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Alterations of Host Resistance to Mouse Typhoid Infection by Sex Hormones
Author(s) -
Kita Eiji,
Yagyu Yoshihiko,
Nishikawa Fumiko,
Hamuro Akiko,
Oku Daisuke,
Emoto Masashi,
Katsui Noriaki,
Kashiba Shuzo
Publication year - 1989
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.46.6.538
Subject(s) - estrogen , hormone , biology , medicine , endocrinology , peritoneal cavity , andrology , immunology , anatomy
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 LD 50 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 LD 50 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.