Send to

Choose Destination
See comment in PubMed Commons below
PLoS One. 2013;8(3):e59174. doi: 10.1371/journal.pone.0059174. Epub 2013 Mar 25.

Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.

Author information

  • 1Institute of Eye and Otorhinolaryngology, Department of Otorhinolaryngology-Head and Neck Surgery, Provincial Hospital affiliated to Shandong University, Jinan, China.



Hygiene hypothesis demonstrates that the lack of microbial exposure would promote the development of allergic airway disease (AAD). Therefore, the gut microbiota, including Escherichia coli (E. coli), would probably offer a potential strategy for AAD.


To investigate whether E. coli infection is able to suppress the induction of AAD and to elucidate the underlying mechanisms.


Nonpathogenic E. coli ATCC 25922 was infected by gavage before AAD phase in three patterns: 10(8) or 10(6) CFU in neonates or 10(8) CFU in adults. Then mice were sensitized and challenged with ovalbumin (OVA) to induce allergic inflammation in both the upper and lower airways. Hallmarks of AAD, in terms of eosinophil infiltration and goblet cell metaplasia in subepithelial mucosa, Th2 skewing of the immune response, and levels of T regulate cells (Tregs), were examined by histological analysis, ELISA, and flow cytometry, respectively.


E. coli, especially neonatally infected with an optimal dose, attenuated allergic responses, including a decrease in nasal rubbing and sneezing, a reduction in eosinophil inflammation and goblet cell metaplasia in subepithelial mucosa, decreased serum levels of OVA-specific IgE, and reduced Th2 (IL-4) cytokines. In contrast, this effect came with an increase of Th1 (IFN-r and IL-2) cytokines, and an enhancement of IL-10-secreting Tregs in paratracheal lymph nodes (PTLN).


E. coli suppresses allergic responses in mice, probably via a shift from Th1 to Th2 and/or induction of Tregs. Moreover, this infection is age- and dose-dependent, which may open up novel possibilities for new therapeutic interventions.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk