4.8 Article

Free Feeding of CpG-Oligodeoxynucleotide Particles Prophylactically Attenuates Allergic Airway Inflammation and Hyperresponsiveness in Mice

期刊

FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.738041

关键词

CpG-ODNs; oral delivery; mouse model of allergic asthma; airway inflammation; airway hyperresponsiveness; pulmonary vein cardiomyocytes; Reg3 gamma; gut microbiota

资金

  1. JSPS KAKENHI [17H03907, 20H03125]
  2. LOTTE Foundation
  3. Kobayashi Foundation
  4. Urakami Foundation for Food and Food Culture Promotion
  5. Grants-in-Aid for Scientific Research [17H03907, 20H03125] Funding Source: KAKEN

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The study found that prophylactic feeding of ODNcap can reduce allergic airway inflammation, hyperresponsiveness, and goblet cell hyperplasia in an ovalbumin-induced asthma model. Transcriptomics-driven approaches demonstrated that ODNcap feeding inhibits injury of pulmonary vein cardiomyocytes. Additionally, airway antimicrobial peptide and fecal microbiota participate in the ODNcap-mediated effects.
CpG-oligodeoxynucleotides (CpG-ODNs) constitute an attractive alternative for asthma treatment. However, very little evidence is available from studies on the oral administration of CpG-ODNs in animals. Previously, we developed acid-resistant particles (named ODNcap) as an oral delivery device for ODNs. Here, we showed that free feeding of an ODNcap-containing feed prophylactically attenuates allergic airway inflammation, hyperresponsiveness, and goblet cell hyperplasia in an ovalbumin-induced asthma model. Using transcriptomics-driven approaches, we demonstrated that injury of pulmonary vein cardiomyocytes accompanies allergen inhalation challenge, but is inhibited by ODNcap feeding. We also showed the participation of an airway antimicrobial peptide (Reg3 gamma) and fecal microbiota in the ODNcap-mediated effects. Collectively, our findings suggest that daily oral ingestion of ODNcap may provide preventive effects on allergic bronchopulmonary insults via regulation of mechanisms involved in the gut-lung connection.

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