Respiratory diseases are a range of diseases that occur in the respiratory system including mild ones such as the self-limiting common cold, and severe ones such as life-threatening bacterial pneumonia or pulmonary embolism. The United States has 100 million people with colds and flu each year, and one in seven people in the United Kingdom suffers from chronic airway disease, primarily chronic obstructive pulmonary disease (COPD) and bronchial asthma. In Canada, respiratory diseases account for 10 percent of hospitalizations and 16 percent of deaths due to respiratory diseases. In China, respiratory diseases are the third leading cause of death, with approximately 1 million deaths and 5 million workforce losses each year. With the development of the economy and the increasing research in respiratory disciplines, significant progress has been made in both basic and clinical research on respiratory medicine. This article will review the research achievements made by Chinese experts in the past few years, including new advances in the pathogenesis, prognosis and treatment of major respiratory diseases such as COPD, asthma, lung cancer, severe acute respiratory syndrome (SARS), acute lung injury/acute respiratory distress syndrome (ALI/ARDS), lung infections, pulmonary embolism and obstructive sleep apnea syndrome (OSAS). Chronic obstructive pulmonary disease (COPD) According to the World Health Organization, COPD will be the first economic burden of disease in China and the fifth economic burden of disease in the world by 2020. A large sample of lung function-based surveys on COPD prevalence showed a significantly higher prevalence of COPD in rural populations, older adults, smokers, low body mass index, lower education, poorly ventilated kitchens, occupational exposure to dust or biofuels, childhood lung disease, and family history of lung disease. Indoor pollutants, especially daily use of biofuels, may be another important risk factor for COPD in rural populations in southern China. A partial genetic susceptibility to COPD has been elucidated. TNF-α and ErbB3 are also involved in the pathogenesis of COPD and both mediate the role of TACE in the course of COPD. A randomized, double-blind, parallel, placebo-controlled study showed that the mucolytic drug carboxymesterol was an effective agent in preventing acute exacerbations in Chinese COPD patients. Moreover, the preventive effect of carboxymesterol was not correlated with COPD severity, smoking, or inhaled corticosteroids. Another study showed that small doses of extended-release theophylline were well tolerated and improved symptoms in patients with stable COPD, although they did not improve lung function. Treatment with salmeterol/fluticasone propionate (sulforaphane, GlaxoSmithKline, UK) consistently improved lung function, quality of life, and symptoms in patients with COPD and was well tolerated in the Chinese population; the improvement in lung function was more pronounced in patients with a history of prior smoking. Bronchial asthma Bronchial asthma is a chronic inflammatory disease of the airways in which numerous cells and cytokines are involved. Eosinophils are characteristically present in the airway lumen of patients with bronchial asthma and promote the expression of MHC class II molecules and costimulatory molecules in vivo, which in turn activate T lymphocytes. Eosinophils in the lumen migrate towards the draining paratracheal lymph nodes and accumulate in the T-cell-rich paracortical area, thereby stimulating the proliferation of antigen-specific T-lymphocytes in vivo. In addition, eosinophils can regulate immune responses in vivo by enhancing Th2 cell responses. migration and in situ differentiation of CD34+ stem cells promote inflammatory eosinophilia, and application of antibodies against chemokine receptor 3 in a mouse model of bronchial asthma inhibits migration and differentiation of CD34+ stem cells . Asthmatic rats express high levels of interleukin (IL)-4 and Th2-like cytokines after antigen excitation. Airway epithelial cells initiate inflammatory responses by releasing systemic inflammatory mediators and regulate allergic rhinitis and asthma through immunopathological feedback. Clinical studies in asthmatic patients have shown that B7-1/B7 2-CD28/CTLA-4 molecules are differentially expressed on the surface of various cells and are present as solubilized molecules in the serum of bronchial asthma patients, which is important for the maintenance of Th1/Th2 homeostasis . The suppressive function of CD4+CD25+ T cells is reduced in allergic patients. CD4+CD25+ T cells suppress Th2 responses by downregulating cytokines required for Th2 activation. Liu et al. conducted a comparative study on three polymorphic loci of the ADA gene: ADA1, ADA2 and ADA6 in 120 Han