Ye Qiao, Nakamura Shinobu, Sarria Rafael, Costabel Ulrich, Guzman Josune
Department of Pneumology and Allergology, Ruhrlandklinik, Medical Faculty, University of Duisburg-Essen, Germany.
Ann Allergy Asthma Immunol. 2009 Feb;102(2):149-54. doi: 10.1016/S1081-1206(10)60246-3.
Hypersensitivity pneumonitis (HP) is characterized by a granulomatous inflammation and may show various forms of clinical presentation, such as the acute, subacute, and chronic forms. The TH1-associated cytokines interleukin (IL) 12 and IL-18 and tumor necrosis factor alpha (TNF-alpha) may be involved in the pathogenesis of both the acute and chronic forms of HP.
To compare the release of IL-12, IL-18, and TNF-alpha from bronchoalveolar lavage (BAL) macrophages in these 2 forms of HP.
Patients underwent BAL 0 to 6 days after the last antigen exposure. Alveolar macrophages (AMs) from BAL in 6 patients with acute HP, 16 with chronic HP, and 11 controls were cultured for 24 hours. Cytokines in the culture supernatants were measured by enzyme-linked immunosorbent assay.
The production of IL-12, IL-18, and TNF-alpha by AMs was increased in patients with both acute and chronic forms in either the absence or presence of lipopolysaccharide compared with controls. The levels of IL-12, IL-18, and TNF-alpha showed no difference between patients with acute and chronic HP. The spontaneous production of IL-12, IL-18, and TNF-alpha did not correlate with the CD4/CD8 ratio in BAL. The spontaneous and lipopolysaccharide-stimulated release of IL-12 showed a positive correlation with the percentage of lymphocytes (r = .470, P = .03; r = .496, P = .02; respectively) in BAL.
This study demonstrates that an increased release of IL-12, IL-18, and TNF-alpha by AMs is associated with both the acute and chronic forms of HP.
过敏性肺炎（HP）以肉芽肿性炎症为特征，可表现出多种临床形式，如急性、亚急性和慢性形式。与TH1相关的细胞因子白细胞介素（IL）-12、IL-18和肿瘤坏死因子α（TNF-α）可能参与HP急性和慢性形式的发病机制。
比较这两种形式HP中支气管肺泡灌洗（BAL）巨噬细胞释放IL-12、IL-18和TNF-α的情况。
患者在最后一次接触抗原后0至6天接受BAL。对6例急性HP患者、16例慢性HP患者和11例对照者的BAL中的肺泡巨噬细胞（AM）进行24小时培养。通过酶联免疫吸附测定法测量培养上清液中的细胞因子。
与对照组相比，无论有无脂多糖，急性和慢性形式患者的AM产生IL-12、IL-18和TNF-α均增加。急性和慢性HP患者之间IL-12、IL-18和TNF-α水平无差异。IL-12、IL-18和TNF-α的自发产生与BAL中的CD4/CD8比值无关。IL-12的自发释放和脂多糖刺激释放与BAL中淋巴细胞百分比呈正相关（分别为r = 0.470，P = 0.03；r = 0.496，P = 0.02）。
本研究表明，AM释放IL-12、IL-18和TNF-α增加与HP的急性和慢性形式均相关。
