Brown M B, Reyes L
Department of Infectious Diseases, College of Veterinary Medicine, University of Florida, Gainesville 32611-0633.
Infect Immun. 1991 Jun;59(6):2181-5. doi: 10.1128/iai.59.6.2181-2185.1991.
Mycoplasma pulmonis causes chronic murine respiratory mycoplasmosis and genital disease in rats. Specific immunoglobulin M (IgM), IgA, and IgG and its subclasses present in sera and tracheal and uterine lavage samples from 36 naturally infected Sprague-Dawley female rats were tested for reactivity with M. pulmonis in an enzyme-linked immunosorbent assay. Ten specific-pathogen-free Sprague-Dawley female rats served as the negative controls. Tracheal and uterine lavage samples were cultured quantitatively for M. pulmonis. M. pulmonis was isolated from the trachea (35 of 36) and uterus (17 of 36) of naturally infected rats; all rats were infected in at least one of the two sites cultured. M. pulmonis was not isolated from any control rat. There was a significant difference in levels of specific antibody of all classes except IgG2c between control and naturally infected animals (P less than 0.001 for IgM, IgG, IgG1, and IgG2a; P less than 0.002 for IgG2b; and P less than 0.02 for IgA). There was no correlation between numbers of M. pulmonis cells isolated and the amount or class of antibody measured in serum or tracheal lavage specimens. The predominant antibodies to M. pulmonis found in the sera of naturally infected rats were IgG and IgM. The IgG2a subclass was responsible for the majority of IgG-positive animals. There were no differences between rats which were positive by culture for M. pulmonis in the uterus (U+) and rats which were negative by culture for M. pulmonis in the uterus (U-) with respect to distribution or amount of antibody classes and subclasses in the serum. However, tracheal wash samples from U+ rats had significantly higher (P less than 0.03) levels of specific IgG1 and IgG2a than those from U- rats. Conversely, IgG2a was present in higher levels in pooled uterine lavage specimens from U- rats than in those from U+ rats.
肺支原体可引起大鼠慢性鼠呼吸道支原体病和生殖系统疾病。采用酶联免疫吸附试验,检测了36只自然感染的斯普拉-道来雌性大鼠血清、气管灌洗液和子宫灌洗液样本中特异性免疫球蛋白M(IgM)、IgA、IgG及其亚类与肺支原体的反应性。10只无特定病原体的斯普拉-道来雌性大鼠作为阴性对照。对气管和子宫灌洗液样本进行肺支原体定量培养。从自然感染大鼠的气管(36只中的35只)和子宫(36只中的17只)中分离出肺支原体;所有大鼠在培养的两个部位中至少有一个部位受到感染。未从任何对照大鼠中分离出肺支原体。对照动物与自然感染动物之间,除IgG2c外,所有类别的特异性抗体水平均存在显著差异(IgM、IgG、IgG1和IgG2a的P值小于0.001;IgG2b的P值小于0.002;IgA的P值小于0.02)。分离出的肺支原体细胞数量与血清或气管灌洗标本中检测到的抗体量或类别之间无相关性。自然感染大鼠血清中发现的针对肺支原体的主要抗体为IgG和IgM。IgG2a亚类占IgG阳性动物的大多数。子宫中肺支原体培养阳性(U+)的大鼠与子宫中肺支原体培养阴性(U-)的大鼠在血清中抗体类别和亚类的分布或数量方面无差异。然而,U+大鼠的气管冲洗样本中特异性IgG1和IgG2a水平显著高于(P值小于0.03)U-大鼠。相反,U-大鼠的合并子宫灌洗标本中IgG2a的水平高于U+大鼠。