Maternal inflammation is hard for offspring to stomach

Kristine E Zengeler; John R Lukens

doi:10.1016/j.immuni.2021.12.005

Maternal inflammation is hard for offspring to stomach

Immunity. 2022 Jan 11;55(1):6-8. doi: 10.1016/j.immuni.2021.12.005.

Authors

Kristine E Zengeler¹, John R Lukens²

Affiliations

¹ Center for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia, Charlottesville, VA 22908, USA; Cell and Molecular Biology Training Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: kez9hf@virginia.edu.
² Center for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia, Charlottesville, VA 22908, USA; Cell and Molecular Biology Training Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: jrl7n@virginia.edu.

PMID: 35021058
DOI: 10.1016/j.immuni.2021.12.005

Abstract

Individuals with neurodevelopmental disorders often experience comorbid gastrointestinal distress and dysregulated immune responses, yet the underlying mechanisms remain unclear. In this issue of Immunity, Kim et al. utilize a murine maternal immune activation model of autism and find that inflammation can alter the microbiota of mothers, which postnatally primes offspring CD4⁺ T cells and increases susceptibility to intestinal inflammation.

Publication types

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MeSH terms

Animals
Gastrointestinal Microbiome*
Humans
Inflammation
Mice
Microbiota*
Prenatal Exposure Delayed Effects*
Stomach