The wound fibroblast and macrophage. II: Their origin studied in a human after bone marrow transplantation

Stewart, Richard J.; Duley, John A.; Dewdney, Janet M.; Allardyce, Randall A.; Beard, Michael; Fitzgerald, P. H.

doi:10.1002/bjs.1800680220

Cited by 25 publications

(13 citation statements)

References 17 publications

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“…Locally administered antimacrophage serum had no effect on the number of circulating monocytes, nor did it affect the number of wound macrophages. Similar conclusions have been drawn conceming the bone marrow origin of macrophages in healing wounds in humans by Stewart et al (1981). By observing the karyotype (sex chromosome markers) ofmacrophages and fibroblasts emigrating from explants of a 5-day skin wound in a 9-year-old girl who had recently received a bone marrow graft from her l1-year-old brother, it was found that the fibroblasts had the karyotype of the recipient, while the macrophages bore the karyotype of the donor.…”

Section: Monocyte Influx Under Inflammatory Conditionssupporting

confidence: 78%

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Riches

1988

The Molecular and Cellular Biology of Wound Repair

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Section: Monocyte Influx Under Inflammatory Conditionssupporting

confidence: 78%

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Riches

1988

The Molecular and Cellular Biology of Wound Repair

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“…There are several different subtypes of lung macrophages identified as morphologically and functionally heterogeneous from one another, including alveolar, interstitial, intravascular, and airway macrophages [90]. Of note, AMs are believed to be long-lived radio-and chemotherapy-resistant cells and they are slow to turn over and be replaced by donor-derived cells following HSCT [57,58,65,71,74,93,94]. Cell-surface receptors and secreted products allow lung macrophages to respond to environmental factors and aid in the clearance of microorganisms in the distal airways and alveolar spaces [90,104].…”

Section: Macrophagesmentioning

confidence: 99%

Eicosanoid regulation of pulmonary innate immunity post-hematopoietic stem cell transplantation

Ballinger

McMillan

Moore

2007

Arch. Immunol. Ther. Exp.

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Hematopoietic stem cell transplantation (HSCT) is a therapeutic option for a number of malignant and inherited disorders. However, the efficacy of this therapy is limited by a number of serious infectious and noninfectious complications. Pulmonary infections represent a significant cause of morbidity and mortality post-HSCT and can occur both pre-and post-hematopoietic reconstitution. Susceptibility to Gram-negative bacterial infections despite full hematopoietic engraftment suggests that innate immunity remains impaired months to years post-HSCT. This review will describe the process and complications of HSCT and will summarize what is known about innate immune reconstitution post-HSCT. Data from the literature as well as our own laboratory will be presented to suggest that an eicosanoid imbalance characterized by overproduction of prostaglandins and under-production of leukotrienes leads to impaired lung phagocyte function post-HSCT. Of therapeutic interest, strategies which limit production of prostaglandins can improve pulmonary host defense in animal HSCT models, which suggests that this may also be beneficial for human HSCT recipients.

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“…It was originally thought that dermal fibroblasts/myofibroblasts involved in the healing of a cutaneous wound were derived from cells situated locally in the dermis. To support that hypothesis many studies are available (Grillo, 1963;Ross et al, 1970;Stewart et al, 1981;Postlethwaite et al, 2004).…”

mentioning

confidence: 90%

Fibroblasts/myofibroblasts that participate in cutaneous wound healing are not derived from circulating progenitor cells

Barisic-Dujmovic

Boban

Clark

2009

Journal Cellular Physiology

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Dermal fibroblasts/myofibroblasts involved in the wound healing are thought to originate from the resident fibroblast progenitors. To test the hypothesis of an extra dermal origin of the dermal fibroblasts/myofibroblasts, bone marrow (BM) transplantation and parabiosis experiments were initiated utilizing a collagen promoter green fluorescent protein (GFP) reporter transgene as a visible marker for dermal fibroblasts/myofibroblasts. BM transplantation experiments using BM from Col3.6GFPsapph transgenic mice showed no evidence that BM derived progenitors differentiated into dermal fibroblasts/myofibroblasts at the wound site. Rather the GFP positive cells (GFP+) observed at the wound site were not dermal fibroblasts/myofibroblasts but immune cells. These GFP+ cells were also detected in the lung and spleen. Furthermore, GFP+ fibroblasts were not detected in primary dermal fibroblast cultures initiated from BM chimeras. Using the same transgenic mice, parabiotic pairs were generated. One partner in the parabiosis carried a GFP expressing transgene while the other partner was a non-transgenic C57BL/6 mouse. Similar to the BM transplantation experiments, GFP+ immune cells were detected in the wound of the non-transgenic parabiont, however, GFP expressing dermal fibroblasts/myofibroblasts were not observed. Collectively, these data suggest that dermal fibroblast/myofibroblast progenitors do not readily circulate. The expression of the Col3.6GFPsapph in the hematopoietic cells confirmed that our methods were sensitive enough to detect Col3.6GFP expressing dermal fibroblasts derived from the peripheral circulation if they had originated in the BM.

show abstract

The wound fibroblast and macrophage. II: Their origin studied in a human after bone marrow transplantation

Cited by 25 publications

References 17 publications

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Eicosanoid regulation of pulmonary innate immunity post-hematopoietic stem cell transplantation

Fibroblasts/myofibroblasts that participate in cutaneous wound healing are not derived from circulating progenitor cells

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