Year: 2021
Type: conference-abstract
Abstract: Background: Evidence shows that CC16 plays a protective role against inflammatory responses in the lung. However, a mechanistic understanding of how CC16 exerts an anti-inflammatory effect in the setting of infection is not entirely known. The gut microbiota is thought to be involved in the pathogenesis of several human diseases. We hypothesized that CC16 modulates the gut microbiome. Objective: To investigate whether CC16 deficiency alters the gut microbiome. Methods: Feces or lung tissue from SCGB1A1 +/+ and SCGB1A1 -/-mice with C57BL/6 background was freshly collected, snap-frozen with liquid nitrogen, then stored at -80C until analysis. DNA was extracted and the hypervariable V4 region of the 16S rRNA gene was amplified by PCR using barcoded primers. Amplicons were pooled and cleaned, then the pooled 16S rRNA library was subjected to the paired-end sequencing. FASTQ files were processed with pair-end read analysis, demultiplexing, denoising, merging and feature table and phylogenic trees were created using QIIME2. The PICRUSt2 was used to predict the microbial function in the microbiota. Differential taxa and pathways were detected using Linear Discriminant Analysis Effect Size (LEfSe). Results: In lung tissue, the DNA was not sufficient to analyze. However, in fecal samples from CC16 deficient mice, there was increased alpha-diversity, decreased abundance of Rikenellaceae and Lachnospiraceae, increased abundance of Bacteroidales S24-7, Porphyromonadaceae (genus Parabacteroides), Deferribacteraceae (genus Mucispirillum), and Desulfovibrionaceae compared to WT mice. Previous studies have shown that Lachnospiraceae in gut microbiota was negatively associated with allergy and asthma (Arrieta MC, et al. 2015; Buendia E, et al. 2018; Stiemsma LT, et al. 2016), Parabacteroides was associated with atopic dermatitis in children (Wopereis H, et al. 2018; Reddel S, et al. 2019), and Mucispirillum has been reported to elicit T cell dependent IgA responses (Bunker JJ, et al. 2015). Regarding functionality of microbiota inferred by PICRUSt2, 20 MetaCyc pathways were enriched and 30 pathways were reduced in CC16 deficient mice. Intriguingly, 11 out of 20 pathways enriched in CC16 deficient mice have been reported to be abundant in the gut of overweight individuals (Zhu Q, et al. 2020), and this may indicate a potential link between obesity-related pathophysiology and CC16 deficiency. Conclusion: CC16 deficient mice demonstrate alterations in their gut microbiota suggesting a pro-allergic phenotype and characteristics of metabolic dysregulation.
Authors: H. Kimura, D. Francisco, D. Laubitz, M. Kraft
Institution: University of Arizona
Language: English
Topic: Gut microbiota and health
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
OpenAlex ID: W4256411885