multivariate logistic regression analysis showed that the incidence of RTAD was significantly decreased(OR=0.27,95%CI 0.07-0.96, P=0.043) when the oversize of stentgraft was 11%-20%, the oversize of stentgraft was ≤10% as the control group, and the difference was statistically significant( P<0.05). The ascending aorta diameter was <40 mm as the control group, and there was no significant difference in the incidence of RTAD between the ≥40 mm group and the control group(OR=2.71,95%CI 0.94-7.84, P=0.065). Conclusions:Aortic dissection is more likely to develop RTAD than other thoracic aortic diseases. A proper stentgraft oversizing ratio could reduce the probability of RTAD. That is to say that a too low stentgraft oversizing ratio is not recommended.

Objective:To investigate the role of IL-21/IL-21R-mediated CD4 + T cells in Chlamydia muridarum ( Cm) respiratory infection. Methods:C57BL/6 mice (WT mice) and IL-21R -/- mice were used to establish the models of Cm respiratory infection through intranasal inhalation of Cm. Flow cytometry was used to detect the proportion, number, activity and function of CD4 + T cells in lung and spleen tissues at 0, 3, 7 and 14 d after Cm respiratory tract infection. IFN-γ and IL-4 levels in spleen cell culture supernatants were detected by ELISA. Na?ve WT mice were transferred with CD4 + T cells in the spleen tissues of IL-21R -/- mice or WT mice on 7 d after infection and given Cm intranasally 2 h later. Then the mice were weighed daily and sacrificed on 14 d after infection. The bacterial load and pathological changes in lung were analyzed. Flow cytometry was performed to detect the proportions and numbers of neutrophils (CD45 + CD11b + Gr-1 high) and alveolar macrophages (CD45 + F4/80 + CD11c high)as well as the proportions of Th1 (IFN-γ + CD4 + ) and Th2 (IL-4 + CD4 + ) cells. ELISA was also performed to measure IFN-γ and IL-4 levels in spleen cell culture supernatants. Results:Compared with WT mice, IL-21R -/- mice showed elevated numbers and enhanced activation of CD4 + T cells, increased proportion of Th1 cells and decreased proportion of Th2 cells in spleen and lung tissues after Cm respiratory infection. Besides, IFN-γ levels increased, while IL-4 levels decreased in spleen cell culture supernatants of IL-21R -/- mice. After Cm infection, the na?ve WT transferred with CD4 + T cells from IL-21R -/- mice showed less body weight loss, reduced bacterial load and alleviated pathological changes in lung tissues, increased proportion of Th1 cells in lung tissue and higher IFN-γ level in spleen cell culture supernatants. Conclusions:IL-21/IL-21R-mediated CD4 + T cells could aggravate Cm respiratory infection by suppressing Th1 cell immune responses.

Objective:To investigate the infiltration and polarization of macrophages in mice during Chlamydia muridarum ( Cm) respiratory infection. Methods:C57BL/6 mice were intranasally infected with 1×10 3 inclusion-forming units (IFU) of Cm to establish the mouse model of Cm respiratory tract infection. The percentages of CD45 + F4/80 + cells and the macrophages expressing CD86, major histocompatibility complex Ⅱ (MHC), inducible nitric oxide synthase (iNOS) and CD206 were detected by flow cytometry. Expression of iNOS, CD206 and CCL2 at mRNA level was detected by real-time quantitative PCR. Results:Cm respiratory tract infection induced the increase of macrophages in mouse lung tissues. Compared with uninfected group, CD45 + F4/80 + macrophages were increased significantly from day 3 and reached the peak on day 7 after Cm infection. Moreover, the expression of CD86, MHCⅡ and CCL2 was increased, and the macrophages were polarized to M1 phenotype. However, the expression of M2 macrophage marker CD206 was decreased gradually. Further studies showed that iNOS expression, the indicator of M1 macrophage activation, was increased after Cm infection and reached to the top on day 7. Conclusions:Cm respiratory infection could induce the infiltration of macrophages in lung tissues and promote the polarization of macrophages to M1 phenotype.