Answers are grounded in this paper and cite their sources.
Preclinical study shows recombinant interleukin-11 dampens inflammation without worsening bacterial burden in mice, indicating preserved host defense against intracellular infection.
To determine whether recombinant human (rh) interleukin (IL)-11 disrupts the clearance of microbial pathogens, mice were challenged with Listeria monocytogenes after receiving high-dose rhIL-11, anti-tumor necrosis factor (TNF) monoclonal antibody (MAb), anti-IL-11 MAb, or saline control. The LD50 was not affected by rhIL-11 but was 10-fold lower in the anti-TNF MAb group (P<.001). Plasma IL-6, IL-1beta, and TNF-alpha levels were not different between rhIL-11-treated animals and the control group; however, interferon-gamma levels were significantly reduced by IL-11 treatment (2477 vs. 0 pg/mL, P<.01). Compared with the control group, the quantitative level of L. monocytogenes in hepatic and splenic tissue was unchanged by rhIL-11 but was significantly increased by TNF or IL-11 inhibition. The results indicate that IL-11 down-regulates cytokine production but does not exacerbate systemic infection in the murine Listeria infection model.
No takes yet. Share an insight, caveat, or question.
Opal et al. (2000) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: