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Updated: Apr 26, 2026

Visualization of Gut Microbiota-host Interactions via Fluorescence In Situ Hybridization, Lectin Staining, and Imaging
Published on: July 9, 2021
Noninvasive molecular fingerprinting of host-microbiome interactions in neonates
Sharon M Donovan1, Mei Wang1, Marcia H Monaco1
1Department of Food Science and Human Nutrition, University of Illinois, Urbana, IL 61801, USA.
Insights
Researchers developed a new method to study infant gut development using exfoliated intestinal cells. This approach reveals differences in gene expression and microbiome interactions between breast-fed and formula-fed infants, aiding in understanding gut health.
Area of Science:
- Developmental Biology
- Microbiology
- Immunology
- Gastroenterology
Background:
- The early postnatal period is crucial for intestinal and immune system maturation.
- Diet (breast milk vs. formula) significantly impacts infant gut microbiome composition and development.
- Studying host-microbe interactions in infant intestines is ethically challenging due to the need for biopsies.
Purpose of the Study:
- To develop a non-invasive analytical framework for examining host and microbial responses in the infant gut.
- To investigate differences in gene expression and microbiome interactions between breast-fed and formula-fed infants.
- To compare host responses in exfoliated intestinal cells between preterm and term infants.
Main Methods:
- Development of a statistically rigorous analytical framework using exfoliated intestinal epithelial cells.
- Simultaneous analysis of host gene expression (transcriptome) and microbiome composition.
- Differential gene expression analysis and canonical correlation analysis to link host and microbial factors.
- Comparison of exfoliated cells from preterm and term infants.
Main Results:
- Significant differential gene expression (approx. 1200 genes) related to intestinal proliferation, differentiation, and barrier function was observed between breast-fed and formula-fed infants.
- A correlation was identified between microbiome virulence genes and host immunity and defense genes.
- Preterm infants showed up-regulated pathways for immune cell function and inflammation, while term infants exhibited up-regulated cell growth-related genes.
Conclusions:
- Coordinate measurement of exfoliated epithelial cell transcriptomes and the microbiome provides a novel approach to study infant gut development and host-microbe interactions non-invasively.
- This method can be used for prospective studies of gut development or retrospective analysis of disease triggers in banked samples.
- Findings highlight diet-specific host responses and differing maturation pathways in preterm versus term infants.
Abstract:
The early postnatal period is a critical window for intestinal and immune maturation. Intestinal development and microbiome diversity and composition differ between breast- (BF) and formula-fed (FF) infants. Mechanistic examination into host-microbe relationships in healthy infants has been hindered by ethical constraints surrounding tissue biopsies. Thus, a statistically rigorous analytical framework to simultaneously examine both host and microbial responses to dietary/environmental factors using exfoliated intestinal epithelial cells was developed. Differential expression of ∼1200 genes, including genes regulating intestinal proliferation, differentiation and barrier function, was observed between BF and FF term infants. Canonical correlation analysis uncovered a relationship between microbiome virulence genes and host immunity and defense genes. Lastly, exfoliated cells from preterm and term infants were compared. Pathways associated with immune cell function and inflammation were up-regulated in preterm, whereas cell growth-related genes were up-regulated in the term infants. Thus, coordinate measurement of the transcriptomes of exfoliated epithelial cells and microbiome allows inquiry into mutualistic host-microbe interactions in the infant, which can be used to prospectively study gut development or, retrospectively, to identify potential triggers of disease in banked samples.
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