Beck J M, Liggitt H D, Brunette E N, Fuchs H J, Shellito J E, Debs R J
Respiratory Care Section, Department of Veterans Affairs Medical Center, San Francisco, California 94121-1598.
Infect Immun. 1991 Nov;59(11):3859-62. doi: 10.1128/iai.59.11.3859-3862.1991.
Pneumocystis carinii pneumonia in patients with AIDS may result from impaired local release of gamma interferon from lung lymphocytes and subsequent failure of macrophage activation. We tested this hypothesis with mice rendered immunodeficient by selective depletion of CD4+ lymphocytes and inoculated intratracheally with P. carinii. After aerosol administration of recombinant murine gamma interferon, the intensity of P. carinii infection in these mice was reduced in comparison with that in mice not treated with gamma interferon. Histologic scoring of lung tissue did not reveal additional pulmonary inflammation attributable to gamma interferon. Aerosol administration of gamma interferon may reduce the intensity of P. carinii infection by augmentation of host defense, despite persistent CD4+ lymphocyte depletion.
艾滋病患者的卡氏肺孢子虫肺炎可能是由于肺淋巴细胞局部释放γ干扰素受损以及随后巨噬细胞激活失败所致。我们用通过选择性清除CD4 +淋巴细胞而导致免疫缺陷的小鼠进行实验,并经气管内接种卡氏肺孢子虫来验证这一假设。在雾化给予重组鼠γ干扰素后,与未用γ干扰素治疗的小鼠相比,这些小鼠体内卡氏肺孢子虫感染的强度有所降低。肺组织的组织学评分未显示γ干扰素引起额外的肺部炎症。尽管CD4 +淋巴细胞持续减少,但雾化给予γ干扰素可能通过增强宿主防御来降低卡氏肺孢子虫感染的强度。