Introduction. The impaired proliferative capacity of alveolar epithelial cells after injury is an important factor causing epithelial repair dysfunction, leading to the occurrence of idiopathic pulmonary fibrosis (IPF). Alveolar type 2 (AT2) cells as the stem cells of alveolar epithelium participate in the repair process after alveolar injury. Lipocalin‐2 (LCN2) participates in multiple processes regulating the pathological process of alveolar epithelial cells, but the mechanisms involved are still unclear. Method. We used a BLM‐treated mouse model to characterize the expression of LCN2 in lung fibrosis regions and analyzed the location of LCN2 in alveolar epithelial cells. Moreover, human pulmonary alveolar epithelial cells (HPAEpiCs) were transfected with the LCN2 overexpression plasmid vector in vitro. Recombinant human interleukin‐17 (IL‐17) protein (rhIL‐17) at different concentrations was administered to intervene in HPAEpiCs, observing cell viability and analyzing the concentration‐dependent effect of IL‐17. Results. LCN2 was increased in the alveolar epithelium post‐BLM injury, and highly expressed LCN2 was mainly concentrated on AT2 cells in BLM‐injured lungs. Meanwhile, LCN2‐overexpressing HPAEpiCs showed impaired cell viability and cell growth. HPAEpiC intervention with rhIL‐17 mildly rescued the impaired cell proliferation induced by LCN2 overexpression, and the effect of IL‐17 intervention was partially concentration‐dependent. Conclusions. The results revealed the reversed effect of IL‐17 on the impaired proliferative capacity of the alveolar epithelium induced by LCN2 overexpression. The target alveolar epithelial cells regulated by this process were AT2 cells, providing new clues for alveolar epithelium repair after injury and the treatment of lung injury diseases.

Although pulmonary infections caused by Schizophyllum commune (S. commune) are still relatively rare in clinical practice, they are increasingly familiar and valued by clinicians. The clinical symptoms and imaging of pulmonary infection with S. commune are not typical, thus diagnosis needs to be confirmed by clinical etiology. S. commune is one of the main fungal species causing allergic bronchopulmonary mycosis. The overall prognosis of S. commune pulmonary infection is good. This paper describes a case of a woman with no underlying disease who had pulmonary infection with S. commune. This report aims to improve clinicians’ awareness of the disease.

Objective: The aim of this study is to investigate the clinical characteristics of acute asthma exacerbations (AEs) with community-acquired pneumonia (CAP) in adults and establish a CAP prediction model for hospitalized patients with AEs.Methods: We retrospectively collected clinical data from 308 patients admitted to Beijing Luhe Hospital, Capital Medical University, for AEs from December 2017 to August 2021. The patients were divided into CAP and non-CAP groups based on whether they had CAP. We used the Lasso regression technique and multivariate logistic regression analysis to select optimal predictors. We then developed a predictive nomogram based on the optimal predictors. The bootstrap method was used for internal validation. We used the area under the receiver operating characteristic curve (AUC), calibration curve, and decision curve analysis (DCA) to assess the nomogram's discrimination, accuracy, and clinical practicability.Results: The prevalence of CAP was 21% (65/308) among 308 patients hospitalized for AEs. Independent predictors of CAP in patients hospitalized with an AE (P < 0.05) were C-reactive protein > 10 mg/L, fibrinogen > 4 g/L, leukocytes > 10 x 10(9)/L, fever, use of systemic corticosteroids before admission, and early-onset asthma. The AUC of the nomogram was 0.813 (95% CI: 0.753-0.872). The concordance index of internal validation was 0.794. The calibration curve was satisfactorily consistent with the diagonal line. The DCA indicated that the nomogram provided a higher clinical net benefit when the threshold probability of patients was 3% to 89%.Conclusions: The nomogram performed well in predicting the risk of CAP in hospitalized patients with AEs, thereby providing rapid guidance for clinical decision-making.

Objective: Smoke inhalation lung injury (SILI) is a common complication in fires and wars, characterized by acute onset and severe condition. Pirfenidone (PFD), a new small‐molecule drug, has been shown to improve lung function and inhibit pulmonary fibrosis and inflammation. This study aimed to elucidate the effect and underlying mechanism of PFD on SILI in rats. Materials and Methods: SILI rats were constructed using a homemade smoking device, which was then treated with PFD. The blood was collected from the abdominal aorta, and the arterial blood gas was detected. The productions of oxidative stress markers and inflammatory cytokines in plasma were measured by enzyme linked immunosorbent assay assay. Moreover, the alveolar surface area, wet:dry weight ratio of the lung tissues, and bronchoalveolar lavage fluid (BALF) were determined as well. The pulmonary histopathology, cell apoptosis, and the related proteins of nuclear factor kappa B (NF‐κB) pathway were determined by hematoxylin‐eosin staining, TdT‐mediated dUTP‐biotin nick end labeling, and western blot assays, respectively. Results: PFD had a significant protective effect on SILI via inhibiting oxidative stress, inflammation, and apoptosis. Mechanistically, PFD inhibited the activation of NF‐κB pathway in vivo. Moreover, activation of NF‐κB pathway attenuated the PFD‐mediated protective effect against SILI. Conclusions: These data demonstrate that PFD alleviates SILI of rats via the NF‐κB signaling pathway, which provides an attractive therapeutic option for SILI treatment.

The purpose of this study was to establish a nomogram for predicting community-acquired pneumonia (CAP) in hospitalized patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The retrospective cohort study included 1249 hospitalized patients with AECOPD between January 2012 and December 2019. The patients were divided into pneumonia-complicating AECOPD (pAECOPD) and non-pneumonic AECOPD (npAECOPD) groups. The least absolute shrinkage and selection operator (LASSO) regression and multivariate logistic regression were utilized to identify prognostic factors. A prognostic nomogram model was established, and the bootstrap method was used for internal validation. Discrimination and calibration of the nomogram model were evaluated by receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA). Logistic and LASSO regression analysis showed that C-reactive protein (CRP) >10 mg/L, albumin (Alb) 50 U/L, fever, bronchiectasis, asthma, previous hospitalization for pAECOPD in the past year (Pre-H for pAECOPD), and age-adjusted Charlson score (aCCI) & GE;6 were independent predictors of pAECOPD. The area under the ROC curve (AUC) of the nomogram model was 0.712 (95% CI: 0.682-0.741). The corrected AUC of internal validation was 0.700. The model had well-fitted calibration curves and good clinical usability DCA curve. A nomogram model was developed to assist clinicians in predicting the risk of pAECOPD.