ABSTRACT
Tracheobronchopathia osteochondroplastica (TBO) is a rare disease with unknown etiology characterized by ossifying nodules in the trachea and bronchial walls without involvement of the posterior wall of trachea. A 35-year-old woman admitted to Second Xiangya Hospital, Central South University, in August 2018 was diagnosed as TBO. She complained of dyspnea for over two years, worsening in autumn and winter, and was detected with tracheal ossification via bronchoscopy and biopsy. The patient received no special treatment, and no improvement or deterioration of symptoms was observed during the 3-month follow-up. We reviewed 60 TBO cases and found that 60％ of them were female, with ages of 20-80 (53.62±15.97) years. The involved lesion sites were from the vocal cords to the bronchial segments, mainly in the trachea and bilateral main trachea, and the lower part of the trachea was more common. Combined respiratory symptoms were common. The diagnosis mainly depends on bronchoscopy and biopsy. Symptomatic treatment is the main strategy for symptomatic TBO patients, including endoscopic intervention and surgery. It is generally believed that the short-term prognosis of TBO is good, but the long-term prognosis still needs to be further studied.
ABSTRACT
<p><b>BACKGROUND</b>Aerobic exercise can improve symptoms, reduce airway inflammation, and even ameliorate airway remodeling in asthmatic animals and patients. However, previous studies have focused mainly on the effect of aerobic exercise on steroid-sensitive asthma (SSA). The goals of this study were to determine the effect of low-intensity aerobic exercise training on airway hyperresponsiveness, inflammation, and remodeling in a rat model of steroid-resistant asthma (SRA) and to identify the potential mechanisms underlying these effects.</p><p><b>METHODS</b>Endotoxin-free ovalbumin with or without lipopolysaccharide were applied to establish rat models of SRA and SSA, respectively. Airway hyperresponsiveness, inflammation, remodeling, expression of interleukin (IL)-25, IL-33, thymic stromal lymphopoietin (TSLP), high mobility group box-1 (HMGB1), and IL-17 in bronchoalveolar lavage fluid (BALF), and the role of dexamethasone (DXM) were compared between these two asthmatic rat models. The effect of low-intensity aerobic exercise training and anti-HMGB1 treatment on airway hyperresponsiveness, inflammation, and remodeling in SRA rats also was evaluated.</p><p><b>RESULTS</b>SRA rats developed neutrophil-dominated airway inflammation ((29.5±4.1)% of the total cell numbers in BALF), whereas SSA rats developed eosinophil-dominated airway inflammation ((24.0±6.1)% of the total cell numbers in BALF). Compared with SSA rats, SRA rats had more severe airway hyperresponsiveness, lower levels of IL-25 ((33.6±10.3) vs. (104.8±24.9) pg/ml), IL-33 ((87.5±25.0) vs. (226.6±40.7) pg/ml), and TSLP ((1 933.2±899.5) vs. (7 224.0±992.1) pg/ml), and higher levels of HMGB1 ((21.2±4.5) vs. (5.4±1.6) ng/ml) and IL-17 ((780.5±261.7) vs. (291.4±76.4) pg/ml) in BALF (all P < 0.05). However, there was no significant difference in goblet cell hyperplasia, subepithelial collagen thickness, and airway smooth muscle remodeling between the two groups. Compared with control SSA rats, airway hyperresponsiveness, inflammation, and remodeling in SRA rats were less sensitive to DXM treatment. Anti-HMGB1 treatment attenuated airway hyperresponsiveness, inflammation, and remodeling in SRA rats to a certain extent and was accompanied by lower levels of IL-17 ((369.2±126.7) vs. (780.5±261.7) pg/ml in control SRA rats) in BALF (P < 0.05). Low-intensity aerobic exercise training decreased the expression of both HMGB1 ((14.1±2.9) vs. (21.2±4.5) ng/ml in control SRA rats) and IL-17 ((545.3±148.6) vs. (780.5±261.7) pg/ml in control SRA rats) in BALF (all P < 0.05) and was accompanied by improved airway hyperresponsiveness, inflammation, and remodeling in SRA rats (all P < 0.05).</p><p><b>CONCLUSIONS</b>Low-intensity aerobic exercise training attenuated airway hyperresponsiveness, inflammation, and remodeling in a rat model of SRA. Decreased HMGB1 and IL-17 levels in BALF by aerobic exercise training at least partly contributed to the improvements of SRA.</p>
Subject(s)
Animals , Male , Rats , Airway Remodeling , Physiology , Asthma , Drug Therapy , Metabolism , Therapeutics , HMGB1 Protein , Metabolism , Physical Conditioning, Animal , Methods , Rats, Sprague-Dawley , Respiratory SystemABSTRACT
Objective To elucidate intracellular transcription factor activation of C_7～T_5 dorsal root ganglia in rats recurrently infected with respiratory syncytial virus (RSV). Methods Eighty 1～2 weeks old Sprague-Dawley rats were randomly divided into 2 groups: a control group and a RSV-infection group. The rats in the RSV-infection group were infected with 5 ×10~5 U/mL RSV once a week and the rats in the control group were treated with culture medium without RSV. Airway response was measured after 8 weeks. Lung tissue was submitted for HE staining and in situ hybridization. The C_7～T_5 dorsal root ganglia were obtained for the preliminary screening of the intracellular transcription factors by TranSignal~(TM) protein/DNA combo array. Nuclear protein of C_7～T_5 dorsal root ganglia were extracted and submitted to Western blot. Results Airway response in the RSV-infection group was higher than that in the control group (P＜0.05). HE staining showed inflammatory cell infiltration, and in situ hybridization demonstrated positive RSV RNA in the RSV-infection rat lung which was not present in the control group, thus validating the efficacy of our model. TranSignalTM protein/DNA combo array screening showed that 55 transcription factors increased by at least 2 folds in the C_7～T_5 DRG cells of the RSV-infection group. The transcription factors Smad and interferon regulatory factor (1 or 2) were the 2 most upregulated transcription factors identified by combo array screening (59 and 43 fold increase compared with the control, respectively). Western blot confirmed Smad(1/2/3) and IRF-1 upregulate while IRF-2 remained unchanged. Conclusion Respiratory syncytial virus infection results in airway hyperresponsiveness and transcription factor activation in C7～T5 spinal adorsal root ganglia in rats, which may contribute to airway nerve network dysfunction and airway hyperresponsiveness.