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Matrix metalloproteinase-7 (matrilysin) controls neutrophil egress by generating chemokine gradients

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Matrilysin matrix metalloproteinase 7 (MMP7) is induced by mucosal injury of many tissues. To assess function of this proteinase, we subjected wild-type and Mmp7 –/– mice to acute colon injury. When matrilysin expression was increasing, 73% of wild-type mice died, whereas only 32% of Mmp7 –/– mice succumbed. Although re-epithelialization was delayed in Mmp7 –/– mice, overall injury did not differ markedly between genotypes. We hypothesized that differences in acute inflammation caused increased mortality in wild-type mice. Indeed, whereas overall neutrophil influx into tissue was similar in wild-type and Mmp7 –/– mice, their location and extent of migration differed between genotypes. Neutrophils were dispersed throughout the mucosa and within the lumen of wild-type mice, but these leukocytes were largely confined to the submucosa in Mmp7 –/– mice. The levels of neutrophil chemokines, keratinocyte-derived chemokine and MIP-2, increased in the colon tissue of both genotypes, but these factors were detected only in lumenal lavages of wild-type mice. Our findings indicate that matrilysin mediates beneficial and deleterious effects in response to injury. On one hand, it promotes re-epithelialization, but it also controls the transepithelial influx of neutrophils, which if excessive, can lead to tissue damage.

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Article Details
Swee, Mei; Wilson, Carole L.; Wang, Ying; McGuire, John K.; Parks, William C.
Journal of Leukocyte Biology , Volume 83 (6): 1404
Fed of American Socs for Experimental Biology – Jun 1, 2008
More Info
  • Publisher Soc Leukocyte Biology
  • Copyright Copyright © 2008 by the Society for Leukocyte Biology.
  • ISSN 0741-5400
  • D.O.I. 10.1189/jlb.0108016

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