Chinese asthmatics and 116 healthy controls, and showed that the DNA sequence associated with asthma susceptibility was localized between the ADA1 and ADA2 loci. This could be a new strategy for the treatment of bronchial asthma. Results from animal models show that early BCG vaccination better regulates Th1/Th2 cytokine production and thus reduces allergic airway inflammation. Further studies on the role of targeted therapies for airway allergic diseases could help establish effective combination therapy for asthma. A questionnaire study of 527 outpatients showed that with the emphasis on long-term asthma management and the promotion of standardized asthma treatment in recent years, the overall level of asthma control has improved significantly and patients’ awareness of the disease has increased to a greater extent. Severe Acute Respiratory Syndrome SARS is a recently emerged respiratory infectious disease that can be widespread, and the pathogen is a novel strain of coronavirus that likely originated in wildlife. The ward environment and management are very important in preventing nosocomial outbreaks of SARS. This SARS outbreak has given us good warnings and experience to prevent the recurrence of SRAS and HPAI attacks. The pathogenesis of SARS is complex, and the most plausible explanation is the direct damage to target cells by SARS-CoV and the indirect damage due to secondary immune system dysfunction. rapid elevation of IL-6, IL-8 and monocyte chemotactic protein-1 signals secondary infection with high mortality. immunopathological processes in the brain . The detection of SARS-CoV N199 protein by ELISA can be used for clinical diagnosis and screening of SARS-CoV infection.Lu et al. used a mass spectrometry decision tree classification algorithm for the initial identification of SARS, which is expected to be an effective tool for early diagnosis. SARS patients can be protected from reinfection with SARS-CoV for 2 years . Animal studies suggest that the development of short interfering RNA has a promising application as a drug for coronavirus-targeted therapy . Another retrospective study showed that hormone therapy in SARS patients did not reduce individual mortality and hospitalization days, but it reduced overall and immediate mortality and shortened overall hospitalization time. Pleural disease Hydrochannel protein-1 may be involved in the transport of pleural fluid in pathological states. Expression of aquaporin-1 on rat pleural mesothelial cells is increased in tuberculous pleural effusion (TPE) and is thought to be associated with the formation of TPE. RNA interference is expected to be a useful tool to study the mechanism of pleural effusion in vivo. Lymphocytic pleural effusion is defined as a pleural effusion in which the number of lymphocytes accounts for more than 50% of total leukocytes, and malignancy and tuberculous pleurisy are the main etiologies, accounting for more than 90% of the total. CD4+CD25+ regulatory T cell numbers are significantly increased in both malignant pleural effusion (MPE) and tuberculous pleural effusion (TPE), and are suppressed by cytotoxic T lymphocyte-associated antigen 4 ( The mechanism of CD4+CD25+ regulatory T cell recruitment into the pleural space is associated with the local production of IL-16 or chemokine CCL22 by pleural cells. It is clinically important to distinguish between TPE and MPE. Many studies have shown that IFN-γ assay is highly sensitive and specific for the diagnosis of pleural effusion. Although adenosine deaminase is valuable for the diagnosis of tuberculous pleurisy, its overall accuracy is lower than that of IFN-γ. Carcinoembryonic antigen is the most widely used tumor marker, and it is a very useful diagnostic tool to confirm the diagnosis of malignant pleural effusion and is also often used to differentiate malignant pleural mesothelioma from metastatic lung cancer. The available evidence does not recommend CA-125, CA 15-3, CA 19-9 and CYFRA 21-1 alone for the diagnosis of malignant pleural effusion, but meta-analysis has shown a greater sensitivity for the combined detection of multiple tumor markers. Detection of soluble trigger receptors on pleural myeloid-1 can help physicians distinguish whether a pleural effusion is bacterial or of other origin. Pulmonary infections The pathogenesis of P. aeruginosa pneumonia in immunosuppressed patients is not fully understood. Xu et al. have demonstrated that the expression of keratinocyte growth factor is lower in the pneumonia model of immunosuppressed rats than in normally immunocompetent rats . Invasive pulmonary aspergillosis is a common form of necrotizing pneumonia. Recent studies have shown that dendritic cells can phagocytose Aspergillus conidia. IL-12 gene-transfected dendritic cells can significantly enhance