Effects of different routes and forms of vitamin D administration on CD4 + T cell homeostasis and renin-angiotensin system-associated lung injury in obese mice complicated with polymicrobial sepsis.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model without human participants
PubMed 36411667 · doi:10.1016/j.biopha.2022.113961
What was done
High-fat diet-induced obese mice underwent cecal ligation and puncture (CLP) to induce polymicrobial sepsis. Mice were divided into four sepsis groups: untreated sepsis control (S), oral cholecalciferol 1 day before CLP (G), intravenous calcitriol 1 hour after CLP (V), or combined pre-CLP oral cholecalciferol and post-CLP intravenous calcitriol (GV). Investigators measured CD4+ T cell subset ratios in blood, inflammatory markers and renin-angiotensin system (RAS) components in lung tissue, and lung injury scores following CLP.
What was found
The abstract reports directional comparisons without numerical values, error metrics, or exact p-values. Blood Th1/Th2 ratios were higher and Th17/Treg ratios were lower in the V and GV groups compared to the S and G groups. At 24 hours post-CLP, pulmonary NF-kB and IL-1beta gene expressions were lowest in the V group, while AT2R, ACE2, and MasR gene expressions were highest in the V group. MasR protein levels in the GV group and the AT2R/AT1R ratio in the V group exceeded those in the G and/or S groups. All vitamin D-treated groups demonstrated lower lung injury scores than the untreated sepsis group.
Why it matters
This animal study suggests that intravenous calcitriol post-injury may exert stronger immunomodulatory and pulmonary RAS-associated anti-inflammatory effects than prophylactic enteral cholecalciferol in obese septic mice.
Limits
Findings are from an animal model and cannot be directly translated to human sepsis. The abstract does not report the total animal sample size (n), absolute numeric measurements, effect sizes, or confidence intervals.
Cited by
- supports In animal models of acute lung injury, high doses of active vitamin D normalize ACE2 levels.