嗜酸粒細胞性支氣管炎(EB)是一種獨立的疾病嗎?答案是否定的，現有的證據也不支持。 廣義的EB是指氣管和支氣管壁存在明顯嗜酸粒細胞浸潤的一種病理狀態，為描記氣道炎癥特征的術語。作為一種常見的發病機制，EB參與多種呼吸系統疾病的發生。哮喘的基本特點就是EB，并與氣道高反應性、氣道重塑和可逆性氣道阻塞密切相關 。除此之外，非哮喘性EB(nonasth— matic eosinophilic bronchitis)、COPD、上氣道咳嗽綜合征和胃食管反流性咳嗽等均可見EB改變，甚至無下呼吸道癥狀的變應性鼻炎或部分健康人也存在這種類型的氣道炎癥。因此，EB在臨床上至少存在哮喘、非哮喘性EB、合并COPD 和無癥狀等表現形式。廣義的EB并不是一種疾病，而是多種呼吸道疾病的共同病理過程。 狹義的EB即非哮喘I生EB，是指以咳嗽為唯一癥狀、肺通氣功能和氣道反應性正常、誘導痰中嗜酸粒細胞明顯增多而皮質激素治療有效者，是慢性咳嗽的常見病因。目前有觀點認為，和咳嗽變異型哮喘相似，EB可能是極輕微的哮喘或哮喘的前期表現。研究發現，EB的病因和發病機制與哮喘很相似。如引起哮喘的環境職業因素和吸入過敏原均可導致EB，Th2炎癥反應是兩者嗜酸粒細胞氣道炎癥的主要基礎。大部分研究顯示介導EB和哮喘的嗜酸粒細胞氣道炎癥的細胞和細胞因子相同，或僅有程度上的差別。EB和哮喘一樣也存在呼出氣一氧化氮濃度增加，氣道上皮基底膜增厚和上皮下纖維化，氣道炎癥及氣道重塑改變程度兩者也相似 。最大的不同在于肥大細胞在氣道壁不同部位的浸潤和激活。哮喘患者肥大細胞主要浸潤支氣管平滑肌層，而在EB則主要位于支氣管黏膜層 。肥大細胞在氣道壁的不同空間分布可以解釋哮喘的氣道高反應性和EB的咳嗽高敏感性，但不足于據此認為兩者為不同的疾病。
Objective To explore the effect of lower airway inflammation on the pathogenesis of upper airway cough syndrome( UACS) . Methods Ten cases of UACS and 10 cases of chronic rhinitis or sinusitis without cough were enrolled as group A and group B, respectively. And 10 healthy volunteers were included as controls( group C) . The cough threshold C2 and C5 to inhaled capsaicin, defined as the lowest concentration of capsaicin required to induce ≥2 and ≥5 coughs, was measured. The total and differential cell counts was determined in induced sputum, and the levels of histamine and prostaglandin E2 were analyzed in supernatant of sputum. Results Cough threshold was significantly lower in group A than group B [ C2: ( 0.65 ±0. 08) μmol / L vs ( 3.90 ±1. 37) μmol / L; C5: ( 1.59 ±0. 28) μmol / L vs ( 33.46 ±23. 71) μmol / L, P lt;0. 05] and comparable between group B and group C( P gt; 0. 05) . Group A, similar to group B( P gt; 0. 05 ) , contained more inflammatory cells, with decreased percentage of macrophages and increased percentage of neutrophils in induced sputum than group C( P lt; 0. 05) . Furthermore, the levels of histamine[ ( 9. 55 ±1. 89) ng/mL vs ( 2. 37 ±0. 25) ng/mL, P lt; 0. 05] and prostaglandin E2 [ ( 361. 71 ±39. 38) pg/mL vs ( 144. 34 ±15. 69) pg/mL, P lt; 0. 05] were higher in supernatant of induced sputum from group A than group B, while the latter was not different from group C( P gt; 0. 05) . Conclusion Increased cough sensitivity caused by airway inflammation may be important for the pathogenesis of UACS, and the activation of mast cells in mucosa of lower airway might be an important factor.