Aspergillus-specific IFN-γ responses, thereby improving the survival of patients with Aspergillus pneumonia . It is suggested that antigen-stimulated dendritic cells and IL-12 gene therapy could be used as an adjuvant therapy for Aspergillosis. Zhan et al. described the clinical features of critically ill patients with chronic respiratory disease (CRD) combined with invasive pulmonary aspergillosis (IPA) and evaluated the value of early diagnosis and treatment. With the rapid expansion of infiltrative lesions in the lungs, bronchial pseudomembranes, rapid increase in peripheral blood leukocytes, and deterioration of imaging were observed. Patients who were given antifungal therapy early before infiltration survived. Invasive pulmonary aspergillosis (IPA) is not uncommon in critically ill patients with chronic respiratory disease (CRD) and has a poor prognosis. Early diagnosis and empirical treatment based on clinical features are expected to improve the prognosis of patients. Recently, He et al. elaborated the structure of the avian AIV virus from the N-terminus PB1 to the C-terminus PA at the atomic level. A randomized controlled trial of 120 Chinese volunteers demonstrated that immune responses elicited by a small dose of inactivated AIV vaccine plus hydrated aluminum hydroxide adjuvant were essentially equivalent to those elicited by adjuvanted or adjuvant-free split virus vaccines. Clinical studies suggest that passive immunotherapy is a viable option for the treatment of AIV infection. There has also been significant progress in research related to mucus hypersecretion. Mucus hypersecretion is a feature of chronic inflammatory diseases such as bronchial asthma, chronic bronchitis, bronchiectasis and cystic fibrosis. Accompanied by cupped cell proliferation and MUC gene abnormalities, mucus hypersecretion leads to impaired mucus cilia clearance, non-normal flora colonization, airway mucus plug formation, and impaired gas exchange. powerful osmotic water channels of Gob-5 and AQP5 are important genes regulating mucus hypersecretion in asthma. In chronic airway inflammation, airway epithelial cells play an important regulatory role in the overall inflammatory system. IL-13, IL-4 and IL-9 are all important cytokines that cause mucus hypersecretion during airway inflammation, and TNF-α can also cause mucus hypersecretion through PKC signaling. In addition, epithelial growth factor receptor (EGFR) can also cause mucus hypersecretion and proliferation of epithelial cells. The alanine-rich cardamomylated kinase C substrate (MARCKS) was identified as the central regulatory molecule. In conclusion, the regulatory mechanisms of mucus secretion and mucin expression have been gradually elucidated. Lung cancer The question of the equivalence of cisplatin- and carboplatin-based chemotherapy regimens for the treatment of progressive non-small cell lung cancer has largely been answered, with Meta-analysis showing no significant survival advantage in either the cisplatin- or carboplatin-based regimen groups. A recent meta-analysis showed that cytology of chest irrigation fluid has a significant contribution to survival and prognosis of lung cancer patients. Chen et al. studied 97 patients with non-small cell lung cancer and found that tissue factor (TF) promotes angiogenesis, whereas urokinase-type fibrinogen activator receptor (uPAR) promotes lymph node and bloodstream metastasis. co-expression of TF and uPAR may play an important role in the metastasis and prognosis of NSCLC. Non-diagnosis of some rare tumors, such as primary pulmonary synovial sarcoma, relies on microscopic identification of epithelioid or spindle cells or immunohistochemical confirmation of positive staining for cytokeratin, wave proteins, and epithelial membrane antigens. Acute lung injury/acute respiratory distress syndrome Recently, the treatment of ARDS has been studied and curcumin has been found to protect the organism from acute lung injury associated with lung transplantation by inhibiting NF-κB-mediated expression of inflammatory genes. Bone marrow mesenchymal stem cells and angiopoietin-1 (Ang-1) have synergistic effects on the treatment of lipopolysaccharide-type acute lung injury, and Ang-1 gene-modified bone marrow mesenchymal stem cells are expected to be a new strategy for the treatment of acute lung injury. Sun et al. suggested that curcumin (CUR) attenuated acute lung injury by ameliorating oxidative stress and inhibiting NF-κB-mediated expression of inflammatory cytokines. Therefore, curcumin may be a new approach for the treatment of ischemia-reperfusion lung injury. Jin et al. showed that elevated serum IL-6 levels in ARDS patients correlated with the severity of lung injury and could be combined with APACHEII scores to determine the prognosis of the