Renata Torres Abib1,2, Alexandru Gaman3,4, Aroldo A Dargél5,6, Ryad Tamouza4,7,8, Flávio Kapczinski7,9,10, Carmem Gottfried11,12,13, Marion Leboyer3,4. 1. Department of Nutrition, Federal University of Pelotas (UFPel), Pelotas, Brazilrenata.abib@ymail.com. 2. Translational Research Group in Autism Spectrum Disorder (GETTEA), Clinical Hospital of Porto Alegre, Porto Alegre, Brazilrenata.abib@ymail.com. 3. Translational Psychiatry Laboratory, INSERM U955, AP-HP, DHU PePSY, Pôle de Psychiatrie des Hôpitaux Universitaires Henri Mondor, Université Paris-Est-Créteil, Paris, France. 4. Fondation FondaMental, Fondation de Coopération Scientifique, Créteil, France. 5. Institut Pasteur, Unité Perception et Mémoire, Paris, France. 6. Centre National de la Recherche Scientifique, Unité Mixte de Recherche 3571, Paris, France. 7. INSERM, U1160, Hôpital Saint Louis, Paris, France. 8. Université Paris Diderot, Sorbonne Paris-Cité, Paris, France. 9. National Institute for Translational Medicine, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil. 10. Molecular Psychiatry Laboratory, Graduate Program in Medicine, Department of Psychiatry, Federal University of Rio Grande do Sul, Porto Alegre, Brazil. 11. Translational Research Group in Autism Spectrum Disorder (GETTEA), Clinical Hospital of Porto Alegre, Porto Alegre, Brazil. 12. Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Brazil. 13. National Institute of Science and Technology on Neuroimmunomodulation-INCT-NIM, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.
Abstract
BACKGROUND/AIMS: Perinatal exposure to infections during critical developmental periods is a promising area of study in autism spectrum disorder (ASD). Epidemiological data has highlighted this relationship, pointing out significant correlations between perinatal exposure to pathogens and the occurrence of ASD. The aim of this review is to critically examine the present state of the art on intracellular pathogenic infection during pregnancy and postnatally, pointing out possible correlations with the development of ASD. METHODS: We reviewed and collected studies concerning potential associations between intracellular pathogens like viral, bacterial, and parasite infection and the risk of ASD. RESULTS: We included 14 publications, considering bacterial and/or viral infection that demonstrated the potential to trigger ASD. Nine case-control studies were included and 5 of them reported an association between infections and ASD. One of the 2 cohorts investigated demonstrated that maternal infection increased the risk of ASD in the offspring. Three cross-sectional studies demonstrated that ASD patients presented with chronic infections and active neuroinflammatory processes. Most of the reports suggest inflammatory response as a common factor, and interleukin 6 appears to be a key-player in this process. CONCLUSION: The immune responses generated by organisms that cause perinatal maternal infection, i.e., bacteria, viruses, or parasites, have been associated with the development of autism in offspring. Physiological changes transmitted from the mother during chronic or acute inflammation should be further investigated so that modulatory preventive measures can be developed.
BACKGROUND/AIMS: Perinatal exposure to infections during critical developmental periods is a promising area of study in autism spectrum disorder (ASD). Epidemiological data has highlighted this relationship, pointing out significant correlations between perinatal exposure to pathogens and the occurrence of ASD. The aim of this review is to critically examine the present state of the art on intracellular pathogenic infection during pregnancy and postnatally, pointing out possible correlations with the development of ASD. METHODS: We reviewed and collected studies concerning potential associations between intracellular pathogens like viral, bacterial, and parasite infection and the risk of ASD. RESULTS: We included 14 publications, considering bacterial and/or viral infection that demonstrated the potential to trigger ASD. Nine case-control studies were included and 5 of them reported an association between infections and ASD. One of the 2 cohorts investigated demonstrated that maternal infection increased the risk of ASD in the offspring. Three cross-sectional studies demonstrated that ASDpatients presented with chronic infections and active neuroinflammatory processes. Most of the reports suggest inflammatory response as a common factor, and interleukin 6 appears to be a key-player in this process. CONCLUSION: The immune responses generated by organisms that cause perinatal maternal infection, i.e., bacteria, viruses, or parasites, have been associated with the development of autism in offspring. Physiological changes transmitted from the mother during chronic or acute inflammation should be further investigated so that modulatory preventive measures can be developed.
Authors: Benjamin J S Al-Haddad; Elizabeth Oler; Blair Armistead; Nada A Elsayed; Daniel R Weinberger; Raphael Bernier; Irina Burd; Raj Kapur; Bo Jacobsson; Caihong Wang; Indira Mysorekar; Lakshmi Rajagopal; Kristina M Adams Waldorf Journal: Am J Obstet Gynecol Date: 2019-06-15 Impact factor: 8.661