Skip NavigationSkip to Content
Return Return to Search Results

PAM3 protects against DSS-induced colitis by altering the M2:M1 ratio

  1. Author:
    Horuluoglu, Begum H
    Kayraklioglu, Neslihan
    Tross,Debra
    Klinman,Dennis

  2. Author Address

    Cancer and Inflammation Program, National Cancer Institute, NIH, Frederick, MD 21720, USA., Cancer and Inflammation Program, National Cancer Institute, NIH, Frederick, MD 21720, USA. klinmand@gmail.com.,
    1. Year: 2020
    2. Date: Apr 08
    3. Epub Date: 2020 04 08
  2. Journal: Scientific reports
    1. 10
    2. 1
    3. Pages: 6078
  4. Type of Article: Article
  5. Article Number: 6078
  6. ISSN: 2045-2322
  1. Abstract:

    Inflammation of the gastrointestinal tract contributes to the development of inflammatory bowel disease (IBD). Human IBD is modeled by administering dextran sulfate sodium (DSS) to mice. In humans and mice, inflammatory M1 macrophages contribute to the progression of IBD whereas immunosuppressive M2 macrophages protect against colitis. The TLR2/1 agonist PAM3CSK4 (PAM3) induces human and murine monocytes to differentiate into immunosuppressive M2 macrophages, suggesting that PAM3 might be of benefit in the prevention/treatment of colitis. PAM3 was therefore administered to mice treated with DSS. As hypothesized, the number of M2 macrophages rose and disease severity decreased. The critical role of M2 macrophages in this process was established by transferring purified M2 macrophages from PAM3 treated control donors into DSS recipients and reducing colitis. These findings suggest that PAM3 may represent a novel approach to the treatment of human IBD.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1038/s41598-020-63143-z
  3. PMID: 32269253
  4. View record in Web of Science®
  5. WOS: 000559751400002
  6. PII : 10.1038/s41598-020-63143-z

Library Notes

  1. Fiscal Year: FY2019-2020
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel