Journal: bioRxiv

Article Title: Gut microbiota within-host evolution enforces colonization resistance against enteric infection

doi: 10.64898/2026.03.27.714693

Figure Lengend Snippet: (A) Microbiota within-host evolution scheme. Germ-free mice were colonized with an OMM 12 community freshly assembled from single species stocks. Mice were housed in two different animal facilities, resulting in two distinct mouse colonies (Evo HAN, Evo MUC2) harboring separately evolved OMM 12 communities. (B) Assessment of colonization resistance against S . Typhimurium ( S . Tm) in mice colonized with the original OMM 12 community or transplanted with evolved OMM 12 communities (Evo HAN, Evo MUC2). Colonization resistance was assessed as described in , but all mice were inoculated with E. coli . (C) Cecum S . Tm loads on day 2 post-infection (d12). Data represent medians with interquartile ranges, and statistical analysis was performed using a Dunn’s post-hoc test. The detection limit is 10 CFU per g. (D) Principal component analyses of cecum metabolomes from mice colonized as described in b with either the original or evolved (Evo HAN, Evo MUC2) OMM 12 communities. Mice ( n = 5 per group) were sacrificed on day 10 post- E. coli colonization or on day two post- S . Tm infection (d12). (E) Fecal microbiota composition on the day of S. Tm infection (d10) in the mice shown in (B) and (C). Absolute abundances were determined via qPCR, quantifying species-specific 16S rRNA gene copies per g feces. Data represent medians with 95% confidence intervals. Statistical analysis was performed using a Dunn’s post-hoc test, comparing the original with each evolved OMM 12 community. Only P -values below 0.05 are shown.

Article Snippet: Isolates were identified via sequencing of the 16S rRNA gene amplicons (Eurofins Genomics Germany GmbH, Germany) using primers fD1, fD2 and rP1 ( Table S2 )

Techniques: Infection

Journal: bioRxiv

Article Title: Gut microbiota within-host evolution enforces colonization resistance against enteric infection

doi: 10.64898/2026.03.27.714693

Figure Lengend Snippet: (A) E. faecalis isolation scheme. Evolved E. faecalis were isolated from the cecal contents of long-term colonized OMM 12 mice (Evo HAN, Evo MUC2) from two different animal facilities. The isolates were subjected to short-read whole genome sequencing ( n = 1 mouse per facility). ( B) Single nucleotide polymorphism-based phylogenetic tree of evolved E. faecalis isolates ( n = 11 isolates per mouse) and original E. faecalis KB1. The tree was created using the Random Accelerated Maximum Likelihood method, and branch lengths represent the substitutions per variable site ( n = 861). A polymorphism allele frequency cut-off of 0.8 was applied. Stars highlight the strains used in (C). ( C) Assessment of colonization resistance against S . Typhimurium ( S . Tm) by original or evolved E. faecalis . Germ-free mice were colonized with the original OMM 11 - E. faecalis community, supplemented with either original E. faecalis KB1 ( E. faecalis Ori) or evolved E. faecalis isolates. The evolved isolates SW161, SW178, and SW180, or SW160 represent E. faecalis HAN and E. faecalis MUC2, respectively. Colonization resistance was assessed as described in . ( D) E. faecalis abundance on the day of S. Tm infection (d10). Absolute abundances were determined via qPCR, quantifying species-specific 16S rRNA gene copies per g feces. The abundances of remaining OMM 12 -species are provided in Fig. S3. ( E) Cecum S . Tm loads on day 2 post-infection (d12). Data represent medians with interquartile ranges. The detection limit is 10 CFU per g. ( D to E) Statistical analysis was performed using a Dunn’s post-hoc test.

Article Snippet: Isolates were identified via sequencing of the 16S rRNA gene amplicons (Eurofins Genomics Germany GmbH, Germany) using primers fD1, fD2 and rP1 ( Table S2 )

Techniques: Isolation, Sequencing, Infection

Journal: Frontiers in Immunology

Article Title: Akkermansia muciniphila primes lung-resident antiviral immunity via the gut–lung axis during SARS-CoV-2 infection

doi: 10.3389/fimmu.2026.1762843

Figure Lengend Snippet: Gut microbiome alterations in mice by SARS-CoV-2 infection. (A) Study design for two types (WA and Omi) of SARS-CoV-2 infection. Fecal samples were collected based on the indicated timeline, and the number of mice per group for 16S rRNA sequencing was n = 5–8, as indicated by dots in the figure. Microbiome analysis was performed on all surviving animals at each time point. Alpha diversity (observed features and Shannon index) of (B) WA-infected mice and (C) Omi-infected mice. (D) Principal coordinate plot of bacterial compositions at 0, 2, and 5 dpi for WA infection and at 0, 2, 5, and 7 dpi for Omi infection (unweighted UniFrac distance). (E) Taxa bar plot of feces microbiome after WA or Omi infection at the family level. Bars represent the average microbial composition across individuals at each time point. (F) Volcano plot of Maaslin2 multivariate analysis results from SARS-CoV-2-infected mice to identify differential abundant species between WA and Omi infection. Virus types and dpi were included as fixed effects and mice ID as a random effect. X-axis indicates Maaslin2 coefficient, and the Y-axis is log10(FDR-corrected p -values). (G) Volatility plots for the two most significant taxa in each group from Maaslin2 analysis based on WA and Omi infection time. The global mean and importance values were calculated by q2-longitudinal plugin in QIIME2. Statistical significance values in box plots were determined using Kruskal–Wallis test with the comparison of 0 dpi group. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: The 16S rRNA gene amplicon datasets obtained by this research were deposited in National Center for Biotechnology Information (NCBI) under accession numbers.

Techniques: Infection, Sequencing, Virus, Comparison