Antibody and cytokine responses to the cilium-associated respiratory bacillus in BALB/c and C57BL/6 mice.

Antibody and cytokine responses to the cilium-associated respiratory bacillus in BALB/c and C57BL/6 mice.
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BALB/c 和 C57BL/6 小鼠对纤毛相关呼吸道杆菌的抗体和细胞因子反应。

DOI:
10.1128/iai.68.9.4961-4967.2000
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发表时间:
2000
影响因子:
3.1
通讯作者:
Franklin,CL
Franklin,CL
中科院分区:
医学2区
文献类型:
--
作者:
Kendall,LV;Riley,LK;HookJr,RR;Besch-Williford,CL;Franklin,CL

文献摘要

相似文献

纤毛相关呼吸道杆菌(CAR)是一种革兰氏阴性滑行细菌,尽管组织学和血清学证据表明其具有显著的免疫反应,但它会导致啮齿动物持续的呼吸道感染。为探讨卡氏杆菌病的体液免疫和细胞因子反应,用105CAR芽孢杆菌对6周龄雌性BALB/c和C57BL/6小鼠进行气管内接种。采用酶联免疫吸附试验检测血清免疫球蛋白(免疫球蛋白M、Ig_1、Ig_2a、Ig_2b、Ig_3、Ig A)和肺局部细胞因子(肿瘤坏死因子-α、干扰素-γ和白介素4),每7天一次,共49天。BALB/c小鼠在病程早期出现碳酸杆菌诱导的损伤,并随着时间的推移变得更加严重。随着疾病严重程度的增加,BALB/c小鼠所有检测的抗体同型均升高,肺组织肿瘤坏死因子-α、干扰素-γ和IL-4也升高。C57BL/6小鼠出现轻度病变,血清IgM、IgG1、IgG2b和IgG3水平轻度升高,最低限度检测到IgG2a和IgA。在C57BL/6小鼠体内未检测到细胞因子的扰动。BALB/c小鼠持续感染,血清抗体反应强烈,干扰素-γ和IL-4反应升高,提示体液免疫和T细胞反应对预防卡氏杆菌病无效。此外,C57BL/6小鼠的抗体反应平淡,细胞因子反应检测不到,提示体液免疫和T细胞反应在抵抗CAR杆菌诱导的疾病中不是关键。
The cilium-associated respiratory (CAR) bacillus is a gram-negative, gliding bacterium that causes persistent respiratory tract infections in rodents despite histologic and serologic evidence of a marked immune response. To assess humoral immunity and cytokine responses in CAR bacillus disease, 6-week-old female BALB/c and C57BL/6 mice were inoculated intratracheally with 105CAR bacillus organisms. CAR bacillus-specific serum immunoglobulins (immunoglobulin M [IgM], IgG1, IgG2a, IgG2b, IgG3, and IgA) and local pulmonary cytokines (tumor necrosis factor alpha [TNF-α], gamma interferon [IFN-γ], and interleukin-4 [IL-4]) were evaluated by enzyme-linked immunosorbent assay every 7 days for 49 days. BALB/c mice developed CAR bacillus-induced lesions early in the course of disease that became more severe with time. Correlating with increasing disease severity, BALB/c mice had elevations in all antibody isotypes tested, and elevations in pulmonary TNF-α, IFN-γ, and IL-4. C57BL/6 mice developed mild lesions with mild increases in serum IgM, IgG1, IgG2b, and IgG3 levels and minimally detectable IgG2a and IgA. Cytokine perturbations were not detected in C57BL/6 mice. The persistence of infection in BALB/c mice with vigorous serum antibody responses and increased IFN-γ and IL-4 responses suggests that humoral immunity and T-cell responses are ineffective at preventing CAR bacillus disease. Furthermore, the lackluster antibody responses and undetectable cytokine responses in C57BL/6 mice suggest that humoral immunity and T-cell responses are not critical in resistance to CAR bacillus-induced disease.