Cytokine production in chorioamnionitis

Saji, Fumitaka; Samejima, Yoshihiro; Kamiura, Shoji; Sawai, Keisuke; Shimoya, Koichiro; Kimura, Tadashi

doi:10.1016/s0165-0378(00)00064-4

Cited by 146 publications

(105 citation statements)

References 45 publications

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“…Explants of amnion and deciduas release prostaglandins in response to stimulation by these cytokines (Romero et al 1989b,d, Mitchell et al 1991, Pollard & Mitchell 1996, Saji et al 2000. We have reported that mares with experimental placentitis have greater mRNA expression of pro-inflammatory cytokines in placental tissues at delivery and have higher concentrations of prostaglandins F and E in allantoic fluids in the last 48 h of gestation than do control mares (LeBlanc et al 2002).…”

Section: Discussionmentioning

confidence: 94%

Alteration in uterine contractility in mares with experimentally induced placentitis

McGlothlin

Lester²,

Hansen³

et al. 2004

Reproduction

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An experimental model of ascending placentitis was developed in the mare to characterize the uterine myoelectrical pattern in late gestation and determine how ascending placentitis altered this pattern. In experiment 1, myometrial electrical activity was analyzed during the early morning, late morning and evening hours in four mares in the last 15 days of gestation to identify patterns of activity. In experiment 2, nine mares received intra-cervical inoculations of Streptococcus equi subspecies zooepidemicus. Myoelectrical activity in the early morning and evening hours in these mares was compared with four control mares. In experiment 1, the number of spike burst clusters >30 s was greater in the evening than in the late morning hours (P < 0.04). Spike burst activity (number 3 duration) of mares in experiment 1 was similar during day and night recordings until the last 6 days of gestation when it gradually increased each evening until parturition (P < 0.05). In experiment 2, control mares experienced a gradual increase in the number of small spike burst clusters in the last 6 days (P 5 0.008) and an increase in large and small spike burst clusters in the evening hours in the last 4 days of gestation (P 5 0.03). Mares with experimentally induced placentitis never exhibited a rise in spike burst clusters but had an increase in the mean duration and activity index of large spike burst clusters in the 4 days before parturition (P < 0.04). In conclusion, control mares had a progressive, reversible rise in myoelectrical activity at night in the week preceding parturition. This was not observed in mares with experimentally induced placentitis. They exhibited an increase in the intensity and duration of large spike burst clusters possibly in response to local inflammation.

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Section: Discussionmentioning

confidence: 94%

Alteration in uterine contractility in mares with experimentally induced placentitis

McGlothlin

Lester²,

Hansen³

et al. 2004

Reproduction

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“…This process might be of importance during an acute inflammatory response in which IL-6 is known to be operational (22). For example, IL-6 is known to be elevated in amniotic fluid from mothers with intrauterine infections and in those with preterm labor (23). It is therefore conceivable that these inflammatory cytokines may up-regulate the FcRn to maintain IgG at the luminal surface or to transport it into the fetal circulation.…”

