Cited by 584Wound Healing and TreatmentsMacrophage Migration Inhibitory FactorChemokine receptors and signaling

Large and Sustained Induction of Chemokines during Impaired Wound Healing in the Genetically Diabetic Mouse: Prolonged Persistence of Neutrophils and Macrophages during the Late Phase of Repair

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Wetzler, Christian, Kämpfer, Heiko, Stallmeyer, Birgit, Pfeilschifter, Josef, Frank, Stefan·2000·Journal of Investigative Dermatology

Abstract

Chemokines are seen as the stimuli that largely control leukocyte migration. To assess whether the severely impaired process of cutaneous repair observed in genetically diabetic db/db mice is associated with a dysregulated infiltration of immune cells, we determined the expressional kinetics for the murine growth-regulated oncogene/melanoma growth stimulatory activity homolog macrophage inflammatory protein-2, and the macrophage chemoattractant protein-1, respectively. Wound repair in db/db mice was characterized by a sustained inflammatory response and a prolonged expression of macrophage inflammatory protein-2 and macrophage chemoattractant protein-1. Immuno-histochemistry revealed that keratinocytes at the wound margins expressed macrophage chemoattractant protein-1, whereas macrophage inflammatory protein-2 immunopositive signals were observed only in keratinocytes of hair follicles located adjacent to the wound site. Inactivation studies using neutralizing antibodies against macrophage chemoattractant protein-1 or macrophage inflammatory protein-2 indicated that sustained expression of these chemokines participated in a prolonged presence of neutrophils and macrophages at the wound site during diabetic repair. Furthermore, our data provide evidence that late infiltration (day 13 after injury) of neutrophils and macrophages into wounds in db/db mice was associated with a simultaneous downregulation of mRNA for receptors specific for macrophage inflammatory protein-2 and macrophage chemoattractant protein-1 in these animals.

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Crossref · 10.1046/j.1523-1747.2000.00029.x

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  • Prolonged secretion of chemokines in the diabetic mouse supports the p38 inhibition mechanism.

    “This is supported by the prolonged secretion of chemokines in the diabetic mouse.105”

    From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [105]

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  1. Knighton DR, Fiegel V. Growth factors and repair of diabetic wounds. In: Levin ME, O'Neal LW, Bowker JH: eds. The Diabetic Foot, 5th edn. St. Louis: Mosby Year Book, 1993:pp

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Authors
Wetzler, C., Kämpfer, H., Stallmeyer, B., Pfeilschifter, J., & Frank, S.
Affiliations
Goethe University Frankfurt (DE)
Corresponding author
Frank, Stefan
Venue
Journal of Investigative Dermatology
Publisher
Elsevier BV
Published
2000-08
Volume
115
Issue
2
Pages
245-253
ISSN
0022-202X (ISSN-L)
OpenAlex
W1965434649
Cited by
584
References
50
Citations by year
2026: 18 · 2025: 25 · 2024: 23 · 2023: 40 · 2022: 31 · 2021: 28 · 2020: 30 · 2019: 36 · 2018: 22 · 2017: 30 · 2016: 31 · 2015: 28 · 2014: 32 · 2013: 28 · 2012: 20
FWCI
10.87
Type
journal article
Language
en
Open access
Locations
  • Journal of Investigative Dermatology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Deutsche Forschungsgemeinschaft (SFB 553)
Topics
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Macrophage Migration Inhibitory Factor
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Keywords
chemokines, wound healing, diabetic wound healing, db/db mice, CXCL2, MCP-1, neutrophil infiltration, macrophage infiltration, keratinocytes, hair follicle, chronic inflammation
MeSH terms
Animals, Dermatitis, Diabetes Mellitus, Macrophages, Mice, Inbred C57BL, Neutrophils, Skin, Time Factors, Wound Healing, Wounds and Injuries, Down-Regulation, Keratinocytes, Receptors, Interleukin, Chemokines, Chemokine CCL2, Receptors, Chemokine, Receptors, Interleukin-8B, Mice, Receptors, CCR2, Chemokine CXCL2

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