Frontiers in microbiology · 2026
Escherichia coli JNL-EC1 enhances type I IFN-mediated antiviral response during DNA and RNA virus infection.
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Li Rui, Pan Zhaoyi, Wang Na, Zhang Shujuan, Geng Xianbo, Yu Yating, Shi Jin, Liu Cunfei, Jin Changzhong, Shang Liang, Wu Haibo, Wu Nanping
Аннотация
INTRODUCTION: The gut microbiota plays a critical role in shaping host antiviral immunity, particularly through the regulation of type I interferon (IFN-I) signaling. Infants are highly vulnerable to viral infections, largely due to their adaptive immune immaturity. Identifying specific commensal bacteria capable of enhancing IFN-I responses represents a promising strategy to boost antiviral defense in this vulnerable population.
METHODS: Forty-five bacterial strains were isolated from fecal samples of infants aged 0-3 years. Their ability to modulate virus-induced IFN-I expression was evaluated using qPCR-based assays in cell lines infected with Sendai virus (SeV). One strain, Escherichia coli JNL-EC1, was selected for further genomic analysis, virulence gene profiling, and hemolysis testing. We assessed IFN-I and ISGs expression, as well as the phosphorylation of STING, TBK1, and IRF3, under conditions of cGAS-STING activation, TBK1 or IRF3-5D overexpression, and HSV-1 or SeV infection. The active components of its metabolites were fractionated using ethanol and chloroform extraction. Antiviral effects were evaluated in HEK293T, INT407, and THP-1 cells, as well as in a SeV-infected mouse model.
RESULTS: Among the 45 isolates, metabolites of E. coli JNL-EC1 significantly enhanced SeV- and HSV-1(herpes simplex virus 1)-induced IFN-I signaling activation. Genomic analysis confirmed that E. coli JNL-EC1 resembles a commensal strain, lacking typical pathogenic determinants and exhibiting a non-hemolytic phenotype. The metabolites potentiated cGAS/STING- and TBK1-mediated IFN-I signaling but did not further enhance IRF3-5D-induced gene expression. Moreover, the metabolites increased the phosphorylation of STING, TBK1, and IRF3 following HSV-1 or SeV infection. Active components were present in both water-soluble (0-60% ethanol) and chloroform-extracted fractions and were heat-stable, suggesting the involvement of multiple non-proteinaceous metabolites. Functionally, metabolite pretreatment reduced the replication of GFP-tagged HSV-1 and vesicular stomatitis virus (VSV) in vitro. E. coli JNL-EC1 significantly upregulated Ifnb1 expression in the spleen and modulated both the composition and activation status of immune cell populations.
DISCUSSION: These findings identify E. coli JNL-EC1 as a gut commensal with broad antiviral-enhancing properties and reveal a microbiota-mediated mechanism that primes antiviral immunity through the IFN-I pathway.
METHODS: Forty-five bacterial strains were isolated from fecal samples of infants aged 0-3 years. Their ability to modulate virus-induced IFN-I expression was evaluated using qPCR-based assays in cell lines infected with Sendai virus (SeV). One strain, Escherichia coli JNL-EC1, was selected for further genomic analysis, virulence gene profiling, and hemolysis testing. We assessed IFN-I and ISGs expression, as well as the phosphorylation of STING, TBK1, and IRF3, under conditions of cGAS-STING activation, TBK1 or IRF3-5D overexpression, and HSV-1 or SeV infection. The active components of its metabolites were fractionated using ethanol and chloroform extraction. Antiviral effects were evaluated in HEK293T, INT407, and THP-1 cells, as well as in a SeV-infected mouse model.
RESULTS: Among the 45 isolates, metabolites of E. coli JNL-EC1 significantly enhanced SeV- and HSV-1(herpes simplex virus 1)-induced IFN-I signaling activation. Genomic analysis confirmed that E. coli JNL-EC1 resembles a commensal strain, lacking typical pathogenic determinants and exhibiting a non-hemolytic phenotype. The metabolites potentiated cGAS/STING- and TBK1-mediated IFN-I signaling but did not further enhance IRF3-5D-induced gene expression. Moreover, the metabolites increased the phosphorylation of STING, TBK1, and IRF3 following HSV-1 or SeV infection. Active components were present in both water-soluble (0-60% ethanol) and chloroform-extracted fractions and were heat-stable, suggesting the involvement of multiple non-proteinaceous metabolites. Functionally, metabolite pretreatment reduced the replication of GFP-tagged HSV-1 and vesicular stomatitis virus (VSV) in vitro. E. coli JNL-EC1 significantly upregulated Ifnb1 expression in the spleen and modulated both the composition and activation status of immune cell populations.
DISCUSSION: These findings identify E. coli JNL-EC1 as a gut commensal with broad antiviral-enhancing properties and reveal a microbiota-mediated mechanism that primes antiviral immunity through the IFN-I pathway.