Interleukin 6 and interleukin 8 play important roles in systemic inflammatory response syndrome of meconium peritonitis

Kanamori, Yutaka; Terawaki, Kan; Takayasu, Hajime; Shimada, Masahiko; Komura, Makoto; Kodaka, Tetsuro; Suzuki, Kan; Kitano, Yoshihiro; Kuroda, Takeshi; Iwanaka, Tadashi

doi:10.1007/s00595-011-0034-3

Cited by 9 publications

(11 citation statements)

References 14 publications

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“…Therefore, we hypothesized that maternal anti‐fetal rejection is linked to a stereotypical derangement of the systemic fetal chemokine milieu, specifically T cell chemokines, just as intra‐amniotic infection/inflammation (IAI) is associated with an elevation of the fetal plasma concentration of IL‐6 . The latter condition observed in human fetuses of patients with preterm labor and preterm pre‐labor rupture of membranes (PPROM) was termed the ‘fetal inflammatory response syndrome’ (FIRS) and has been associated with a higher rate of adverse neonatal outcome, a short interval to delivery, and multi‐systemic involvement . We have recently reported that an elevation of amniotic fluid CXCL10 concentration during the mid‐trimester is a risk factor for preterm delivery after 32 weeks of gestation, while an elevation of amniotic fluid IL‐6 concentration is associated with preterm delivery before 32 weeks of gestation .…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Fetal Blood Transcriptome and Proteome in Maternal Anti‐Fetal Rejection: Evidence of a Distinct and Novel Type of Human Fetal Systemic Inflammatory Response

Lee

Romero

Chaiworapongsa

et al. 2013

American J Rep Immunol

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Background The human fetus is able to mount a systemic inflammatory response when exposed to microorganisms. This stereotypic response has been termed the “fetal inflammatory response syndrome” (FIRS), defined as an elevation of fetal plasma interleukin-6 (IL-6). FIRS is frequently observed in patients who delivered preterm associated with intra-amniotic infection (IAI), acute inflammatory lesions in the placenta, and a high rate of neonatal morbidity. Recently, a novel form of fetal systemic inflammation, characterized by an elevation of fetal plasma CXCL10, has been identified in patients with placental lesions suggestive of “maternal anti-fetal rejection”. These lesions include chronic chorioamnionitis, plasma cell deciduitis and villitis of unknown etiology (VUE). In addition, a seropositivity for HLA panel-reactive antibodies (PRA) in maternal sera can also be used as an index of suspicious for “maternal anti-fetal rejection”. The purpose of this study was to determine: 1) the frequency of pathologic evidence of “maternal anti-fetal rejection” in term and spontaneous preterm births; 2) the fetal serum concentration of CXCL10 in patients with and without evidence of maternal anti-fetal rejection; and 3) the fetal blood transcriptome and proteome in pregnancy with evidence of fetal inflammatory response associated with maternal anti-fetal rejection. Methods Maternal and fetal sera were obtained from normal term birth (N=150) and spontaneous preterm births (N=150). Fetal inflammatory response associated with maternal anti-fetal rejection was diagnosed when the patients met two or more of the following criteria: 1) presence of chronic placental inflammation; 2) ≥80% of maternal HLA class I panel-reactive antibody (PRA) seropositivity; and 3) fetal serum CXCL10 concentration > 75th percentile of normal. Maternal HLA PRA was analyzed by flow cytometry. The concentration of fetal CXCL10 and IL-6 were determined by ELISA. Transcriptome analysis was undertaken after extraction of total RNA from white blood cells with a whole-genome DASL assay. Proteomic analysis of fetal serum was conducted by two-dimensional difference gel electrophoresis. Differential gene expression was considered significant when there was a p<0.01 and a fold-change >1.5. Results 1) The frequency of placental lesions consistent with maternal anti-fetal rejection was higher in patients with preterm delivery than in those with term delivery (56% vs. 32%; P<0.001); 2) patients with spontaneous preterm births had a higher rate of maternal HLA PRA class I positivity than those who delivered at term (50% vs. 32%; P=0.002); 3) fetuses who were born to mothers with positive maternal HLA PRA results had a higher median serum CXCL10 concentration than in those with negative HLA PRA results (P<0.001); 4) the median serum CXCL10 concentration (but not IL-6) was higher in fetuses with placental lesions associated with maternal anti-fetal rejection than in those without such lesions (P<0.001); 5) a whole-genome DASL assay of fetal blood RNA demonstrated ...

