Infection and prematurity and the role of preventive strategies

Romero, Roberto; Espinoza, Jimmy; Chaiworapongsa, Tinnakorn; Kalache, Karim

doi:10.1053/siny.2002.0121

Cited by 194 publications

(117 citation statements)

References 128 publications

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“…3 A causal relationship between intrapartal infections and an increased risk of premature birth has been well documented in many studies. 5 Maternal genetic predisposition to infections is therefore likely to play a role in premature birth but it is unknown whether fetal genetic predisposition may contribute to this risk as well. Consequently we examined fetal MBL2 genotypes in a group of premature infants and compared them to a group of infants born at term.…”

Section: Discussionmentioning

confidence: 99%

“…4 Among identifiable causes of pre-term birth, infections seem to be the most prevalent and it is therefore conceivable that genetic factors that predispose to infections may play an important role. 5 A candidate gene study focusing on genes that encode cytokines, mediators of apoptosis and of host defense found associations with allelic variants in the genes for interleukin 4 and 10 (IL4, IL10), the tumor necrosis factor alpha (TNF-␣), and the mannose-binding lectin gene (MBL2). 6 The possible genetic context between infection, inflammation and pre-term delivery is also supported by other findings, in particular for the IL4 and TNF-␣ genes.…”

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confidence: 99%

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Evidence for an association between mannose-binding lectin 2 (MBL2) gene polymorphisms and pre-term birth

Bodamer

Mitterer

Mäurer

et al. 2006

Genetics in Medicine

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Purpose: Human mannose-binding lectin, encoded by the MBL2 gene, is an important component of innate immunity and an important regulator of inflammatory processes. MBL2 gene polymorphisms are associated with an increased risk of neonatal infections and some data suggest a relation between the maternal MBL2 genotype and the risk of premature delivery. In this study, we evaluated whether there is an association between the fetal MBL2 genotype and prematurity. Methods: A microarray-based on-chip PCR method was used to simultaneously detect five common MBL2 polymorphisms (codon 52, 54, 57; promoter -550, -221) in 204 DNA samples isolated from archival blood cards. MBL2 genotypes of infants born before the 36 th week of pregnancy (N ϭ 102) were compared to a control group of infants born at term after the 37 th week (N ϭ 102). Results: The frequency of the codon 52 polymorphism was significantly higher in the pre-term group compared to the term group (10.8% versus 4.9%, P ϭ 0.04), while the frequency of the codon 54 polymorphism was equal in both groups (11.3% versus 11.8%). Interestingly, carriers of genotypes (O/O) likely conferring deficient MBL plasma levels were more common in the group of premature birth (9.8% versus 2.9%, P ϭ 0.05), while the promoter -550 C/C genotype was underrepresented in the pre-term birth group (24.5% versus 39.2%, P ϭ 0.03). Conclusion: Our data add to the knowledge about genetic predisposition to prematurity and suggest that the fetal MBL2 genotype might be an additional genetic factor contributing to the risk of premature delivery. Genet Med 2006:8(8):518-524.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Evidence for an association between mannose-binding lectin 2 (MBL2) gene polymorphisms and pre-term birth

Bodamer

Mitterer

Mäurer

et al. 2006

Genetics in Medicine

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“…Chorioamnionitis, or inflammation of the amniotic membranes, placenta, and/or uterus, is a frequent cause of preterm delivery and premature rupture of the amniotic membranes (Romero et al, 2002). Infants born in the presence of chorioamnionitis have a lower risk of surfactant deficiency and respiratory distress syndrome in the immediate perinatal period (Watterberg et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Toll‐like receptor signaling inhibits structural development of the distal fetal mouse lung

Prince

Dieperink

Okoh

et al. 2005

Developmental Dynamics

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We tested the hypothesis that innate immune signaling in utero could disrupt the structural development of the fetal lung, contributing to the pathogenesis of bronchopulmonary dysplasia. Injection of Escherichia coli lipopolysaccharide (LPS) into the amniotic fluid of E15 BALB/cJ mice increased the luminal volume density of fetal mouse lungs at embryonic day (E) 17 and E18. LPS also increased luminal volume and decreased distal lung branching in fetal mouse lung explants. This effect required NF-B activation and functional Toll-Like Receptor 4. Airway branching may require fibronectin-dependent epithelial-mesenchymal interactions, representing a potential target for innate immune signaling. Anti-fibronectin antibodies and LPS both blocked distal lung branching. By immunofluorescence, fibronectin localized to the clefts between newly formed airways but was restricted to peripheral mesenchymal cells in LPS-exposed explants. These data suggest that LPS may alter the expression pattern of mesenchymal fibronectin, potentially disrupting epithelial-mesenchymal interactions and inhibiting distal airway branching and alveolarization. This mechanism may link innate immune signaling with defects in structural development of the fetal lung. Developmental Dynamics 233:553-561, 2005.

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“…The benefits provided by gentamicin, however, often outweigh the risks. For instance, infection during pregnancy has been causally linked to premature birth, and, as a result, an increasing number of pregnant women are being exposed to gentamicin during the perinatal period (2). Thus, their offspring are also being exposed to this ototoxic agent during a period of development when they are more vulnerable (3).…”

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confidence: 99%

Pivotal role of Harakiri in the induction and prevention of gentamicin-induced hearing loss

Kalinec

Fernández-Zapico

Urrutia

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Gentamicin is a widely used ototoxic agent. In this study, we shed light on the mechanisms underlying gentamicin-induced hearing loss. More importantly, we demonstrate in vivo and in vitro the effectiveness of a strategy for preventing drug-induced hearing loss using L Together, these results outline pathways for gentamicin-induced hearing loss and its prevention and assign a key role to Hrk in these processes. Thus, our data offer a conceptual framework for designing clinical trials using a safe micronutrient, LCAR, as a simple preventive strategy for iatrogenically induced ototoxicity.apoptosis ͉ ototoxicity ͉ L-carnitine ͉ extracellular signal-regulated kinase 1͞2 ͉ HEI-OC1 cells

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Infection and prematurity and the role of preventive strategies

Cited by 194 publications

References 128 publications

Evidence for an association between mannose-binding lectin 2 (MBL2) gene polymorphisms and pre-term birth

Evidence for an association between mannose-binding lectin 2 (MBL2) gene polymorphisms and pre-term birth

Toll‐like receptor signaling inhibits structural development of the distal fetal mouse lung

Pivotal role of Harakiri in the induction and prevention of gentamicin-induced hearing loss

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