Background: AECOPD is a severe status of COPD. The prolonged length of hospital stay (LHS) was associated with poor prognosis and higher medical costs in AECOPD patients. Identification of the risk factors for prolonged LHS will help physicians provide targeted and personalized interventions, reduce LHS, and avoid unnecessary health services in COPD patients. This study aimed to explore the risk factors for prolonged LHS in hospitalized AECOPD patients. Methods: In this multicenter cross-sectional study, 598 AECOPD patients were screened. In the end, the LHS of 111 were <7 days (Normal LHS, N-LHS), 218 were 7-10 days (Mild Prolonged LHS, MP-LHS), and 100 were≥11 days (Severe Prolonged LHS, SP-LHS). Demographic data, underlying diseases, symptoms, and laboratory findings were collected. Multiple logistics regression was performed to investigate the independent risk factors for prolonged LHS in AECOPD patients. Results: The significant differences in 11 variables were found by univariate analysis. Since significant collinearities among white blood cells (WBC), neutrophils (NS), and NS% were observed, WBC and NS% were excluded. Therefore, 9 factors were included in multiple logistics regression. Subsequently, our results identified that the rates of hypertension and chronic cor pulmonale (CCP) were independently associated with prolonged LHS in AECOPD patients. Conclusions: Collectively, our results suggested that complications of hypertension and CCP were at a higher risk of prolonged LHS in AECOPD patients. It also indicated that AECOPD combined with hypertension and/or CCP probably more severe. Then, more extensive management should be initially administrated.

LPS produced by Gram-negative bacteria effectively stimulates the maturation of BMDCs. Previous studies have shown that DClps might induce tolerance in autoimmune diseases and cancer in vivo, whereas it remains unclear whether DClps can modulate the immune microenvironment in allergic asthma. We sought to elucidate the potential effects of DClps on OVA-sensitized/challenged airway inflammation in a mouse model of asthma, which may help facilitate the application of specific tolDCs in allergic asthma patients in the future. We generated and obtained DClps from wild-type mice to evaluate their functional characteristics by ELISA and FACS. We also induced OVA-sensitized/challenged asthmatic mice and intraperitoneally treated these mice with DClps to assess the effects of these injected cells by histopathologic analysis and performing inflammatory cell counts in BALF. Changes in memory CD4+ T cells, Tregs and phosphorylated protein in lung digests were analyzed. DClps exhibited lower levels of CD80 and MHCII and increased levels of anti-inflammatory cytokines such as IL-10 and TGF-β than DCia. Additionally, DClps treatment dramatically ameliorated airway inflammation and diminished the infiltration of pulmonary inflammatory cells. In addition, we prolonged the modeling time of asthmatic mice and demonstrated that DClps treatment decreased the proliferation activity of pulmonary memory CD4+ T cells, which further rendered the downregulation of Th2 cytokines. However, the number of pulmonary Tregs did not discernibly change. DClps treatment also markedly reduced the phosphorylation level of STAT6 protein.