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Autor(en) / Beteiligte
Titel
IL-22 reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosi s
Ist Teil von
  • The Journal of immunology (1950), 2019-05, Vol.202 (1_Supplement), p.181-181.19
Erscheinungsjahr
2019
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
  • Abstract IL-22 play an important role in protective immune responses against bacterial infections including Mtb and maintains homeostasis by regulating excess inflammation. IL-22 can also regulate glucose homeostasis, suggesting IL-22 pathway as a novel target for therapeutic intervention. Previously, we developed a mouse model of type 2 diabetes mellitus (T2DM) and found that pathological immune response enhances mortality of Mycobacterium tuberculosis (Mtb) infected T2DM mice. In the current study, we determined the role of IL-22 during Mtb infection in T2DM mice. We found innate lymphoid 3 cells (ILC3) are the major source for IL-22 and IL- 22 production was significantly reduced in the lungs and serum of T2DM mice infected with Mtb. Recombinant IL- 22 or adoptive transfer of ILC3 cells prolonged the survival of Mtb infected T2DM mice. Recombinant IL-22 prevented neutrophil accumulation near alveoli, reduced the serum insulin level and improved the lipid metabolism. Recombinant IL-22 also prevented neutrophil-mediated epithelial cell damage by inhibiting elastase production by neutrophils. Further, we found serum IL-22 levels were significantly less in tuberculosis (TB) patients with T2DM compared to TB patients without T2DM. Our findings suggest that IL-22 produced by ILC3 cells is essential to inhibit excess inflammation, epithelial cell damage in T2DM mice infected with Mtb.
Sprache
Englisch
Identifikatoren
ISSN: 0022-1767
eISSN: 1550-6606
DOI: 10.4049/jimmunol.202.Supp.181.19
Titel-ID: cdi_crossref_primary_10_4049_jimmunol_202_Supp_181_19
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