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MCP-3 in inflammatory bowel disease
  1. U HELWIG,
  2. K M LAMMERS,
  3. P GIONCHETTI,
  4. F RIZZELLO,
  5. M CAMPIERI
  1. Department of Internal Medicine and Gastroenterology
  2. University of Bologna, Bologna, Italy
  3. Email: paolo{at}meol.unibo.it
  4. Theodor Kocher Institute
  5. University of Bern, Bern, Switzerland
    1. M UGUCCIONI
    1. Department of Internal Medicine and Gastroenterology
    2. University of Bologna, Bologna, Italy
    3. Email: paolo{at}meol.unibo.it
    4. Theodor Kocher Institute
    5. University of Bern, Bern, Switzerland
      1. J WEDEMEYER,
      2. A LORENTZ,
      3. M P MANNS,
      4. S C BISCHOFF
      1. Department of Gastroenterology and Hepatology
      2. Medical School of Hannover, Hannover, Germany
      3. Email: bischoff.stephan{at}mh-hannover.de

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        Editor,—We read with interest the article by Wedemeyer and colleagues (Gut1999; 44:629–35) on chemokines in inflammatory bowel disease.

        Monocyte chemotactic protein 3 (MCP-3) expression in inflammatory bowel diseases is a very interesting observation and we agree with the authors that MCP-3 might play an important role in the pathophysiology of these diseases.

        We have recently published an article on the C-X-C chemokines interleukin (IL)-8 and IP-10, and the C-C chemokines MCP-1 and MCP-3 in the mucosa of active ulcerative colitis.1 It concerns an immunohistochemical study in which we showed increased expression of these chemokines in the lamina propria of patients with ulcerative colitis compared with normal controls. Furthermore, we observed a significant difference in expression between inactive and moderate/severe ulcerative colitis based on the histological grading in MCP-1, MCP-3, and IL-8.

        Wedemeyer and colleagues state in their discussion that MCP-1 is expressed in the epithelial cells and lamina propria whereas MCP-3 is almost exclusively produced by epithelial cells. However, in the results section and further in the discussion the authors mentioned sporadic MCP-3 expression in the lamina propria of inflamed tissue. The photographs show only epithelial cells and it is not possible to see the staining pattern of the lamina propria.

        We found MCP-3 expressing cells in the lamina propria which was significantly increased in active ulcerative colitis compared with both inactive ulcerative colitis and normal controls. Furthermore, MCP-3 expression in lamina propria was also enhanced in patients suffering from pouchitis compared with patients with a normal pouch (unpublished data).

        In the study of Wedemeyer et al, unfortunately the data on MCP-3 expression in Crohn's disease were not significant which might be because of the small number of patients examined. It would be interesting to further evaluate the role of chemokines in Crohn's disease.

        In conclusion, albeit with some minor differences, both studies have shown that MCP-3 plays an important role in ulcerative colitis.

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        Editor,—We thank Dr Helwig and colleagues for their interest in our recent paper in which we showed enhanced expression of the C-C chemokine MCP-3 in inflammatory bowel disease mucosa. In the article by Uguccioni and colleagues,1-1 we noted their slightly different findings in terms of localisation of MCP-3 expression. Using different techniques (cryostat and paraformaldehyde fixatives, different anti-MCP-3 antibodies) we found consistent expression of MCP-3 in the intestinal epithelium and sporadically in the lamina propria. Uguccioni et al reported MCP-3 expression in the lamina propria. The reason why they did not find MCP-3 expression in the epithelium remains unclear. A possible explanation could be that patients received different therapies at the time of colonoscopy. Only one of the patients investigated in the study by Uguccioni et al received steroids while most patients with macroscopic inflamed mucosa enrolled in our study received either oral or parenteral steroid medication at the time of biopsy. As mentioned in the results, we also found occasional MCP-3 staining cells within the lamina propria but did not focus our investigation on these cells. Which lamina propria cells express MCP-3 remains to be determined. We found that human isolated mast cells are capable of expressing MCP-3 mRNA (unpublished data) which makes them a possible candidate. Other candidates are macrophages and endothelial cells, as reported by Ying and colleagues,1-2 who found MCP-3 expression in bronchial biopsies located in these two cell types and in epithelial cells.

        In conclusion, we agree with Dr Helwig and colleagues that the role of chemokines in inflammatory bowel disease needs to be evaluated in more detail. Further data are necessary to answer the question of whether or not these alterations in chemokine expression are restricted to specific disorders such as ulcerative colitis or resemble a more general finding associated with any type of intestinal inflammation and host defence mechanisms.

        References

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