disease. Continuous renal replacement therapy (CRRT) can reduce serum IL-6 levels, decrease the duration of mechanical ventilation and ICU admission, and reduce the incidence of ventilator-associated pneumonia (VAP).CRRT may be the most important treatment for ARDS. Pulmonary embolism The function of endothelial cells to lyse fibrin plays an important role in the pathophysiology of pulmonary vascular disease. Binding of urokinase-type fibrinogen activator to its receptor may be a key pathway for urokinase-type fibrinogen activator expression. The detection of a single protein or the combination of several proteins plus available markers such as D-dimer has greatly improved the accuracy of the diagnosis of acute pulmonary embolism. Thromboendarterectomy is an effective treatment for chronic pulmonary thromboembolism. Right heart insufficiency, right and left ventricular end-diastolic internal and external diameter ratios, and cardiac troponin I are all independent factors in determining disease prognosis. Early detection of right heart insufficiency is beneficial in distinguishing high-risk patients. A study by Pang (64) and Yin et al. found that patients with acute pulmonary thromboembolism (PTE) had damage to the pulmonary vascular endothelium and significant imbalances in the coagulation and fibrinolytic systems. Combined testing of plasma D-dimer, antithrombin III, protein S, protein C, thrombomodulin, tissue-type fibrinogen activator, and fibrinogen activator inhibitor-1 better identified imbalances in the coagulation and fibrinolytic systems. Anticoagulation and thrombolytic therapy help balance the coagulation and fibrinolytic system in PTE patients and protect the function of pulmonary vascular endothelial cells. Obstructive sleep apnea syndrome Meta-analysis showed that continuous positive airway pressure ventilation did not improve the overall quality of life scores of patients with OSAS, but it did improve their physical and mental status. Study design and quality of life questionnaires are important to obtain patient information and assess it effectively. However, general quality of life indicators may not assess important changes in the quality of life of OSAS patients. Yue et al. found that 5-hydroxytryptamine (related to circadian and respiratory rhythms) transporter genes were associated with OSAS susceptibility, especially in male patients, through a study of 5-hydroxytryptamine transporter gene polymorphisms in Chinese OSAS patients. In patients with OSAS combined with hypertension, recurrent motor microarousals and hypoxia occurring at the end of apnea are important factors affecting their circadian blood pressure levels and may lead to elevated blood pressure at night and during the day in patients with OSAS. Patients with OSAS are prone to congestive heart failure, suggesting that OSAS has a detrimental effect on myocardial contractility. There is a strong correlation between right and left myocardial work done index and apnea hypoventilation index. Thus, OSAS is often associated with impaired right and left myocardial function. Conclusions Significant advances have been made in research in respiratory medicine in the past 5 years. As the molecular mechanisms of respiratory diseases continue to be studied, effective preventive and therapeutic measures have greatly reduced the morbidity and mortality of respiratory diseases. Much of today’s research involves the level of molecular immunity, targeted therapies and gene therapy. Despite being in the early stages of exploration, the results of clinical trials are very encouraging. As the understanding of respiratory disease pathogenesis, disease progression factors and therapeutic targets continues to improve, we can better assess disease risk and prognosis and discover new therapeutic strategies. It should also be recognized that in the field of respiratory medicine research, we lack cutting-edge research results and evidence-based medical studies regarding diagnosis and treatment. In addition, because of the difficulty in obtaining histological specimens of human lungs, most of the above-mentioned advances in respiratory medicine have come from animal experiments. We should pay attention to the differences between humans and animals and be able to use advanced experimental techniques, such as transgenic or knockout mice, to conduct research. Also, we need to organize more multicenter, randomized, double-blind, parallel-controlled, placebo-controlled clinical studies. In conclusion, the ultimate goal of respiratory disease research is to reduce the physical and psychological toll of disease on people and to protect the airways and lungs from disease. For this, we need more and more in-depth clinical and basic research. Respiratory medicine researchers have a long way to go.