Cited by 33Wound Healing and TreatmentsImmune Response and InflammationNitric Oxide and Endothelin Effects

Bacterial colonization and the expression of inducible nitric oxide synthase in murine wounds

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Mahoney, Eric, Reichner, Jonathan, Robinson Bostom, Leslie, Mastrofrancesco, Balduino, Henry, William, Albina, Jorge·2002·The American Journal of Pathology

Abstract

The expression of inducible nitric oxide synthase (iNOS) in two different murine wound models was investigated. Animals were subjected to either full-thickness linear skin incision with subcutaneous implantation of sterile polyvinyl alcohol sponges, or to 1.5 x 1.5-cm dorsal skin excision. Reverse transcriptase-polymerase chain reaction detected iNOS mRNA in all cell samples retrieved from the sponges. Immunoblotting of lysates of inflammatory cells harvested from the sponges failed to detect iNOS protein, and immunohistochemistry of the incisional wound was mildly positive. Inflammatory cells of excisional wounds stained strongly positive for iNOS. Cutaneous wounds were found to be colonized with Staphylococcus aureus. The detection of iNOS in cells from sponges inoculated in vivo with heat-killed bacteria and the reduction of immunohistochemical signal for iNOS in excisional wounds of animals treated with antibiotics support a role of bacteria in the induction of iNOS in wounds. The expression of iNOS in excisional wounds requires interferon-gamma and functional lymphocytes because interferon-gamma knockout and SCID-Beige mice exhibited attenuated iNOS staining in excisional wounds. The expression of iNOS in the inflammatory cells of murine wounds is a response to bacterial colonization and not part of the normal repair process elicited by sterile tissue injury.

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Crossref · 10.1016/s0002-9440(10)64492-6

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  • Mp in incisional mouse skin wounds appear to express iNOS only in response to invading pathogens and not as an inherent feature of the tissue-repair response.

    “However, Mp in incisional mouse skin wounds appear to express iNOS only in response to invading pathogens and not as an inherent feature of the tissue-repair response [33,67].”

    From Macrophage phenotypes during tissue repair (2013) · cites this paper as [67]

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Authors
Mahoney, E., Reichner, J., Robinson Bostom, L., Mastrofrancesco, B., Henry, W., & Albina, J.
Affiliations
Brown University (US)
Corresponding author
Albina, Jorge
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2002-12
Volume
161
Issue
6
Pages
2143-2152
ISSN
0002-9440 (ISSN-L)
OpenAlex
W2077985932
Cited by
33
References
24
Citations by year
2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2017: 1 · 2014: 3 · 2013: 2 · 2012: 1
FWCI
3.11
Type
journal article
Language
en
Open access
Locations
  • American Journal Of Pathology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of General Medical Sciences (R01GM042859, GM-42859)
Topics
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
inducible nitric oxide synthase, wound healing, bacterial colonization, Staphylococcus aureus, skin wounds, interferon-gamma, lymphocytes, inflammatory cells, SCID/beige mice, excision wound, incisional wounds
MeSH terms
Animals, Anti-Bacterial Agents, Immunohistochemistry, Interferon-gamma, Macrophages, Skin, Staphylococcus aureus, Wound Healing, Wound Infection, Surgical Sponges, Mice, SCID, Mice, Knockout, Nitric Oxide Synthase, Mice, Nitric Oxide Synthase Type II

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