Immunological Responsiveness to Escherichia coli During Pregnancy

Abstract

To determine whether immunological responsiveness to a bacterial antigen is altered during pregnancy and lactation, Swiss mice (gestation, 19 to 21 days) were studied during early, middle, and late pregnancy and in the early postpartum period. Pregnant and nursing mice, each along with a virgin female littermate control, were injected with 2 x 106 heat-killed Escherichia coli and sacrificed 4 days later for the enumeration of splenic anti-E. coli plaque-forming cells (PFC). For 72 4to 10-day pregnant and control mice ranked together, total PFC per spleen ranged from 0 to 312,650, with 61% of the counts from pregnant animals ranking above the median of 12,700. The mean number of PFC for the pregnant animals was greater than for sister controls in 19 of 23 litters studied (P = 0.001). Responsiveness was also increased for 72 mice tested in later pregnancy. Counts of PFC of 72% of mice 11 to 18 days pregnant were above the median when ranked with those of their controls (P < 0.001). In 18 of 21 litters studied, pregnant animals responded better than littermate controls (P = 0.001). Responses of mice at term (19 to 21 days) were depressed when compared with those of controls, but nursing animals 6 to 9 postpartum responded like virgin animals. Previous studies suggested that low concentrations of estradiol stimulate the mitosis of PFC. To determine if progesterone also increases numbers of PFC, concentrations in a range physiological for pregnancy were added to cultures of spleen cells from male mice injected with E. coli 3 days before. After 24 h of incubation, numbers of PFC in these suspensions were compared to those of the same suspensions incubated without hormone. In 19 of 25 and 48 of 68 suspensions tested at concentrations of 500 pg and 50 ng of progesterone per ml, the numbers of PFC were increased over those of the same suspensions without hormone (P < 0.01). Geometric mean number of PFC for progesterone-treated cells was 45% greater than that for the controls. Findings suggest that female sex hormones, important for the normal growth and differentiation of fetal cells, may also enhance division and/or maturation of immunocompetent cells in the mother.

Protection against Escherichia coli K1 infection in newborn rats by antibody to K1 capsular polysaccharide antigen

“…Administration of a larger bacterial inoculum or another schedule and route of immunization may have improved the antibody response in these adult rats. It is unlikely that pregnancy altered this immune response, since Kenny and Diamond have shown that pregnant rats have enhanced antibody production after immunization with various bacterial antigens when compared with nonpregnant control animals (14).…”

Corticosterone regulation of the effector function of malarial immunity during pregnancy

“…A decreased maternal immunoreactivity during pregnancy, contributing to tolerance of the fetal allograft, has been suggested frequently (6). Humoral immunity is either not affected or even slightly stimulated during pregnancy (12,22,32). The decreased mixed-lymphocyte reaction, phytohemagglutinin stimulation, and lymphocyte cytotoxicity, as well as delayed rejection of cardiac allografts, during pregnancy reflect impairment of T-cell function in vitro and in vivo (3,8,15,16,28,42).…”

Altered Humoral Immunoregulation During Human Pregnancy

“…While neutralizing antibodies have been reported in the sera of pregnant women following therapeutic vaccinationl'<'" and natural infection,22-24 animal experiments monitoring specific antibody-producing cell and immunoglobulin levels following immunization provide contrasting information, depending largely on the T-dependence or otherwise of the antigen involved and the route of inoculation. [25][26][27][28][29] The most convincing evidence for B-cell activity during human pregnancy comes from observations of maternal anti-paternal antibodiesv? and maternal anti-idiotype antibodies!"…”