The surgical implications of chronic granulomatous disease

Eckert, Jordan W.; Abramson, Stuart L.; Starke, Jeffrey R.; Brandt, Mary L.

doi:10.1016/s0002-9610(99)80167-6

Cited by 44 publications

(11 citation statements)

References 12 publications

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“…More recently, non-phagocytic cells have been identified to generate ROS by a NADPH oxidase-dependent system (31). Deficiencies in NADPH oxidase function causes chronic granulomatous disease, a disorder that is associated with wound infection and impaired wound healing (32). Recent studies indicate that ROS may serve as signaling mediators (4).…”

Section: Discussionmentioning

confidence: 99%

Oxidant-induced Vascular Endothelial Growth Factor Expression in Human Keratinocytes and Cutaneous Wound Healing

Sen

Khanna

Babior

et al. 2002

Journal of Biological Chemistry

293

218

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Neutrophils and macrophages, recruited to the wound site, release reactive oxygen species by respiratory burst. It is commonly understood that oxidants serve mainly to kill bacteria and prevent wound infection. We tested the hypothesis that oxidants generated at the wound site promote dermal wound repair. We observed that H 2 O 2 potently induces vascular endothelial growth factor (VEGF) expression in human keratinocytes. Deletion mutant studies with a VEGF promoter construct revealed that a GC-rich sequence from bp ؊194 to ؊50 of the VEGF promoter is responsible for the H 2 O 2 response. It was established that at M concentrations oxidant induces VEGF expression and that oxidant-induced VEGF expression is independent of hypoxia-inducible factor (HIF)-1 and dependent on Sp1 activation. To test the effect of NADPH oxidase-generated reactive oxygen species on wound healing in vivo, Rac1 gene transfer was performed to dermal excisional wounds left to heal by secondary intention. Rac1 gene transfer accelerated wound contraction and closure. Rac1 overexpression was associated with higher VEGF expression both in vivo as well in human keratinocytes. Interestingly, Rac1 gene therapy was associated with a more well defined hyperproliferative epithelial region, higher cell density, enhanced deposition of connective tissue, and improved histological architecture. Overall, the histological data indicated that Rac1 might be an important stimulator of various aspects of the repair process, eventually enhancing the wound-healing process as a whole. Taken together, the results of this study indicate that wound healing is subject to redox control.

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Section: Discussionmentioning

confidence: 99%

Oxidant-induced Vascular Endothelial Growth Factor Expression in Human Keratinocytes and Cutaneous Wound Healing

Sen

Khanna

Babior

et al. 2002

Journal of Biological Chemistry

293

218

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“…Once recruited, PMNs produce and release copious amounts of reactive oxygen species (ROS) that target potential bacterial invaders. A failure in sufficient production of ROS leads to frequent and recurrent bacterial and fungal infections; as observed in chronic granulomatous disease (CGD), a disease prompted by a deficient oxidase system in PMNs (Eckert et al, 1995). Conversely, excess ROS production contributes to the pathophysiology of conditions such as impaired wound healing (Gordillo and Sen, 2003), cardiovascular disease (Cave et al, 2006), sepsis (Guo and Ward, 2007)or ischemia/reperfusion injury(Kaminski et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

The down regulation of neutrophil oxidative metabolism by S100A8 and S100A9: Implication of the protease-activated receptor-2

Sroussi

Villines

et al. 2012

Molecular Immunology

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S100A8 and S100A9 regulate polymorphonuclear neutrophils (PMNs) recruitment and represent 40% of PMN cytosolic protein weight. We have shown that S100A8/S100A9 inhibit PMN oxidative metabolism. The present study was designed to elucidate the mechanisms of this anti-oxidative effect. We hypothesized that the protease activated receptor-2 (PAR-2) played a role in the down-regulation of PMN oxidative metabolism by S100A8/S100A9. Freshly isolated PMNs were tested for their ability to oxidize dichlorofluorescin-diacetate. Functional inhibition of PAR-2 with ENMD-1068, the pepducin P2pal-21 or an antibody directed at PAR-2 cleavage/activation site, resulted in a significant inhibition of S100A8 and S100A9 anti-oxidative effect. Conversely, the controlled activation of PAR-2 potentiated S100 anti-oxidative effect. Taken together, the data indicate that the anti-oxidative effect of S100A8/A9 is initiated by PAR-2 activation. S100A8/S100A9 may therefore dampen inflammation without interfering with its initial strength. This finding opens translational possibilities to limit deleterious PMN activation with a dual PAR-2/S100 strategy.

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“…In contrast, the series examining thoracic surgery in nontuberculous mycobacterial disease identified only two instances of wound infections in 265 operations [19]. Previous series of CGD patients have reported rates of wound complications ranging from 20 to 40 %, likely reflecting the unique inflammatory defect in CGD that leads to exuberant granulation tissue formation and wound dehiscence [11, 12]. It is relatively unique to CGD that wound dehiscence is treated most effectively with systemic corticosteroids, which rapidly reverse it.…”

Section: Discussionmentioning

confidence: 99%

“…In one series of ten children with CGD who underwent surgery, 30 % experienced wound dehiscence [12]. In a separate series of patients undergoing colonic resections, 75 % (3/4) of patients receiving a colostomy developed pyoderma gangrenosum, two of whom required additional surgical interventions [13].…”

Section: Introductionmentioning

confidence: 99%

Thoracic Surgery in Chronic Granulomatous Disease: a 25-Year Single-Institution Experience

et al. 2016

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The surgical implications of chronic granulomatous disease

Cited by 44 publications

References 12 publications

Oxidant-induced Vascular Endothelial Growth Factor Expression in Human Keratinocytes and Cutaneous Wound Healing

Oxidant-induced Vascular Endothelial Growth Factor Expression in Human Keratinocytes and Cutaneous Wound Healing

The down regulation of neutrophil oxidative metabolism by S100A8 and S100A9: Implication of the protease-activated receptor-2

Thoracic Surgery in Chronic Granulomatous Disease: a 25-Year Single-Institution Experience

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