ABSTRACT
OBJECTIVE: We aimed to investigate whether PM2.5 has the potential to exacerbate neutrophil airway inflammation and to analyze the underlying mechanisms. MATERIALS AND METHODS: The high-volume air sampler (Laoying 2033B, Qingdao, China) was used to collect PM2.5 from January 01, 2016 to December 21, 2016 in Yantai, Shandong Province, China. BALB/c mice were divided into the following four groups: control group, ovalbumin (OVA) group, low-dose PM2.5 group and high-dose PM2.5 group. Mice except for control group were sensitized and challenged by OVA, and those in low-dose PM2.5 group and high-dose PM2.5 group were intranasally administered by PM2.5 suspension. Airway responsiveness of mice was measured. Enzyme-linked immunosorbent assay (ELISA) kit was used to evaluate the expressions of interleukin 17 (IL-17) and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF) and serum samples. Cell counting in BALF and histological examination were measured to explore PM2.5-induced airway inflammation. Protein expression of Integrin ß4 (ITGB4) was assessed by Western blot. RESULTS: Airway hyperresponsiveness (AHR) exacerbated in PM2.5 exposed asthmatic mice in progressively increased doses of acetylcholine chloride (ACH). Levels of IL-17 and TNF-αin BALF and serum increased significantly in PM2.5 groups compared with other groups with significant differences between two PM2.5 groups. PM2.5 exposure exacerbated inflammatory cell infiltration and mucus secretion in airways of asthmatic mice. Percentage of neutrophils in PM2.5 groups was significantly higher in dose-dependent manner. OVA and PM2.5 co-exposure inhibited the expression of ITGB4. In particular, ITGB4 expression in mice of high-dose PM2.5 group was significantly lowered than the low-dose PM2.5 group. CONCLUSIONS: We showed that PM2.5 exposure exacerbates neutrophil airway inflammation in asthmatic mice though up-regulating expressions of IL-17 and TNF-α but down-regulating the expression of ITGB4.
Subject(s)
Air Pollutants/adverse effects , Asthma/metabolism , Down-Regulation/drug effects , Inflammation/chemically induced , Integrin beta4/genetics , Respiratory System/drug effects , Respiratory System/metabolism , Animals , Asthma/pathology , China , Disease Models, Animal , Environmental Monitoring , Female , Inflammation/pathology , Integrin beta4/metabolism , Mice , Mice, Inbred BALB C , Neutrophils/metabolism , Neutrophils/pathology , Respiratory System/pathologyABSTRACT
OBJECTIVE: To investigate the role of IL-9 in chronic obstructive pulmonary disease (COPD), and to explore its potential mechanism. MATERIALS AND METHODS: A mouse COPD model was established by exposure to cigarette smoke. COPD mice were then randomly assigned into two groups, including: the PBS group and the IL-9 antibody group. The above two groups were treated with phosphate-buffered saline (PBS) or IL-9 injection, respectively. The histopathological changes in lung tissues of mice were observed by hematoxylin-eosin (H&E) staining. Immunohistochemistry was performed to detect IL-9-positive (IL-9+) cells in lung tissues. Expression levels of IL-9, sIL-9R, STAT3, and p-STAT3 in peripheral blood of mice were determined by quantitative Real time-polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blot, respectively. In addition, the expression levels of superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS) were detected. RESULTS: H&E staining results showed that the airway wall structure of COPD mice in the PBS group was irregular. Ciliated columnar epithelium exhibited marked degeneration, necrosis and shedding. Besides, numerous inflammatory cell infiltration, narrowing and rupture of the alveolar septa, and larger cysts fused by adjacent alveoli were observed. H&E staining also indicated that the structure of alveolar epithelium was severely impaired in COPD mice. However, the pathological changes in lung tissues of mice in the IL-9 antibody group were much milder than those of the PBS group. Immunohistochemistry results showed a significant deposition of IL-9+ cells in the lung tissues of the PBS group. Meanwhile, the mRNA and protein levels of IL-9, sIL-9R, and p-STAT3 in the PBS group were also remarkably higher than those of the IL-9 antibody group. In addition, SOD content in the PBS group was significantly decreased, whereas the levels of MDA and ROS were significantly increased than those of the IL-9 antibody group. CONCLUSIONS: IL-9 activated STAT3 and aggravated lung injury in COPD mice by increasing inflammatory and oxidative stress.
Subject(s)
Interleukin-9/physiology , Oxidative Stress , Pulmonary Disease, Chronic Obstructive/etiology , Animals , Disease Models, Animal , Lung/pathology , Male , Mice , Mice, Inbred C57BL , Pulmonary Disease, Chronic Obstructive/pathology , Receptors, Interleukin-9/analysis , Receptors, Interleukin-9/physiology , STAT3 Transcription Factor/physiologyABSTRACT
OBJECTIVE: To explore the feasibility of the telescopic technique associated with mucosectomy in preventing pancreatic fistula after pancreaticoduodenectomy (PD). METHODS: The data of 39 patients who received PD in the Affiliated Hospital of Nantong University was retrospecively analyzed. We developed a safe and simple method of pancreaticojejunostomy in 39 patients, in whom approximately 3 cm of jejunal mucosa was cut to improve the adhesion between the loop and pancreatic parenchyma after end-to-end invagination. RESULTS: This procedure was proved to be much more expeditious, and only 2 of 39(5.1%)patients had pancreatic leakages, who were treated with drainage only. No hemorrhage or cholangitis was observed. No postoperative mortality was observed. CONCLUSION: The telescopic technique associated with mucosectomy is an acceptable and safe surgery for pancreaticojejunal anastomosis.
