Neonatal exposure to estradiol induces resistance to helminth infection and changes in the expression of sex steroid hormone receptors in the brain and spleen in adult mice of both sexes.

Abstract

A single injection of 17beta-estradiol administered to 4-day-old male and female mice increased the cellular immune response, and induced resistance to Taenia crassiceps cysticercosis as well as changes in the expression pattern of progesterone (PR) and estrogen receptor (ER) isoforms in the brain and splenocytes. Regardless of gender, when treated mice reached adulthood, they were highly resistant to infection. Female mice presented early vaginal opening and altered estrous cycles. In male and female mice, the expression of the PR and ER isoforms in the brain was differentially regulated after neonatal exposure to estradiol. Moreover, an increase in the expression of IL-4 and IFN-gamma was found in the serum of experimentally infected neonatally estrogenized animals, which correlated with the observed protection against T. crassiceps infection. In conclusion, early exposure to estradiol permanently modifies immune system activity and sex steroid hormone receptors in the brain, and causes profound changes in sex-associated susceptibility, leading to resistance to helminth parasite infection.

• Authors: Carolina Guzmán, Ignacio Camacho-Arroyo, Marco A De León-Nava, Jorge Morales-Montor
• Journal: Brain, behavior, and immunity (Brain Behav Immun) Vol. 23 Issue 5 Pg. 709-15 (Jul 2009) ISSN: 1090-2139 [Electronic] Netherlands
• PMID: 19258031 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Estrogen Receptor alpha
• Receptors, Estrogen
• Receptors, Progesterone
• Interleukin-4
• Estradiol
• Interferon-gamma

Topics

• Age Factors
• Animals
• Animals, Newborn (immunology)
• Brain (metabolism)
• Brain Chemistry (drug effects)
• Cysticercosis (immunology, metabolism, parasitology, physiopathology, prevention & control)
• Estradiol (pharmacology)
• Estrogen Receptor alpha (biosynthesis, genetics)
• Estrus (drug effects)
• Female
• Immune System (drug effects, growth & development)
• Immunity, Innate (drug effects)
• Interferon-gamma (blood)
• Interleukin-4 (blood)
• Male
• Mice
• Mice, Inbred BALB C
• Receptors, Estrogen (biosynthesis, genetics)
• Receptors, Progesterone (biosynthesis, genetics)
• Sexual Maturation (drug effects)
• Spleen (metabolism)
• Taenia
• Th1 Cells (immunology)
• Th2 Cells (immunology)