Role of Maternal Infections and Inflammatory Responses on Craniofacial Development

Bhagirath, Anjali Y.; Medapati, Manoj Reddy; Jesus, Vivianne Cruz de; Yadav, Sneha; Hinton, Martha; Dakshinamurti, Shyamala; Atukorallaya, Devi

doi:10.3389/froh.2021.735634

Cited by 6 publications

(3 citation statements)

References 318 publications

(328 reference statements)

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“…An association between the development of OFC and maternal illness and infections has previously been described. Studies in Latin America showed that maternal acute and chronic viral infections were significantly associated with the incidence of cleft lip cases, which is hypothesized to be secondary to vascular disruption during the embryonic period associated either with hyperthermia and/or the use of salicylates 16 . Half of our cohort experienced upper urinary tract infections; however, pathogen identification was not recorded.…”

Section: Discussionmentioning

confidence: 81%

“…Studies in Latin America showed that maternal acute and chronic viral infections were significantly associated with the incidence of cleft lip cases, which is hypothesized to be secondary to vascular disruption during the embryonic period associated either with hyperthermia and/or the use of salicylates. 16 Half of our cohort experienced upper urinary tract infections; however, pathogen identification was not recorded. Other studies have reported a larger association with Chlamydia exposure, apparently secondary to the 60 kD heat shock protein (hsp60), considered a potent inflammation inducer.…”

Section: Discussionmentioning

confidence: 99%

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Characterization of 554 Mexican Patients With Nonsyndromic Cleft Lip and Palate: Descriptive Study

Pérez-González,

Lavielle-Sotomayor,

López-Rodríguez

et al. 2023

Journal of Craniofacial Surgery

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Orofacial clefts are one of the most common birth defects and the most common craniofacial malformation worldwide. The most common orofacial clefts (OFCs) are congenital cleft lip with or without cleft palate (CL ± P) and isolated cleft palate (CP). The incidence of OFCs varies depending on region and ethnicity; however, it affects approximately 1 in 600 newborns worldwide. In most cases, CL ± P and CP are multifactorial congenital malformations, where both exogenous and genetic factors play an important role. The objective of this study was to describe the frequency of potential risk factors associated with the development of CL ± P and CP in Mexican population. Patients were referred for multisystemic treatment, from private and public institutions in different regions of the country (center, north, and south). Sociodemographic information, prenatal and parental history were obtained through direct interviews with the patients or the patients' mothers in the case of underaged patients. Referred patients were invited to participate in the study. No interventions were applied for this study. The relationship between these factors and the prevalence of CL ± P and CP was studied. A total of 554 patients were included, the majority with CLP (30% to 7%), statistically significant differences were found for folic acid (P = 0.02) consumption. Familial aggregation did not reach statistical significance for first-degree family members (P = 0.34) but was significant for second-degree family members (P = 0.007). More risk factors associated with CL ± P and CP may still be unknown, prompting more epidemiological research and research in other little-studied areas, such as; specific genetic factors in Mexican population.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Characterization of 554 Mexican Patients With Nonsyndromic Cleft Lip and Palate: Descriptive Study

Pérez-González,

Lavielle-Sotomayor,

López-Rodríguez

et al. 2023

Journal of Craniofacial Surgery

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“…On the other hand, epidemiological studies have associated pro-inflammatory conditions as diabetes, maternal infections, and obesity to CLP 29 – 37 , however, with no experimental demonstration of how those risk factor could affect craniofacial development. Concurrently, there is evidence that pro-inflammatory activation modulates CDH1 /E-cadherin levels in multiple cell models 38 – 45 .…”

Section: Introductionmentioning

confidence: 99%

Neural crest E-cadherin loss drives cleft lip/palate by epigenetic modulation via pro-inflammatory gene–environment interaction

et al. 2023

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Gene–environment interactions are believed to play a role in multifactorial phenotypes, although poorly described mechanistically. Cleft lip/palate (CLP), the most common craniofacial malformation, has been associated with both genetic and environmental factors, with little gene–environment interaction experimentally demonstrated. Here, we study CLP families harbouring CDH1/E-Cadherin variants with incomplete penetrance and we explore the association of pro-inflammatory conditions to CLP. By studying neural crest (NC) from mouse, Xenopus and humans, we show that CLP can be explained by a 2-hit model, where NC migration is impaired by a combination of genetic (CDH1 loss-of-function) and environmental (pro-inflammatory activation) factors, leading to CLP. Finally, using in vivo targeted methylation assays, we demonstrate that CDH1 hypermethylation is the major target of the pro-inflammatory response, and a direct regulator of E-cadherin levels and NC migration. These results unveil a gene–environment interaction during craniofacial development and provide a 2-hit mechanism to explain cleft lip/palate aetiology.

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Congenital infectious encephalopathies from the intrapartum period to postnatal life

Fortin,

DeBiasi,

Mulkey

2024

Seminars in Fetal and Neonatal Medicine

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Role of Maternal Infections and Inflammatory Responses on Craniofacial Development

Cited by 6 publications

References 318 publications

Characterization of 554 Mexican Patients With Nonsyndromic Cleft Lip and Palate: Descriptive Study

Characterization of 554 Mexican Patients With Nonsyndromic Cleft Lip and Palate: Descriptive Study

Neural crest E-cadherin loss drives cleft lip/palate by epigenetic modulation via pro-inflammatory gene–environment interaction

Congenital infectious encephalopathies from the intrapartum period to postnatal life

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