IL-4 Is Required for Defense against Mycobacterial Infection
-
- Sugawara Isamu
- Department of Molecular Pathology, The Research Institute of Tuberculosis
-
- Yamada Hiroyuki
- Department of Molecular Pathology, The Research Institute of Tuberculosis
-
- Mizuno Satoru
- Department of Molecular Pathology, The Research Institute of Tuberculosis
-
- Iwakura Yoichiro
- Laboratory Animal Research Center, Institute of Medical Sciences, The University of Tokyo
抄録
Although the involvement of T helper (Th1) cells is central to protection against intracellular bacteria, including Mycobacterium tuberculosis, the involvement of Th2 cells, characterized by potent interleukin (IL)-4 secretion in mycobacterial infection is still unclear. In order to clarify the role of IL-4 in murine tuberculosis, IL-4-deficient mutant mice, IL-4 knockout (IL-4 KO) mice, were utilized. The mice were infected with H37Rv, Kurono or BCG Pasteur via an airborne infection route by placing them in the exposure chamber of a Middlebrook airborne infection apparatus. Their capacity to control mycobacterial growth, granuloma formation, cytokine secretion, and nitric oxide (NO) production were examined. These mice developed large granulomas, but not necrotic lesions in the lungs, liver or spleen (P<0.05). This was consistent with a significant increase in lung colony-forming units (CFU). Compared with levels in wild-type mice, upon stimulation with mycobacteria, splenic IL-10 levels were low and IL-6 levels were intermediate, but interferon (IFN)-γ and IL-12 levels were significantly higher. IL-18 levels were within the normal range. The level of NO production by alveolar macrophages of the IL-4 KO mice was similar to that of the wild-type mice. Granulomatous lesion development by IL-4 KO mice was inhibited significantly by treatment with exogenous recombinant IL-4. These findings were not specific to the IL-4 KO mice used. Our data show that IL-4 may play a protective role in defense against mycobacteria, although IFN-γ and TNF-α play major roles in it. Our data do not rule out an IFN-γ-independent function of IL-4 in controlling tuberculosis.
収録刊行物
-
- MICROBIOLOGY and IMMUNOLOGY
-
MICROBIOLOGY and IMMUNOLOGY 44 (12), 971-979, 2000
Center For Academic Publications Japan
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1571135653081185536
-
- NII論文ID
- 130003484806
-
- ISSN
- 03855600
-
- 本文言語コード
- en
-
- データソース種別
-
- CiNii Articles