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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis
Peter Zanvit1, Joanne E Konkel1,2, Xue Jiao1,3
1Mucosal Immunology Section, OPCB, NIDCR, NIH, Bethesda, Maryland 20892, USA.
Abstract:
Psoriasis is an inflammatory skin disease affecting ∼2% of the world's population, but the aetiology remains incompletely understood. Recently, microbiota have been shown to differentially regulate the development of autoimmune diseases, but their influence on psoriasis is incompletely understood. We show here that adult mice treated with antibiotics that target Gram-negative and Gram-positive bacteria develop ameliorated psoriasiform dermatitis induced by imiquimod, with decreased pro-inflammatory IL-17- and IL-22-producing T cells. Surprisingly, mice treated neonatally with these antibiotics develop exacerbated psoriasis induced by imiquimod or recombinant IL-23 injection when challenged as adults, with increased IL-22-producing γδ(+) T cells. 16S rRNA gene compositional analysis reveals that neonatal antibiotic-treatment dysregulates gut and skin microbiota in adults, which is associated with increased susceptibility to experimental psoriasis. This link between neonatal antibiotic-mediated imbalance in microbiota and development of experimental psoriasis provides precedence for further investigation of its specific aetiology as it relates to human psoriasis.
Insights
Antibiotic exposure in adult mice reduced psoriasis symptoms. However, early-life antibiotic treatment worsened psoriasis later in life by altering gut and skin microbiota, increasing susceptibility.
Area of Science:
- Dermatology
- Immunology
- Microbiology
Background:
- Psoriasis is a prevalent inflammatory skin condition with an unclear etiology.
- The role of microbiota in autoimmune disease development is increasingly recognized.
- The specific influence of microbiota on psoriasis pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the impact of antibiotic-induced microbiota alterations on experimental psoriasis.
- To determine how the timing of antibiotic exposure influences psoriasis development.
- To explore the link between dysregulated microbiota and psoriasis susceptibility.
Main Methods:
- Antibiotic treatment targeting Gram-negative and Gram-positive bacteria in adult and neonatal mice.
- Induction of psoriasiform dermatitis using imiquimod or recombinant IL-23.
- Flow cytometry to analyze T cell populations (IL-17, IL-22, γδ T cells).
- 16S rRNA gene sequencing for gut and skin microbiota composition analysis.
Main Results:
- Adult antibiotic treatment ameliorated imiquimod-induced psoriasis, decreasing pro-inflammatory T cells.
- Neonatal antibiotic treatment exacerbated adult psoriasis, increasing IL-22-producing γδ T cells.
- Neonatal antibiotic exposure led to gut and skin microbiota dysbiosis in adult mice, correlating with increased psoriasis susceptibility.
Conclusions:
- The timing of antibiotic exposure significantly influences psoriasis development.
- Neonatal antibiotic-induced microbiota dysbiosis is linked to increased susceptibility to experimental psoriasis.
- These findings highlight the critical role of early-life microbiota in immune system development and its implications for psoriasis etiology.
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