Peritoneal macrophages are impaired in cathelicidin-deficient mice systemically challenged with Escherichia coli.
Boucher. Emily E; Brown. Luke L; Lahiri. Priyoshi P; Cobo. Eduardo R ER
Key Findings
- Cathelicidin‑deficient mice recruit fewer peritoneal macrophages during E. coli infection
- Macrophages in these mice show reduced ability to phagocytose bacteria
- Synthetic human LL‑37 does not restore phagocytosis in a mouse cell line
Practical Outcomes
- The study suggests that simply taking LL‑37 supplements may not boost immune cell function, at least not in the same way the body’s native peptide does. For biohackers, it highlights the importance of supporting the body’s own production of cathelicidins rather than relying on external LL‑37.
Summary
Mice that lack their own cathelicidin peptide have fewer immune cells called macrophages go to the belly cavity and those cells are worse at eating bacteria. Adding the human version of the peptide (LL‑37) didn’t fix the problem in mouse cells, suggesting the body’s own version is needed for proper function.
Abstract
Cathelicidins are small, cationic peptides produced by macrophages with protective effects against infection although their involvement in phagocytosis is not fully understood. This study demonstrates that fewer macrophages were recruited in mice genetically deficient in cathelicidin (Camp<sup>-/-</sup>) during acute Escherichia coli-induced peritonitis and those macrophages had impaired phagocytosis. These defects seem due to endogenous functions of murine cathelicidin (CRAMP) as phagocytosis was not improved by synthetic human cathelicidin (LL-37) in a murine phagocytic cell line. This knowledge contributes to understanding the function of cathelicidins in the recruitment and function of phagocytic cells and differential roles between endogenous and exogenous cathelicidins.
Study Information
pubmed
2021
2021-01-26T00:00:00.000Z
10.1007/s00441-020-03362-y
33