Background: Methicillin-resistant Staphylococcus aureus (MRSA) pneumonia is an important issue with significant morbidity and mortality in clinical practice, especially in diabetes mellitus (DM). Studies focusing on S. aureus pneumonia in DM is limited, we sought to make a relatively comprehensive exploration of clinical characteristics, antimicrobial resistance, and risk factors for mortality of S. aureus pneumonia in DM and non-diabetics mellitus (non-DM). Methods: A retrospective study was conducted in Ruijin Hospital from 2014 to 2017. The characteristics of DM and non-DM patients were assessed, including demographics, comorbidities, using of invasive mechanical ventilation, Hemoglobin A1c (HbA1C), confusion, urea, respiratory rate, blood pressure, age ≥65 years (CURB-65) score, length of hospital stay, clinical outcomes, antimicrobial susceptibility. Independent risk factors for mortality were identified by univariate and multivariate logistic regression analysis. Results: A total of 365 patients with S. aureus pneumonia were included in our study, including 144 with DM and 221 non-DM. DM patients were more susceptible to MRSA infection (65.3% vs. 56.1%, P > 0.05), suffered from much severer pneumonia with a higher CURB-65 score, invasive mechanical ventilation rate (46.5% vs. 28.1%, P < 0.01) and mortality rates (30.6% vs. 23.1%, P > 0.05); almost all DM patients had higher antimicrobial resistance than non-DM patients, the DM group had a higher co-infection rate (47.2% vs. 45.7%, P > 0.05), and Acinetobacter baumannii was the most common bacterium in DM, while Klebsiella pneumoniae ranked first in patients with non-DM. Independent risk factors for pneumonia-related mortality were MRSA and CURB-65. Higher HbA1c levels were linked to a higher MRSA infection and co-infection rate and more severe pneumonia, leading to an increase in mortality. Conclusions: DM patients with poor glucose control are more susceptible to MRSA infection. They suffer from higher antimicrobial resistance, a higher co-infection rate, and much severer pneumonia than non-DM. MRSA itself is an independent risk factor for mortality in all patients.

Abstract. Suppressor of cytokine signaling-1 (SOCS1) is a protein that negatively regulates cytokine and growth factor signaling. However, little is known regarding the precise role it plays in idiopathic pulmonary fibrosis. The aim of the present study was to construct a recombinant lentiviral vector for RNA interference targeting the SOCS1 gene and to detect the expression in human alveolar epithelial cells. A lentiviral vector-mediated RNA interference method was used to establish a SOCS1-negative cell line of alveolar origin (A549). Three pairs of complementary small hairpin RNA (shRNA) oligonucleotides targeting the SOCS1 gene were designed, synthesized and inserted into the pPll3.7 vector. Packaged lentivirus particles were obtained after 48 h, and the supernatant was used to transfect the human alveolar epithelial cell line A549. The expression of the SOCS1 protein was detected by Western blotting. MTT assay was used to detect the cell proliferation of alveolar epithelial cells with SOCS1 knockdown. The recombinant plasmids were confirmed by sequencing. The lentivirus-containing supernatant effectively infected the A549 cell line, and the expression of SOCS1 protein was inhibited, which was confirmed by Western blotting in the target cells. MTT assay indicated the inhibition effect for cell proliferation of A549 cells in the SOCS1-RNA interference group, compared to the control group with no interference-mediated silencing of the SOCS1 gene. A lentiviral vector for RNA interference targeting the SOCS1 gene was successfully constructed, and cell survival tests showed that knockdown of the SOCS1 gene promotes the apoptosis of alveolar cells.