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Section: Introductionmentioning

confidence: 99%

Characterization of the Fetal Blood Transcriptome and Proteome in Maternal Anti‐Fetal Rejection: Evidence of a Distinct and Novel Type of Human Fetal Systemic Inflammatory Response

Lee

Romero

Chaiworapongsa

et al. 2013

American J Rep Immunol

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“…Perforation is associated with bowel obstruction and/or ischemia, which can be caused by intestinal atresia, volvulus, viral infection, ischemia in the mesentery, or cystic fibrosis . Meconium promotes intraperitoneal inflammatory reactions by activating macrophages and inflammatory mediators . The inflammatory reaction can cause intraperitoneal adhesions and damage to the intestinal wall and circulation.…”

Section: Introductionmentioning

confidence: 72%

“…2 Meconium promotes intraperitoneal inflammatory reactions by activating macrophages and inflammatory mediators. 3,4 The inflammatory reaction can cause intraperitoneal adhesions and damage to the intestinal wall and circulation. Some of the perforations may seal spontaneously during pregnancy.…”

mentioning

confidence: 99%

Predicting poor outcomes and the need for surgical treatment in neonates with meconium peritonitis

et al. 2019

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Objective The objective of this study is to determine factors associated with poor outcomes and the need for surgical treatment in neonates with meconium peritonitis (MP). Methods We evaluated the association between prenatal ultrasound features, maternal characteristics, and the likelihood of surgery, mortality, and serious morbidity in 49 neonates with a prenatal diagnosis of MP, who were born in Guangzhou Women and Children's Medical Center between January 2011 and December 2016. Results Thirty of 49 neonates (61.2%) required surgical treatment, and 17 (34.7%) had a poor outcome. Independent predictors of need for surgical treatment were polyhydramnios, maternal intrahepatic cholestasis of pregnancy (associated with lower risk), and persistence of peritoneal fluid. The model correctly predicted 70.0% of the neonates who required surgery (at a 10% false‐positive rate; area under the curve [AUC]: 0.86 [95% CI, 0.75‐0.97]). For poor outcomes, independent predictors were low gestational age at birth, persistence of peritoneal fluid, and polyhydramnios. For the latter, the model only achieved a detection rate of 52.9% (10% false‐positive rate, AUC: 0.82 [95% CI, 0.70‐0.94]). Conclusions A combination of prenatal ultrasound features and maternal characteristics correctly predicted 70.0% the need for neonatal surgery. Prediction of poor outcome‐based prenatal ultrasound features and gestational age did not perform well.

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“…Reported causes of neonatal death include prematurity, necrotizing enterocolitis, and postoperative sepsis. [25] Furthermore, the SIRS has been reported as a possible complication,[3] but there are no previous reports of this complication during the fetal period.…”

Section: Discussionmentioning

confidence: 99%

“…[12] Meanwhile, some affected infants result in death, and systemic inflammatory response syndrome (SIRS) is thought to be a possible cause in the field of neonatology. [3]…”

Section: Introductionmentioning

confidence: 99%

A rare case of fetal meconium peritonitis developing coagulopathy in utero

et al. 2019

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Hydrops fetalis in association with meconium peritonitis is a rare condition, and the mechanism underlying hydropic changes has not been fully recognized. We present a case of fetal meconium peritonitis with hydrops and coagulopathy. Clinically, the cause of fetal disseminated intravascular coagulation is considered to be a consequence of a systematic inflammatory response based on progressive, but mild fetal anemia without other apparent triggers, thrombocytopenia, elevated white blood cell count and serum C reactive-protein, hypoalbuminemia, and increased vascular permeability. The infant was born at 32 weeks of gestation and survived after postnatal multidisciplinary treatment. Our experience suggests that recognition of this rare condition will enable early diagnosis and better clinical management for fetuses with meconium peritonitis.

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Interleukin 6 and interleukin 8 play important roles in systemic inflammatory response syndrome of meconium peritonitis

Cited by 9 publications

References 14 publications

Characterization of the Fetal Blood Transcriptome and Proteome in Maternal Anti‐Fetal Rejection: Evidence of a Distinct and Novel Type of Human Fetal Systemic Inflammatory Response

Characterization of the Fetal Blood Transcriptome and Proteome in Maternal Anti‐Fetal Rejection: Evidence of a Distinct and Novel Type of Human Fetal Systemic Inflammatory Response

Predicting poor outcomes and the need for surgical treatment in neonates with meconium peritonitis

A rare case of fetal meconium peritonitis developing coagulopathy in utero

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