Recent evidence has shown the importance of the gut and asthma. The gut biome is linked to airway disease through modification of the the immune response, which is called the gut-lung axis. In allergic asthma, altered gut microbiome has been reported to augment allergic sensitization. Studies have shown that the use of antibiotics and a modern lifestyle in infancy increase the prevalence of asthma.
Antibiotics induce changes in the gut microbiome even after a short period of 1 to 2 weeks. Azithromycin has been discussed as a candidate treatment for airway inflammatory disease.
Azithromycin for Asthma, as Add-On Therapy
A study published in the Journal of Allergy and Clinical Immunology aimed to evaluate whether changes in the gut microbiota could change the airway inflammation in allergic asthma. The authors reported the following:
- Airway inflammation induced dysbiosis in the gut but it didn’t affect the airway microbiome
- Antibiotic (azithromycin) treatment could change gut micorbiota and decrease airway inflammation in allergic asthma, which was confirmed by microbiota transplantation in allergic mice.
- Azithromycin treatment could increase commensal clostridium proportion and acetate levels. (These have anti-inflammatory effects).
Based on this study and other ones, it seems that the gut microbiome plays a strong role in asthma and other allergic diseases.
Gut microbiome in food allergy
Altered Gut Microbes in Chronic Hives
Food Allergy and C-sections, what is the influence?
Do antibiotics or acid suppressor meds in infants promote allergy?
A very important period is during the maturation of gut microbiota in early infancy. Many antibiotics can disrupt the gut microbiome, but azithromycin (Zithromax) seems to contain anti-inflammatory properties and its administration may reduce airway inflammation. This suggests that the gut and asthma play a close interaction. This may provide a new strategy for immune modulators to treat asthma in the future. More studies will need to be done. This study was done on mice.