Immunoglobulin class- and subclass-specific responses to Mycoplasma pulmonis in sera and secretions of naturally infected Sprague-Dawley female rats

Abstract

Mycoplasma pulmonis causes chronic murine respiratory mycoplasmosis and genital disease in rats. Specffic 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 < 0.001 for IgM, IgG, IgGl, and IgG2a; P < 0.002 for IgG2b; and P < 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 IgGpositive 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 < 0.03) levels of specific IgGl 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.

Genital Mycoplasmosis in Rats: A Model for Intrauterine Infection1

“…Specific IgM, IgA, IgG and its subclasses present in the sera, tracheal, and uterine lavages of 36 naturallyinfected SD female rats were tested for reactivity with M. pulmonis in an enzyme-linked immunosorbent assay (ELISA). 48 Sera of all naturally-infected rats were seropositive in both IgG and IgM classes; 31% were positive in the IgA class. Naturally infected rats were positive in IgG1, IgG2a, IgG2b, and IgG2c subclasses (72, 100, 44, and 22%, respectively) The serum levels between rats with M. pulmonis uterine infection (U+) and rats without M. pulmonis uterine infection (U−) were not statistically different for any immunoglobulin class.…”

“…We have demonstrated conclusively that in utero transmission does occur during pregnancy. 48,52 Therefore, Caesarean-derivation alone may be inadequate to eliminate M. pulmonis from rodent colonies.…”

Hematogenous infection of Sprague-Dawley rats with Mycoplasma pulmonis: development of a model for maternal and fetal infection

“…The tropism of M pulmonis for the reproductive tissues appears to be pregnancy-specific; in a previous study M pulmonis was recovered from the trachea in 35 of 36 naturally infected nonpregnant rats but was isolated from the uterus of only 17 of these same rats. 21 Further, in rats experimentally infected in the vagina before breeding, the reproductive tissues were more commonly colonized than the trachea once pregnancy was established. 22,25,26 The current paradigm is that infectious agents colonize the placenta, breach the placental barrier, and infect the AF, thereby gaining access to the fetus directly or via hematogenous spread from the placenta.…”

“…In addition, significant intrauterine infection is seen only in animals infected before breeding rather than at time points throughout gestation. [20][21][22] The IV model is more useful for studying acute, temporal effects of infection, whereas the vaginal infection model is better suited for chronic situations. Studies focused on mechanisms of low birthweight would be more appropriate for the vaginal model 20 as acute infection established in IV-infected rats did not result in low birthweight.…”

“…2,7,9,18,19 Mycoplasma pulmonis genital disease is the only naturally occurring reproductive disease in laboratory animals that is caused by a member of the class Mollicutes, and infection of the uterus can be accomplished by both intravaginal and intravenous (IV) routes. [20][21][22][23] Once infected, dams that have varying complications develop similar to ureaplasmal-associated reproductive disease of humans, including chorioamnionitis, fetal infection of the lung and central nervous system, low birthweight, and fetal and neonatal death. 20 The contribution of the fetal immune response to infection is now recognized as a key determinant of APO.…”