title: Gestational hypothyroidism increases the severity of experimental autoimmune encephalomyelitis in adult offspring.
abstract: BACKGROUND
  Maternal thyroid hormones play a fundamental role in appropriate fetal development during gestation. Offspring that have been gestated under maternal hypothyroidism suffer cognitive impairment. Thyroid hormone deficiency during gestation can significantly impact the central nervous system by altering the migration, differentiation, and function of neurons, oligodendrocytes, and astrocytes. Given that gestational hypothyroidism alters the immune cell ratio in offspring, it is possible that this condition could result in higher sensitivity for the development of autoimmune diseases.
  
  
  METHODS
  Adult mice gestated under hypothyroidism were induced with experimental autoimmune encephalomyelitis (EAE). Twenty-one days after EAE induction, the disease score, myelin content, immune cell infiltration, and oligodendrocyte death were evaluated.
  
  
  RESULTS
  We observed that mice gestated under hypothyroidism showed higher EAE scores after disease induction during adulthood compared to mice gestated in euthyroidism. In addition, spinal cord sections of mice gestated under hypothyroidism that suffered EAE in adulthood showed higher demyelination, CD4(+) and CD8(+) infiltration, and increased oligodendrocyte death.
  
  
  CONCLUSIONS
  These results show for the first time that a deficiency in maternal thyroid hormones during gestation can influence the outcome of a central nervous system inflammatory disease, such as EAE, in their offspring. These data strongly support evaluating thyroid hormones in pregnant women and treating hypothyroidism during pregnancy to prevent increased susceptibility to inflammatory diseases in the central nervous system of offspring.
authors.affiliation: 1 Department of Biological Sciences, Faculty of Biological Sciences, Andrés Bello National University, Santiago, Chile .
authors.forename: Eduardo A
authors.initials: EA
authors.lastname: Albornoz
authors.forename: Leandro J
authors.initials: LJ
authors.lastname: Carreño
authors.forename: Claudia M
authors.initials: CM
authors.lastname: Cortes
authors.forename: Pablo A
authors.initials: PA
authors.lastname: Gonzalez
authors.forename: Pablo A
authors.initials: PA
authors.lastname: Cisternas
authors.forename: Kelly M
authors.initials: KM
authors.lastname: Cautivo
authors.forename: Tamara P
authors.initials: TP
authors.lastname: Catalán
authors.forename: M Cecilia
authors.initials: MC
authors.lastname: Opazo
authors.forename: Eliseo A
authors.initials: EA
authors.lastname: Eugenin
authors.forename: Joan W
authors.initials: JW
authors.lastname: Berman
authors.forename: Susan M
authors.initials: SM
authors.lastname: Bueno
authors.forename: Alexis M
authors.initials: AM
authors.lastname: Kalergis
authors.forename: Claudia A
authors.initials: CA
authors.lastname: Riedel
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000503:physiopathology*; D005260:Female; D007037:Hypothyroidism / Q000276:immunology / Q000503:physiopathology*; D008214:Lymphocytes / Q000276:immunology*; D051379:Mice; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012720:Severity of Illness Index; D013116:Spinal Cord / Q000276:immunology / Q000503:physiopathology*