Cryptogenic organising pneumonia (COP) has long been unrecognised by clinicians, and its concept has been vague, having previously been referred to as “occlusive bronchitis” or “proliferative bronchitis”. “In 1969, Liebow and Carrington summarized several cases of “mechanized pneumonia” and referred to it as “occlusive bronchitis and interstitial pneumonia”. COP is usually referred to as idiopathic BOOP, and in 2002 the American and European Respiratory Societies recommended that COP be classified as a subcategory of idiopathic interstitial pneumonia (IIP). COP is a histopathological description characterized by lesions mainly of alveolar ducts and alveolar lumen filled with loose connective tissue composed of proliferating fibroblasts and myofibroblasts, with varying degrees of involvement of the fine bronchial lumen [2]. However, the lung tissue structure usually remains intact, with mild widening of the alveolar interstitium and mild chronic inflammatory cell infiltration in the interstitium, and there may be hyperplasia of alveolar type II epithelial cells, making it almost impossible to develop a “cellular lung”. Organized pneumonia (OP) can be caused by a variety of diseases, such as infections (bacteria, Mycobacterium, Cryptococcus, Nocardia, viruses), connective tissue diseases (systemic lupus erythematosus, leukoarthritis, rheumatoid arthritis, polymyositis and dermatomyositis, systemic sclerosis, mixed connective tissue disease, dry syndrome, etc.), allergic alveolitis, drugs, radiation, and aspiration. Only a fraction of those of unknown etiology are called idiopathic mechanized pneumonia, or COP. It occurs in patients mostly aged 50 to 70 years, occasionally in children, and can also occur in the elderly. The onset is usually subacute, with symptoms of cough and dyspnea (usually lasting several weeks). The cough is usually dry and without sputum, but can also be accompanied by fever, fatigue, anorexia and weight loss. In some cases, COP can manifest as acute respiratory distress syndrome (ARDS) and respiratory failure. The predominant signs are “popping sounds” and increased respiratory rate, elevated white blood cells and granulocytes, and elevated ESR and CRP. The most common imaging sign of COP is multiple patchy infiltrative shadows in both lungs, which may appear as “ground glass” with normal lung volumes. The shadows can also be “wandering” and the lesions can change from site to site within a few weeks. These patchy infiltrative shadows tend to be peripheral and resemble “eosinophilic pneumonia”. Sometimes, the lesions appear as multi-located solid lesions, mostly bilateral and rarely unilateral [5]. No more than 20% of patients show diffuse interstitial infiltrates on imaging, often secondary to connective tissue disease, and the presence of interstitial pulmonary infiltrates is a poor prognosis. Some patients present with focal pulmonary solids. Pleural effusions do not exceed 25%. BALF of bronchoalveolar lavage fluid in patients with COP suggests an increased total and proportion of lymphocytes, as well as increased neutrophils and eosinophils. lung function in patients with COP is usually mild to moderate with restrictive ventilatory dysfunction and diffusion dysfunction. A small number of patients may have airway obstruction (FEV1/FVC <70%), mostly in patients who smoke. Mild resting and/or post-exertional hypoxemia may be present. The diagnosis of COP requires a combination of clinical and imaging examinations, but the definitive diagnosis relies on histopathological evidence. Transbronchoscopic lung biopsy of TBLB can confirm the diagnosis if the tissue is large enough (including alveoli, alveolar ducts, and interstitial lung). However, if sufficiently large tissue is not available for TBLB, open lung biopsy is often required to obtain pathological specimens. On the basis of imaging, COP with solid lung lesions needs to be differentiated from alveolar carcinoma, lymphoma, vasculitis, especially Wegener's granulomatosis, nodular disease, and infection (especially tuberculosis or atypical mycobacterial infection). When the solid lesion is subpleural, it should be differentiated from chronic eosinophilic pneumonia. In the case of multiple large nodules, the presence of metastatic tumors, lymphoma, and early lung abscess should be considered in the differential diagnosis. The possibility of COP should be considered in the presence of peribronchial and subpleural distribution of solid lesions, and in the presence of both ground glass shadow and cyst, it should also be differentiated from lymphocytic interstitial pneumonia (LIP) or desquamative interstitial pneumonia (DIP). In the process of diagnosing COP it is important to note: 1. Cryptogenic mechanized pneumonia is highly confused with bacterial pneumonia and others because of its low incidence, usually between 40 and 65 years of age, and in some cases even up to 80 years of age or older, and the non-specific nature of the symptoms. 2. Patients often have malaise, flu-like symptoms, weight loss, increased ESR, and images are dominated by solid inflammation with a tendency to spread along the bronchi, combined with an early history of tuberculosis, which is easily misdiagnosed as pneumonia and tuberculosis or even lung cancer. The diagnosis of cryptogenic mechanized pneumonia is based on pathological changes and requires a combination of symptoms, signs and significant imaging changes, with the exception of other similar interstitial pneumonia, to obtain a definitive diagnosis, which is more difficult. The majority of COP patients have significant improvement in imaging after corticosteroid treatment, and COP is a disease that is sensitive to glucocorticoids. The prognosis for patients is often very satisfactory, with more than 2/3 of patients experiencing complete resorption of the lung lesions. The dosage of hormone is prednisone 0.75 mg/kg/d, and the hormone is gradually reduced after 2 to 4 weeks. In COP patients with rapidly progressive disease, short-term high-dose glucocorticoid shock therapy may be required. The total duration of hormone therapy is 6 to 12 months, and relapse can occur in about 1/3 of patients if the duration of therapy is less than 3 months. About 10-15% of COP patients do not respond to glucocorticoids, and the efficacy of immunosuppressive agents, such as cyclophosphamide and azathioprine, is still unclear.