Gestational Hypothyroidism Increases the Severity of Experimental Autoimmune Encephalomyelitis in Adult Offspring

Albornoz, Eduardo A; Carreño, Leandro J.; Cortés, Claudia; González, Pablo A; Cisternas, Pablo; Cautivo, Kelly M.; Catalán, Tamara P.; Opazo, María Cecilia; Eugenín, Eliseo A.; Berman, Joan W.; Bueno, Susan M.; Kalergis, Alexis M.; Riedel, Claudia A.

doi:10.1089/thy.2012.0401

Cited by 21 publications

(22 citation statements)

References 47 publications

(51 reference statements)

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“…Albornoz et al demonstrated the impact of maternal THs deficiency during gestation on the outcome of offspring central nervous system (CNS) in response to autoimmune inflammatory encephalomyelitis disease. 16 Their animal study suggests that gestational hypothyroidism modulates the offspring immune system in a way that increases the likelihood of the offspring to suffer from severe autoimmune inflammatory diseases in the CNS. 16 In another study, Nieto et al evaluated whether adult mice gestated in hypothyroid mothers display an altered response to pneumococcal pneumonia.…”

Section: Discussionmentioning

confidence: 99%

“…16 Their animal study suggests that gestational hypothyroidism modulates the offspring immune system in a way that increases the likelihood of the offspring to suffer from severe autoimmune inflammatory diseases in the CNS. 16 In another study, Nieto et al evaluated whether adult mice gestated in hypothyroid mothers display an altered response to pneumococcal pneumonia. 17 They observed that female mice exposed in utero to maternal hypothyroidism had higher survival rates and fewer bacterial dissemination following an intranasal challenge with Streptococcus pneumoniae.…”

Section: Discussionmentioning

confidence: 99%

“…14,15 Furthermore, the link between maternal hypothyroidism during gestation and offspring future immune response was recently described. 13,16,17 Albornoz et al and Nieto et al found increased autoimmune response 16 and improved resistance to bacterial infection 17 in these offspring, respectively. These data suggest a novel pattern of intrauterine imprinting that expand the knowledge about a possible impact of maternal hypothyroidism during pregnancy on offspring immune response.…”

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confidence: 90%

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Maternal Hypothyroidism during Pregnancy and the Risk for Infectious Morbidity of the Offspring

et al. 2019

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Objective Animal studies indicate a possible intrauterine immunological imprinting in pregnancies complicated by hypothyroidism. We aimed to evaluate whether exposure to maternal hypothyroidism during pregnancy increases the risk of long-term infectious morbidity of the offspring. Study Design A retrospective cohort study compared the long-term risk of hospitalization associated with infectious morbidity in children exposed and unexposed in utero to maternal hypothyroidism. Outcome measures included infectious diagnoses obtained during any hospitalization of the offspring (up to the age of 18 years). Results The study included 224,950 deliveries. Of them, 1.1% (n = 2,481) were diagnosed with maternal hypothyroidism. Children exposed to maternal hypothyroidism had a significantly higher rate of hospitalizations related to infectious morbidity (13.2 vs. 11.2% for control; odds ratio: 1.2; 95% confidence interval: 1.08–1.36; p = 0.002). Specifically, incidences of ear, nose, and throat; respiratory; and ophthalmic infections were significantly higher among the exposed group. The Kaplan–Meier curve indicated that children exposed to maternal hypothyroidism had higher cumulative rates of long-term infectious morbidity. In the Cox proportional hazards model, maternal hypothyroidism remained independently associated with an increased risk of infectious morbidity in the offspring while adjusting for confounders. Conclusion Maternal hypothyroidism during pregnancy is associated with significant pediatric infectious morbidity of the offspring.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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confidence: 90%

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Maternal Hypothyroidism during Pregnancy and the Risk for Infectious Morbidity of the Offspring

et al. 2019

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“…Furthermore, these TH-stimulated OPCs differentiate into myelinating oligodendrocytes (OLs) to repair demyelinated axons. Through this effect, TH may promote remyelination and contribute to the suppression of MS deterioration significantly impact the CNS by altering the migration, differentiation, and function of OLs [93]. Moreover, an example of hyperthyroidism that initially induces the accelerated maturation process, including cell migration and differentiation, extension of dendritic processes, and synaptogenesis, implicates the effects of TH on cell migration and differentiation [94,95].…”

