Intestinal mononuclear cells primed by systemic interleukin-12 display long-term ability to aggravate colitis in mice

Area of Science:

• Immunology
• Gastroenterology
• Inflammation Research

Background:

• Systemic cytokines can influence localized inflammation.
• The role of interleukin-12 (IL-12) bursts in modulating intestinal inflammation requires further investigation.

Purpose of the Study:

• To determine if a systemic interleukin-12 (IL-12) burst impacts intestinal inflammation induced by luminal stimuli.
• To assess the duration of IL-12-induced priming on intestinal inflammatory responses.

Main Methods:

• Mice (C57BL/6) received cDNA injection to induce IL-12 release, followed by dextran sulphate sodium administration to elicit colitis.
• Inflammatory responses were evaluated by myeloperoxidase activity and histological damage in colon samples.
• Colitis was induced at different time points (7 and 60 days) after IL-12 induction to assess priming persistence.

Main Results:

• IL-12 priming led to accelerated and selective infiltration of inflammatory mononuclear cells in the lamina propria.
• Inflammatory cell recruitment was driven by systemic cytokines, not luminal antigens.
• Intestinal cells retained their heightened inflammatory potential and ability to worsen colitis even 7 or 60 days post-IL-12 burst.

Conclusions:

• A systemic IL-12 burst effectively primes intestinal cells, making them more susceptible to inflammatory responses.
• This IL-12-mediated priming is long-lasting, indicating a persistent inflammatory potential in intestinal cells.