Biochemical factors of neutrophils in exudates from acute surgical wounds have been investigated. However, the fate and functions of neutrophils in the exudates have not been clarified and no prior study had compared exudates in the early and late surgical wound stages. The purpose of this study was to investigate the differing effects of exudates on human neutrophils between the early and late phases of inflammation, and to clarify the factors affecting neutrophil function. Exudates from 30 surgical patients with oral cancer who underwent radical neck dissection were collected on the 1st and 5th day after surgery (EX1, EX5). Neutrophils were obtained from two healthy volunteers. Following incubation of the neutrophils with the exudates we examined superoxide anion production and hAPO-1/Fas expression by the neutrophils, apoptosis of the neutrophils and cytokine concentration in the exudates, and the factors related to neutrophil apoptosis. Superoxide anion production by neutrophils incubated with EX1 was significantly higher than by those incubated with EX5, while hAPO-1/Fas expression by the neutrophils was also significantly greater upon incubation with EX5. The DNA ladder was detected only in human neutrophils incubated with EX5. The level of IL-10 in EX1 was significantly lower than that in EX5. Apoptosis of the neutrophils incubated with EX5 was suppressed by the addition of anti-IL-10 antibody. These results indicate that neutrophils have their functions augmented and apoptosis is inhibited in the early phase of inflammation. Furthermore, IL-10 is involved in apoptosis of neutrophils in the late phase of inflammation.

Tumor blood vessels play an important role in tumor progression and metastasis. Thus, targeting tumor blood vessels is an important strategy for cancer therapy, especially for head and neck cancer patients. Tumor blood vessels generally sprout from pre-existing vessels and have been thought to be genetically normal. However, tumor blood vessels have been shown to differ from their normal counterparts, for example, by changes in morphology. The authors isolated tumor endothelial cells (TECs) from mouse tumor xenografts and have shown that the TECs are abnormal. TECs up-regulate many genes and proliferate more rapidly and migrate more than normal endothelial cells (NECs). Furthermore, TECs were found to be cytogenetically abnormal. We conclude that TECs can acquire cytogenetic abnormalities while in a tumor microenvironment.To develop ideal antiangiogenic therapies, understanding the crosstalk between blood vessels and the tumor microenvironment is important.Here, we provide an overview of the current studies on TEC abnormalities and a discussion about possible mechanisms for how tumor the microenvironment makes TECs abnormal.