The healing of peritoneum under normal and pathological conditions

Ellis, Harold; Harrison, Walford; Hugh, Thomas B.

doi:10.1002/bjs.1800520616

Cited by 231 publications

(117 citation statements)

References 6 publications

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“…Previous reports showed that peritoneal injury is triggered by leakage of plasma proteins, followed by formation of fibrinous deposits and proliferation of fibroblasts (3). A rapid and transient influx of neutrophils into the peritoneal cavity also occurs followed by an accumulation of mononuclear cells, largely macrophages (M) 3 (4,5). CD4-positive T cells also play a significant role in peritoneal adhesions together with the T cell-derived proinflammatory cytokine, IL-17 (6), and the programmed death-1 inhibitory pathway (7).…”

Section: Inhibition Of Ccl1-ccr8 Interaction Prevents Aggregation Of mentioning

confidence: 99%

Inhibition of CCL1-CCR8 Interaction Prevents Aggregation of Macrophages and Development of Peritoneal Adhesions

Hoshino¹,

Kawamura²,

Yasuhara

et al. 2007

The Journal of Immunology

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Peritoneal adhesions are a significant complication of surgery and visceral inflammation; however, the mechanism has not been fully elucidated. The aim of this study was to clarify the mechanism of peritoneal adhesions by focusing on the cell trafficking and immune system in the peritoneal cavity. We investigated the specific recruitment of peritoneal macrophages (PMφ) and their expression of chemokine receptors in murine models of postoperative and postinflammatory peritoneal adhesions. PMφ aggregated at the site of injured peritoneum in these murine models of peritoneal adhesions. The chemokine receptor CCR8 was up-regulated in the aggregating PMφ when compared with naive PMφ. The up-regulation of CCR8 was also observed in PMφ, but not in bone marrow-derived Mφ, treated with inflammatory stimulants including bacterial components and cytokines. Importantly, CCL1, the ligand for CCR8, a product of both PMφ and peritoneal mesothelial cells (PMCs) following inflammatory stimulation, was a potent enhancer of CCR8 expression. Cell aggregation involving PMφ and PMCs was induced in vitro in the presence of CCL1. CCL1 also up-regulated mRNA levels of plasminogen activator inhibitor-1 in both PMφ and PMCs. CCR8 gene-deficient mice or mice treated with anti-CCL1-neutralizing Ab exhibited significantly reduced postoperational peritoneal adhesion. Our study now establishes a unique autocrine activation system in PMφ and the mechanism for recruitment of PMφ together with PMCs via CCL1/CCR8, as immune responses of peritoneal cavity, which triggers peritoneal adhesions.

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Section: Inhibition Of Ccl1-ccr8 Interaction Prevents Aggregation Of mentioning

confidence: 99%

Inhibition of CCL1-CCR8 Interaction Prevents Aggregation of Macrophages and Development of Peritoneal Adhesions

Hoshino¹,

Kawamura²,

Yasuhara

et al. 2007

The Journal of Immunology

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“…Similar shifts in cell differentiation following peritoneal trauma have been demonstrated in other animal models. [12][13][14] The exact role of PMN in post-surgical enhanced tumor development is not yet clear. In the early post-operative inflammatory reaction PMN are responsible for clearing dead tissue and invading organisms by producing and releasing reactive oxygen species (ROS).…”

Section: Introductionmentioning

confidence: 99%

The Influence of Reactive Oxygen Species on the Adhesion of Pancreatic Carcinoma Cells to the Peritoneum

Raa

Grevenstein

Kate

et al. 2007

Cell Adhesion & Migration

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Postoperative peritoneal carcinomatosis is a significant clinical problem after "curative" resection of pancreatic carcinoma. Preoperative surgical trauma activates a cascade of peritoneal defense mechanisms responsible for postoperative intra-abdominal tumor recurrence. Reactive oxygen species (ROS) play a pivotal role in this postoperative inflammatory reaction. This study explores the influence of ROS on adhesion of human pancreatic carcinoma cells to human mesothelial cells. Furthermore this study explores the influence of ROS on the presentation of adhesion molecules on Panc-1 and mesothelial cells. ROS were produced using the enzymatic reaction of xanthine with xanthine oxidase (X/XO). A reproducible in vitro assay to study adhesion of human Panc-1 carcinoma tumor cells to a mesothelial cell monolayer of primary human mesothelial cells was used. Mesothelial monolayers were incubated with ROS produced prior to adhesion of the tumor cells. Incubation of the mesothelial cells with X/XO resulted in a significant increase (69.5%) in adhesion of Panc-1 in all patients. SOD/catalase, anti-oxidants, could reduce this increase by 56.7%. ROS significantly influenced the expression of the adhesion molecules ICAM-1, VCAM-1 and CD44h on mesothelial cells, but did not influence adhesion molecule expression on Panc-1. The ROS released during the post-operative inflammatory reaction may play an important role in the adhesion of pancreatic tumor cells to the mesothelium-possibly by influencing adhesion molecule expression on mesothelial cells. Therefore ROS can partly be responsible for the enhanced post-operative intra-abdominal tumor recurrence.

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“…Failure of the peritoneum to heal is an important prerequisite of the rupture of any laparotomy incision. Of relevance to patients with advanced malignant disease, it has been demonsstrated that protein deficiency (Mott et al, 1969), uraemia (Mott and Ellis, 1967), vitamin C deficiency (Ellis et al, 1965), and local x-ray therapy (Venables et al, 1967) impaired the fibroblastic proliferation in peritoneal defects and the subsequent healing process. However, cytotoxic drugs administered within the therapeutic range had no overall effect on the rate or quality of the healing of such defects (Gordon et al, 1967).…”

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confidence: 99%