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Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa.

ABSTRACT: BACKGROUND:The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models. RESULTS:Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, ovalbumin-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice. CONCLUSION:Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.

SUBMITTER: Jeon YJ

PROVIDER: S-EPMC7542126 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa.

Jeon Yung Jin YJ Gil Chan Hee CH Won Jina J Jo Ara A Kim Hyun Jik HJ

BMC microbiology 20201007 1

<h4>Background</h4>The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to ...[more]

PMID: 33028252

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Project description:ObjectivesHost-microbial commensalism can shape the innate immune response in the nasal mucosa, and the microbial characteristics of nasal mucus directly impact the mechanisms of the initial allergic responses in the nasal epithelium. We sought to determine alterations of the microbial composition in the nasal mucus of patients with allergic rhinitis (AR) and to elucidate the interplay between dysbiosis of the nasal microbiome and allergic inflammation.MethodsIn total, 364,923 high-quality bacterial 16S ribosomal RNA-encoding gene sequence reads from 104 middle turbinate mucosa samples from healthy participants and patients with AR were obtained and analyzed using the Quantitative Insights into Microbial Ecology pipeline.ResultsWe analyzed the microbiota in samples of nasal mucus from patients with AR (n=42) and clinically healthy participants (n=30). The Proteobacteria (Ralstonia genus) and Actinobacteria (Propionibacterium genus) phyla were predominant in the nasal mucus of healthy subjects, whereas the Firmicutes (Staphylococcus genus) phylum was significantly abundant in the nasal mucus of patients with AR. In particular, the Ralstonia genus was significantly dominant in the clinically healthy subjects. Additional pyrosequencing data from 32 subjects (healthy participants: n=15, AR patients: n=17) revealed a greater abundance of Staphylococcus epidermidis, Corynebacterium accolens, and Nocardia coeliaca, accounting for 41.55% of mapped sequences in the nasal mucus of healthy participants. Dysbiosis of the nasal microbiome was more pronounced in patients with AR, and Staphylococcus aureus exhibited the greatest abundance (37.69%) in their nasal mucus, in association with a positive response to house dust mites and patients' age and height.ConclusionThis study revealed alterations in the nasal microbiome in the nasal mucus of patients with AR at the levels of microbial genera and species. S. aureus-dominant dysbiosis was distinctive in the nasal mucus of patients with AR, suggesting a role of host-microbial commensalism in allergic inflammation.

Project description:UnlabelledMuch of the morbidity and mortality associated with influenza virus respiratory infection is due to bacterial coinfection with pathogens that colonize the upper respiratory tract such as methicillin-resistant Staphylococcus aureus (MRSA) and Streptococcus pneumoniae. A major component of the immune response to influenza virus is the production of type I and III interferons. Here we show that the immune response to infection with influenza virus causes an increase and restructuring of the upper respiratory microbiota in wild-type (WT) mice but not in Il28r(-/-) mutant mice lacking the receptor for type III interferon. Mice lacking the IL-28 receptor fail to induce STAT1 phosphorylation and expression of its regulator, SOCS1. Il28r(-/-) mutant mice have increased expression of interleukin-22 (IL-22), as well as Ngal and RegIIIγ, in the nasal cavity, the source of organisms that would be aspirated to cause pneumonia. Proteomic analysis reveals changes in several cytoskeletal proteins that contribute to barrier function in the nasal epithelium that may contribute to the effects of IL-28 signaling on the microbiota. The importance of the effects of IL-28 signaling in the pathogenesis of MRSA pneumonia after influenza virus infection was confirmed by showing that WT mice nasally colonized before or after influenza virus infection had significantly higher levels of infection in the upper airways, as well as significantly greater susceptibility to MRSA pneumonia than Il28r(-/-) mutant mice did. Our results suggest that activation of the type III interferon in response to influenza virus infection has a major effect in expanding the upper airway microbiome and increasing susceptibility to lower respiratory tract infection.ImportanceS. aureus and influenza virus are important respiratory pathogens, and coinfection with these organisms is associated with significant morbidity and mortality. The ability of influenza virus to increase susceptibility to S. aureus infection is less well understood. We show here that influenza virus leads to a change in the upper airway microbiome in a type III interferon-dependent manner. Mice lacking the type III interferon receptor have altered STAT1 and IL-22 signaling. In coinfection studies, mice without the type III interferon receptor had significantly less nasal S. aureus colonization and subsequent pneumonia than infected WT mice did. This work demonstrates that type III interferons induced by influenza virus contribute to nasal colonization and pneumonia due to S. aureus superinfection.

Dataset Information

Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa.

Publications

Symbiotic microbiome Staphylococcus aureus from human nasal mucus modulates IL-33-mediated type 2 immune responses in allergic nasal mucosa.

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