Section: Thyroid Hormone Activates Oligodendrocyte Precursor Cells Tomentioning

confidence: 99%

Thyroid Hormone Potentially Benefits Multiple Sclerosis via Facilitating Remyelination

Zhang

Qin

et al. 2015

Mol Neurobiol

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Myelin destruction due to inflammatory damage of oligodendrocytes (OLs) in conjunction with axonal degeneration is one of the major histopathological hallmarks of multiple sclerosis (MS), a common autoimmune disorder affecting the central nervous system (CNS). Therapies over the last 20 years mainly focus on the immune system and, more specifically, on the modulation of immune cell behavior. It seems to be effective in MS with relapse, while it is of little benefit to progressive MS in which neurodegeneration following demyelination outweighs inflammation. Otherwise, remyelination, as a result of oligodendrocyte production from oligodendrocyte precursor cells (OPCs), is considered to be a potential target for the treatment of progressive MS. In this review, positive effects of remyelination on MS will be discussed in view of the critical role played by thyroid hormone (TH), focusing on the following points: (1) promising treatment of TH on MS that potentially targets to remyelination; (2) the active role of TH that is able to promote remyelination; (3) the regulative role of TH that works on endogenous stem and precursor cells; (4) the effect of TH on gene transcription; and (5) a working hypothesis which is developed that TH can alleviate MS by promoting remyelination, and the mechanism of which is its regulative role in gene transcription of OPCs.

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“…In susceptible individuals, immune tolerance shaped by self-antigens recognition may fail, leading to a harmful autoimmune response (Shum et al 2009). Unfortunately, up to date the etiology for many autoimmune diseases remains unknown, but a number of studies have suggested that these ailments are strongly associated with factors such as genetics, hormonal status, infections and/or environment factors (Albornoz et al 2013;Bentham et al 2015;Luo et al 2011). The fact that systemic lupus erythematosus (SLE), as well as other autoimmune diseases, preferentially affects women over male would suggest that the female hormonal status could play a pivotal role during autoimmunity onset and progression (Whitacre et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Hormonal Modulation of Dendritic Cells Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity

Mackern-Oberti

Jara

Riedel

et al. 2016

Arch. Immunol. Ther. Exp.

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Hormonal homeostasis is crucial for keeping a competent and healthy immune function. Several hormones can modulate the function of various immune cells such as dendritic cells (DCs) by influencing the initiation of the immune response and the maintenance of peripheral tolerance to self-antigens. Hormones, such as estrogens, prolactin, progesterone and glucocorticoids may profoundly affect DCs differentiation, maturation and function leading to either a pro-inflammatory or an anti-inflammatory (or tolerogenic) phenotype. If not properly regulated, these processes can contribute to the pathogenesis of autoimmune disease. An unbalanced hormonal status may affect the production of pro-inflammatory cytokines, the expression of activating/inhibitory receptors and co-stimulatory molecules on conventional and plasmacytoid DCs (pDCs), conferring susceptibility to develop autoimmunity. Estrogen receptor (ER)-α signaling in conventional DCs can promote IFN-α and IL-6 production and induce the expression of CD40, CD86 and MHCII molecules. Furthermore, estrogen modulates the pDCs response to Toll-like receptor ligands enhancing T cell priming. During lupus pathogenesis, ER-α deficiency decreased the expression of MHC II on pDCs from the spleen. In contrast, estradiol administration to lupus-prone female mice increased the expression of co-stimulatory molecules, enhanced the immunogenicity and produced large amounts of IL-6, IL-12 and TNF-α by bone marrow-derived DCs. These data suggest that estradiol/ER signaling may play an active role during lupus pathology. Similarly, understanding hormonal modulation of DCs may favor the design of new therapeutic strategies based on autologous tolerogenic DCs transfer, especially in sex-biased systemic autoimmune diseases. In this review, we discuss recent data relative to the role of different hormones (estrogen, prolactin, progesterone and glucocorticoids) in DC function during systemic autoimmune pathogenesis.

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Gestational Hypothyroidism Increases the Severity of Experimental Autoimmune Encephalomyelitis in Adult Offspring

Cited by 21 publications

References 47 publications

Maternal Hypothyroidism during Pregnancy and the Risk for Infectious Morbidity of the Offspring

Maternal Hypothyroidism during Pregnancy and the Risk for Infectious Morbidity of the Offspring

Thyroid Hormone Potentially Benefits Multiple Sclerosis via Facilitating Remyelination

Hormonal Modulation of Dendritic Cells Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity

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