Martin William J, Wu Min, Pasula Rajamouli
Department of Internal Medicine, University of Cincinnati, PO Box 670557, Cincinnati, Ohio 45267-0557, USA.
Trans Am Clin Climatol Assoc. 2005;116:221-6; discussion 226-7.
Systemic immunosuppression accounts for significant morbidity and mortality worldwide. Pulmonary infections represent the most common cause of death in these patients. The resident inflammatory cell in the lung is the alveolar macrophage (AM) and its function is markedly diminished by immunosuppression. We hypothesized that AMs from normal mice with or without gene transfer of the gamma interferon gene inside the macrophages, can restore alveolar immunity in immunosuppressed mice with severe combined immunodeficiency syndrome (SCID). To test this hypothesis we intratracheally instilled normal and IFN-gamma activated macrophages to the lungs of SCID mice. We demonstrated that airway delivery of macrophages results in widespread alveolar distribution, improved phagocytic function and ability to clear opportunistic infections such as Pneumocystis carinii. Airway delivery of IFN-gamma expressing macrophages further increased the function of alveolar macrophages. Reconstitution of the lungs of immunosuppressed mice with normal or activated AMs can restore alveolar immunity despite ongoing systemic immunosuppression.
全身性免疫抑制在全球范围内导致了显著的发病率和死亡率。肺部感染是这些患者最常见的死亡原因。肺内的常驻炎性细胞是肺泡巨噬细胞(AM),其功能在免疫抑制状态下会显著减弱。我们推测,来自正常小鼠的AM,无论其巨噬细胞内是否进行了γ干扰素基因的转染,都能够恢复患有严重联合免疫缺陷综合征(SCID)的免疫抑制小鼠的肺泡免疫功能。为了验证这一假设,我们将正常的和经γ干扰素激活的巨噬细胞经气管内注入SCID小鼠的肺部。我们证明,经气道递送巨噬细胞可使其在肺泡中广泛分布,改善吞噬功能以及清除诸如卡氏肺孢子虫等机会性感染的能力。经气道递送表达γ干扰素的巨噬细胞可进一步增强肺泡巨噬细胞的功能。尽管存在持续的全身性免疫抑制,但用正常或激活的AM重建免疫抑制小鼠的肺部能够恢复肺泡免疫功能。