Alterations of the phenotype of colonic macrophages in... : European Journal of Gastroenterology & Hepatology (original) (raw)

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Alterations of the phenotype of colonic macrophages in inflammatory bowel disease

Rogler, Gerhard1; Andus, Tilo1; Aschenbrenner, Elisabeth1; Vogl, Daniela1; Falk, Werner1; Schölmerich, Jürgen1; Gross, Volker1

From the 1Department for Internal Medicine I, University of Regensburg, Germany.

Requests for reprints to Dr med. Dr phil. Gerhard Rogler, Klinik und Poliklinik für Innere Medizin I, Universität Regensburg, D-93042 Regensburg, Germany.

Date received: 28 January 1997; revised: 24 March 1997; accepted: 19 June 1997.

Abstract

Background:

Intestinal macrophages play an important role in mucosal inflammation. In normal colonic mucosa we recently demonstrated a unique macrophage phenotype with attenuated immune functions. Here we present an analysis of the alterations of the phenotype of colonic macrophages in inflammatory bowel disease (IBD).

Methods:

Intestinal macrophages were isolated from biopsies of patients with IBD (n = 20). Flow cytometric triple fluorescence analysis was applied to study CD14, CD16, CD33, HLA-DR, CD44, CD11b, CD11c and CD3/CD19 expression.

Results:

In IBD there was an increase in expression not only of CD14 compared to control mucosa (36.0%±13.2% vs. 10.5%±3.8%, P<0.0001) but also of CD16 (28.6%±10.3% vs. 10.1%±3.9%, P<0.0001), HLA-DR (53.1%±15.9% vs. 27.3%± 9.2%, P<0.0005), CD11b (42.8%±14.2% vs. 17.4%±6.8%, P<0.0001) and CD11c (35.1% ± 15.9% vs. 17.8%±10.4%, P<0.005.). Furthermore, a hitherto undescribed new population of macrophages could be detected by flow cytometry only in patients with ulcerative colitis (CD16++, CD11b++, CD14low, CD33low, CD11c-) accounting for 5.8% of all cells isolated.

Conclusion:

In contrast to colonic macrophages from normal mucosa, there is a significantly higher expression of CD14, CD16, HLA-DR, CD11b and CD11c in IBD, indicating additional macrophage populations in the inflamed mucosa. This may reflect either a recruitment of new cells from the circulation or a change in phenotype of resident cells.