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Gut 38:248-253 doi:10.1136/gut.38.2.248
  • Research Article

Differential expression of complement proteins and regulatory decay accelerating factor in relation to differentiation of cultured human colon adenocarcinoma cell lines.

  1. M F Bernet-Camard,
  2. M H Coconnier,
  3. S Hudault,
  4. A L Servin
  1. INSERM CJF 94-07, Pathogénie Cellulaire et Moléculaire des Microorganismes Entérovirulents, Châtenay-Malabry, France.

      Abstract

      Self protection of host cells against inadvertent injury resulting from attack by autologous complement proteins is well reported for vascular epithelium. In intestinal epithelium, the expression of C complement proteins and regulatory proteins remains currently poorly reported. This study looked at the distribution of C complement proteins and regulatory decay accelerating factor (DAF) in four cultured human intestinal cell lines of embryogenic or colon cancer origins. C3 and C4 proteins and DAF were widely present in human colon adenocarcinoma T84, HT-29 glc-/+ cells compared with human embryonic INT407 cells. In contrast, no expression of C5, C5b-9, and CR1 was seen for any of the cell lines. Taking advantage of the Caco-2 cells, which spontaneously differentiate in culture, it was seen that the C3, C4, and DAF were present in undifferentiated cells and that their expression increased as a function of the cell differentiation. These results, taken together with other reports on the presence of C complement proteins and DAF in the intestinal cells infer that the expression of regulatory C complement proteins develops in parallel with the expression of C proteins to protect these cells against the potential injury resulting from the activation of these local C proteins. Moreover, the finding that the pathogenic C1845 Escherichia coli binds to the membrane bound DAF in the cultured human intestinal cells synthetising locally C proteins and regulatory C proteins supports the hypothesis that E coli could promote inflammatory disorders by blocking local regulatory protein function.