Fetal thymic involution: A sonographic marker of the fetal inflammatory response syndrome

Naro, Edoardo Di; Cromi, Antonella; Ghezzi, Fabio; Raio, Luigi; Uccella, Stefano; D’Addario, Vincenzo; Loverro, Giuseppe

doi:10.1016/j.ajog.2005.05.036

Cited by 112 publications

(117 citation statements)

References 22 publications

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“…The fetal organ systems involved include the skin [61–63], heart [64–66], lungs [67–74], eyes [75], kidneys [76], adrenal glands [77], hematologic system [78–80], thymus [81–83] and the central nervous system [84–97]. Although FIRS is frequently found in patients with intra-amniotic infection/inflammation (IAI), it can also be observed in fetuses with congenital viral infection [98–104] or alloimmunization [105].…”

Section: Introductionmentioning

confidence: 99%

Soluble ST2 in the fetal inflammatory response syndrome:in vivoevidence of activation of the anti-inflammatory limb of the immune response

Stampalija

Romero

Korzeniewski

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Inflammation is a mechanism of host response to infection which can be harmful when inappropriately modulated. Soluble ST2 (sST2) is a decoy receptor of interleukin (IL)-33, and this complex modulates the balance in the Th1/Th2 immune response. Moreover, sST2 inhibits the production of pro-inflammatory cytokines in cooperation with an anti-inflammatory cytokine, IL-10. The objectives of this study were to: 1) determine whether umbilical cord plasma sST2 concentration differ between comparing preterm neonates with and without funisitis and between those with and without the fetal inflammatory response syndrome (FIRS); and 2) evaluate the relationship between sST2 and IL-10 among neonates with funisitis and/or FIRS. Methods Umbilical cord plasma was collected from neonates delivered prematurely due to preterm labor or preterm prelabor rupture of membranes with (n=36), and without funisitis (n=30). FIRS (umbilical cord IL-6 concentration ≥17.5 pg/mL) was identified in 29 neonates. Plasma sST2 and IL-10 concentrations were determined by ELISA. Results The median umbilical cord plasma sST2 concentration was 6.7-fold higher in neonates with FIRS than in those without FIRS (median 44.6 ng/mL, interquartile range [IQR] 13.8–80.3 ng/mL vs. median 6.7 ng/mL, IQR 5.6–20.1 ng/mL; p<0.0001). Similarly, the median umbilical cord plasma sST2 concentration was 2.6-fold higher in neonates with funisitis than in those without funisitis (median 19.1 ng/mL; IQR 7.1–75.0 ng/mL vs. median 7.2 ng/mL; IQR 5.9–23.1 ng/mL; p=0.008). There was a strong positive correlation between sST2 and IL-10 in neonates with funisitis and/or FIRS (Spearman’s Rho=0.7, p<0.0001). Conclusions FIRS and funisitis are associated with an elevation of umbilical cord plasma concentrations of soluble ST2. This protein represents an important mediator of the immune response in neonates diagnosed with fetal inflammatory response syndrome by promoting an anti-inflammatory effect in association with IL-10.

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Section: Introductionmentioning

confidence: 99%

Soluble ST2 in the fetal inflammatory response syndrome:in vivoevidence of activation of the anti-inflammatory limb of the immune response

Stampalija

Romero

Korzeniewski

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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“…Although fetal thymus size is decreased in women with PPROM and chorioamnionitis, the measurement of the fetal thymus (for example, using ultrasound) might give additional information in subclinical cases. 42,43 Di Naro et al 44 suggested that fetal thymus involution in preterm labor patients was strongly associated with funisitis, as the histological manifestation of the FIRS. In addition, significant morphological changes are present in the thymus that include increased organ complexity, severe reduction of thymocytes, and monocytic and macrophagic infiltration of Hassall's bodies.…”

Section: Thymusmentioning

confidence: 99%

Chorioamnionitis: a multiorgan disease of the fetus?

et al. 2010

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The bacterial infection of chorion and amnion is a common finding in premature delivery and is referred to as chorioamnionitis. As the mother rarely shows symptoms of a systemic inflammation, the course of chorioamnionitis is frequently asymptomatic and chronic. In contrast, the fetal inflammatory response syndrome represents a separate phenomenon, including umbilical inflammation and increased serum levels of proinflammatory cytokines in the fetus. Ascending maternal infections frequently lead to systemic fetal inflammatory reaction. Clinical studies have shown that antenatal exposure to inflammation puts the extremely immature neonates at a high risk for worsening pulmonary, neurological and other organ development. Interestingly, the presence of chorioamnionitis is associated with a lower rate of neonatal mortality in extremely immature newborns. In the following review, the pathogeneses of inflammation-associated perinatal morbidity are outlined. The concept of fetal multiorganic disease during intrauterine infection is introduced and discussed.

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“…Clinically, chorioamnionitis is however associated with a decreased thymus size in very low-birth weight preterm infants. 13,14 De Felice et al demonstrated that preterm neonates exposed to subclinical chorioamnionitis had smaller thymuses at birth on chest radiographs than preterm neonates without chorioamnionitis. 15 Histological examination at autopsy showed severe morphological changes in the fetal thymus with a reduced corticomedullary (CM) ratio and low thymocytes count when fetuses were exposed to intrauterine infection.…”

Section: Introductionmentioning

confidence: 99%

Intraamniotic Lipopolysaccharide Exposure Changes Cell Populations and Structure of the Ovine Fetal Thymus

et al. 2013

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Rationale: Chorioamnionitis induces preterm delivery and acute involution of the fetal thymus which is associated with postnatal inflammatory disorders. We studied the immune response, cell composition, and architecture of the fetal thymus following intraamniotic lipopolysaccharide (LPS) exposure. Methods: Time-mated ewes received an intraamniotic injection of LPS 5, 12, or 24 hours or 2, 4, 8, or 15 days before delivery at 125 days gestational age (term ¼ 150 days). Results: The LPS exposure resulted in decreased blood lymphocytes within 5 hours and decreased thymic corticomedullary ratio within 24 hours. Thymic interleukin 6 (IL6) and IL17 messenger RNA (mRNA) increased 5-fold 24 hours post-LPS exposure. Increased toll-like receptor 4 (TLR4) mRNA and nuclear factor kB positive cells at 24 hours after LPS delivery demonstrated acute thymic activation. Both TLR4 and IL1 mRNA increased by 5-fold and the number of Foxp3-positive cells (Foxp3þ cells) decreased 15 days after exposure. Conclusion: Intraamniotic LPS exposure caused a proinflammatory response, involution, and a persistent depletion of thymic Foxp3þ cells indicating disturbance of the fetal immune homeostasis.

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Fetal thymic involution: A sonographic marker of the fetal inflammatory response syndrome

Cited by 112 publications

References 22 publications

Soluble ST2 in the fetal inflammatory response syndrome:in vivoevidence of activation of the anti-inflammatory limb of the immune response

Soluble ST2 in the fetal inflammatory response syndrome:in vivoevidence of activation of the anti-inflammatory limb of the immune response

Chorioamnionitis: a multiorgan disease of the fetus?

Intraamniotic Lipopolysaccharide Exposure Changes Cell Populations and Structure of the Ovine Fetal Thymus

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