Differential expression of uterine NO in pregnant and nonpregnant rats with intrauterine bacterial infection
| Autor: | C. Yallampalli, L. Fang, B. Nowicki |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
medicine.medical_specialty
Nitric Oxide Synthase Type III Transcription Genetic Physiology Ovariectomy medicine.medical_treatment Uterus Nitric Oxide Synthase Type II Biology Nitric Oxide Nitric oxide Rats Sprague-Dawley Andrology chemistry.chemical_compound Pregnancy Reference Values Physiology (medical) Internal medicine medicine Animals RNA Messenger Pregnancy Complications Infectious Enzyme inducer Escherichia coli Infections Tumor Necrosis Factor-alpha medicine.disease Rats Nitric oxide synthase Endocrinology medicine.anatomical_structure Cytokine Gene Expression Regulation chemistry Enzyme Induction Urinary Tract Infections biology.protein Pregnancy Animal Gestation Female Nitric Oxide Synthase |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 280:R1356-R1363 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.2001.280.5.r1356 |
| Popis: | Previous studies have demonstrated that nitric oxide (NO) is involved in the uterine host defense against bacterial infection. In nonpregnant rats, NO production in the uterus was shown to be lower, and inducible NO synthase (NOS) expression was undetectable. However, studies in pregnant rats show abundant expression of inducible NOS with significant elevation in NO production in the uterus. We have recently reported that intrauterine Escherichia coli infection caused a localized increase in uterine NO production and inducible NOS expression in the nonpregnant rat. In our present study, we examined whether the uterine NO production, NOS expression, and uterine tumor necrosis factor-α protein are increased in pregnant rats with intrauterine pathogenic Escherichia coli infection. Unlike the nonpregnant state, the NO production in the infected uterine horn of pregnant rats was not significantly elevated after bacterial inoculation compared with the contralateral uterine horn. The expression of uterine NOS (types II and III) also did not show significant upregulation in the infected horn. This is in contrast to that in nonpregnant animals, in which type II NOS was induced in the uterus on infection. Moreover, intrauterine infection induced an elevated expression of tumor necrosis factor-α protein in the infected horn both of nonpregnant and of pregnant rats. These data suggest that the sequential stimulation of NOS expression, especially the inducible isoform, and generation of uterine NO are lacking during pregnancy despite an elevated tumor necrosis factor-α after infection. In summary, NO synthesis response may be maximal at pregnancy, and infection may not further induce the NO system. Present studies, together with our previous report that intrauterine infection-induced lethality in pregnancy rats was amplified with the inhibition of NO, suggest that pregnancy is a state predisposed for increased complications associated with intrauterine infection and that the constitutively elevated uterine NO during pregnancy may help contain or even reduce the risk of infection-related complications. |
| Databáze: | OpenAIRE |
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