The gut as a source of inflammatory cytokines after stimulation with endotoxin

Eur J Surg. 1997 Jan;163(1):45-51.


Objective: To find out if endotoxin (LPS) can mediate the production of inflammatory cytokines by enterocytes.

Design: Laboratory experiment.

Setting: Teaching hospital and burns unit, USA.

Material: Caco-2 cells (HTB38, human adenocarcinoma, and colon).

Main outcome measures: Concentrations of tumour necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and prostaglandin E2 (PGE2) in cell culture supernatants.

Results: LPS significantly increased the production of TNF from 8.9 to 26.4 units/ml in 24 h and this increase persisted at a lower level for 4 days with an increase from 2.3 to 9 units/ml at a cell concentration of 2 x 10(5) cells/ml. There was no increase in TNF production when the cells were cultured at 5 x 10(5) cells ml with LPS. At a concentration of 2 x 10(5) cells/ml, the cells produced small amounts of IL-6 in 24 h or 4 day cultures with or without LPS. At a concentration of 5 x 10(5) cells/ml, LPS significantly increased IL-6 production in 24 h from 142 to 433 units/ml and from 106 to 250 units/ml in 4 days. The amount of IL-6 produced by LPS-stimulated cells was greater at 1 day than at 4 days. There was no significant difference in PGE2 production by the cells under any of the incubation conditions.

Conclusion: Enterocytes can produce TNF and IL-6, and endotoxin can increase the production of these cytokines by enterocytes. The gut therefore has the potential to become an important source of inflammatory cytokines.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Caco-2 Cells
  • Cytokines / biosynthesis*
  • Dinoprostone / biosynthesis*
  • Humans
  • Inflammation / metabolism*
  • Interleukin-6 / biosynthesis
  • Lipopolysaccharides / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Cytokines
  • Interleukin-6
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Dinoprostone