Section: Discussionmentioning

confidence: 99%

Distribution of the IgG Fc Receptor, FcRn, in the Human Fetal Intestine

Shah¹,

Dickinson²,

Blumberg³

et al. 2003

Pediatric Research

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The intestinal Fc receptor, FcRn, functions in the maternofetal transfer of gamma globulin (IgG) in the neonatal rodent. In humans, most of this transfer is presumed to occur in utero via the placenta. Although the fetus swallows amniotic fluid that contains immunoglobulin, it is unknown whether this transfer also occurs via the fetal intestine. A human FcRn has been identified in the syncytiotrophoblast that mediates the maternofetal transfer of antibody. It has also been identified in human fetal intestine and is postulated to function in IgG transport. We hypothesize that the human fetal intestinal FcRn may play a role in IgG transport from the amniotic fluid into the fetal circulation. The aim of this study was to characterize the distribution of the FcRn along the human fetal intestine. Lysates prepared from human fetal intestine and from a nonmalignant human fetal intestinal epithelial cell line (H4) were subjected to Western blot analysis and probed using anti-FcRn antibodies. A 42-kD band, consistent with the known molecular weight of the FcRn, was detected along the human fetal intestine and in H4 cells. Expression of the human FcRn was confirmed with immunohistochemistry. Our study demonstrates the expression of FcRn along the human fetal intestine and in a human nonmalignant fetal intestinal epithelial cell line (H4), which by location indicates that FcRn could play a role in the uptake and transport of IgG in the human fetus.Humoral immunity acquired via maternofetal transfer of antibody is critical in the prevention of perinatal infections. In rodents, this transfer occurs through the yolk sac and the intestine via a Fc receptor for IgG (FcRn). This receptor has been considered important in the maternofetal transmission of IgG in the yolk sac of mice and rats and also in the human placental syncytiotrophoblast (1). The FcRn is also expressed in the small intestine of suckling mice and rats, where the receptor functions in the uptake of IgG from ingested maternal milk. Although a FcRn has been demonstrated on the human fetal small intestine, a similar function for this receptor in the human fetal intestine has not been demonstrated to date.The acquisition of humoral immunity early in life may have a significant lifelong impact on the prevention of infectious and inflammatory diseases. Because IgG synthesis in the human fetus is reduced, most IgG in the blood of newborns is maternal in origin. Low levels of IgG

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“…To shed light on these questions, immunohistochemistry was used to localize IL-6 at the maternal-placental interface in DCs of placental sections from patients with CAM and gestational age-matched control placentas. The effects of IL-1␤, a classic proinflammatory cytokine present at elevated levels in the amniotic fluid of women with CAM, 15 were evaluated on IL-6 mRNA and protein expression in cultured human term DCs. In these experiments, IL-1␤ was added with either estradiol (E 2 ) as the control incubation or with E 2 plus medroxyprogesterone acetate (MPA) to mimic the steroid milieu of pregnancy.…”

mentioning

confidence: 99%

Regulation of Interleukin-6 Expression in Human Decidual Cells and Its Potential Role in Chorioamnionitis

Lockwood

Murk

Kayisli

et al. 2010

The American Journal of Pathology

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Chorioamnionitis frequently precedes both genital tract and placental inflammation and is both a primary cause of maternal morbidity and a major antecedent of preterm premature rupture of the membranes (PPROM) as well as preterm delivery (PTD). In most cases of chorioamnionitis , neutrophils dominate the decidua. In a subset of these cases , a predominance of monocytes is uniquely associated with both neonatal intraventricular hemorrhage and death. The multifunctional cytokine , interleukin-6 , promotes local monocyte dominance via several mechanisms. In this study , immunostaining of placental sections revealed significantly higher interleukin-6 HSCOREs in decidual cells (DCs) but not in interstitial trophoblasts , in chorioamnionitis versus gestational agematched control placentas (P < 0.05). In confluent leukocyte-free term DCs , secreted interleukin-6 levels in incubations with estradiol-17␤ were increased 2500-fold by IL-1␤ (P < 0.05). This up-regulation was inhibited by more than 50% in parallel incubations that included medroxyprogesterone acetate (n ‫؍‬ 12, P < 0.05). Western blotting data confirmed these enzyme-linked immunosorbent assay results; quantitative RT-PCR findings demonstrated corresponding changes in interleukin-6 mRNA levels. Specific inhibitors of signaling for both nuclear factor-B activation and p38-mitogen-activated protein kinase , but not for protein kinase C , significantly decreased IL-1␤-enhanced interleukin-6 expression levels in cultured DCs. In conclusion , in situ and in vitro results indicate that significantly enhanced interleukin-6 expression levels in DCs during chorioamnionitis could be pivotal in skewing decidual monocyte differentiation to macrophages.

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Cytokine production in chorioamnionitis

Cited by 146 publications

References 45 publications

Alteration in uterine contractility in mares with experimentally induced placentitis

Alteration in uterine contractility in mares with experimentally induced placentitis

Distribution of the IgG Fc Receptor, FcRn, in the Human Fetal Intestine

Regulation of Interleukin-6 Expression in Human Decidual Cells and Its Potential Role in Chorioamnionitis

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