title: Alterations of host resistance to mouse typhoid infection by sex hormones.
abstract: The effect on mouse typhoid infection of a 3-day treatment of female virgin mice with 1 mg/day of female sex hormones (estrogen or progesterone), maintaining the same hormonal levels observed in pregnant mice for 30 days, was investigated in order to clarify the mechanisms of altered resistance during pregnancy. Estrogen-exposed mice were more susceptible to the intraperitoneal challenge with Salmonella typhimurium as compared with the vehicle control mice, while progesterone treatment increased the survival times of mice. Estrogen exposure increased the number of peritoneal cells after treatment, but the inflammatory cellular response after infection was significantly suppressed. Although the estrogen-treated and vehicle control mice had the same degrees of peritoneal cellular responses after infection, the death rates in the estrogen-treated mice were higher than those in the vehicle control mice against challenge with 1 LD50 of S. typhimurium. On the other hand, progesterone treatment resulted in the marked influx of peritoneal cells after treatment was terminated, and also it induced a significant increase in the number of peritoneal cells after infection. Although survival times in the progesterone group were higher than those in other groups, all progesterone-treated mice died after a challenge with 1,000 LD50 of S. typhimurium. These results suggest that progesterone enhances nonspecific resistance by increasing the influx of peritoneal cells after infection, while estrogen affects the acute inflammatory responses.
authors.affiliation: Department of Bacteriology, Nara Medical College, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Kita
authors.forename: Y
authors.initials: Y
authors.lastname: Yagyu
authors.forename: F
authors.initials: F
authors.lastname: Nishikawa
authors.forename: A
authors.initials: A
authors.lastname: Hamuro
authors.forename: D
authors.initials: D
authors.lastname: Oku
authors.forename: M
authors.initials: M
authors.lastname: Emoto
authors.forename: N
authors.initials: N
authors.lastname: Katsui
authors.forename: S
authors.initials: S
authors.lastname: Kashiba
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000276:immunology; D001770:Blood Bactericidal Activity; D004967:Estrogens / Q000097:blood; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D007111:Immunity, Cellular; D008099:Liver / Q000276:immunology / Q000382:microbiology; D051379:Mice; D008815:Mice, Inbred Strains; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology*; D011374:Progesterone / Q000097:blood; D012486:Salmonella typhimurium / Q000276:immunology / Q000472:pathogenicity; D013154:Spleen / Q000276:immunology / Q000382:microbiology; D016019:Survival Analysis; D014435:Typhoid Fever / Q000276:immunology*
chemical_list: D004967:Estrogens; D012739:Gonadal Steroid Hormones; D011374:Progesterone