[Recent developments in head and neck immunology : A basis for novel therapeutic strategies?] / Jüngste Entwicklungen in der Kopf-Hals-Immunologie : Grundlage für neue Therapiestrategien?

Immunological processes play a key role in the pathogenesis of head and neck pathologies. Besides allergies or infections of the tonsils, the paranasal sinuses, and the ear, initiation, progression, and metastasis of malignant tumors are particularly dependent on the immune system. The recruitment of white blood cells to the site of injury or infection is a critical event in the pathogenesis of these diseases. This article will provide a compact overview about recent developments in this rapidly growing field in otorhinolaryngology which might establish the basis for promising therapeutic strategies for previously insufficiently treatable disorders of the head and neck.

Factor VII-activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation.

Essentials Factor VII-activating protease (FSAP) is a plasma protease involved in vascular processes. Neointima formation was investigated after vascular injury in FSAP-/- mice. The neointimal lesion size and the accumulation of macrophages were increased in FSAP-/- mice. This was due to an increased activity of the chemokine (C-C motif) ligand 2 (CCL2). SUMMARY: Background Factor VII-activating protease (FSAP) is a multifunctional circulating plasma serine protease involved in thrombosis and vascular remodeling processes. The Marburg I single-nucleotide polymorphism (MI-SNP) in the FSAP-coding gene is characterized by low proteolytic activity, and is associated with increased rates of stroke and carotid stenosis in humans. Objectives To determine whether neointima formation after vascular injury is increased in FSAP-/- mice. Methods and Results The neointimal lesion size and the proliferation of vascular smooth muscle cells (VSMCs) were significantly enhanced in FSAP-/- mice as compared with C57BL/6 control mice after wire-induced injury of the femoral artery. Accumulation of leukocytes and macrophages was increased within the lesions of FSAP-/- mice at day 3 and day 14. Quantitative zymography demonstrated enhanced activity of gelatinases/matrix metalloproteinase (MMP)-2 and MMP-9 within the neointimal lesions of FSAP-/- mice, and immunohistochemistry showed particular costaining of MMP-9 with accumulating leukocytes. Using intravital microscopy, we observed that FSAP deficiency promoted the intravascular adherence and the subsequent transmigration of leukocytes in vivo in response to chemokine ligand 2 (CCL2). CCL2 expression was increased in FSAP-/- monocytes but not in the vessel wall. There was no difference in the expression of platelet-derived growth factor (PDGF-BB). Conclusions FSAP deficiency causes an increase in CCL2 expression and CCL2-mediated infiltration of leukocytes into the injured vessel, thereby promoting SMC proliferation and migration by the activation of leukocyte-derived gelatinases. These results provide a possible explanation for the observed association of the loss-of-function MI-SNP with vascular proliferative diseases.

Quantum dots modulate leukocyte adhesion and transmigration depending on their surface modification.

Although different nanosized materials, including quantum dots (QDs), are intended to be used for biomedical applications, their interactions with microvessels and their inflammatory potential are largely unknown. In this in vivo study we report that leukocyte recruitment is modulated in the presence of quantum dots. We found that the surface chemistry of QDs strongly affects their localization in postcapillary venules, their uptake by perivascular macrophages, and their potential to modify steps of leukocyte recruitment.

A comparison of irrigation solutions for microanastomoses.

A comparative study of irrigating solutions that contained various clot-active substances and/or vasodilating substances was done using a crush injury model of the rat's femoral artery. A routine microanastomosis was done with one of seven irrigation solutions employed in the study. The patency rate of lactated Ringer's solution (10%) (the control solution) was compared with solutions of heparin (35%) urokinase (50%), phentolamine (35%) tissue plasminogen activator (tPA) (15%), a combination of urokinase, heparin, and phentolamine (55%), and a combination of tPA, heparin, and phentolamine (42.5%). Statistically significant improvement in patency rates were obtained with heparin (p less than 0.0005), phentolamine (p less than 0.03), urokinase (p less than 0.001), the tPA, heparin and phentolamine combination (p less than 0.001), and the urokinase, heparin, and phentolamine combination (p less than 0.0001). There seems to be a benefit with the addition of either vasoactive agents or clot-active agents to the microvascular irrigating solution during construction of a compromised microanastomosis.

A critical look at capsule contracture in subglandular versus subpectoral mammary augmentation.

A critical comparison of the contracture rate in subglandular versus subpectoral augmentations was done in a personal series (senior author's) of 100 consecutive augmentation patients, 50 with subglandular augmentation and 50 with subpectoral augmentation. The average followup for the series was 27 months. Baker's classification of capsule contracture was utilized. Overall contracture rate in the subglandular group was 58% (29 of 50 patients) while in the subpectoral group it was 22% (11 of 50 patients), p less than 0.0002. Considering only the more severe contractures (Baker III & IV), the subglandular patients had 48% (24/50) while the subpectoral patients had 14% (7/50), p less than 0.0002. Comparing the more severe contractures in individual breasts, the subglandular group had 41% and the subpectoral group had 8%, p less than 0.0001. We conclude that in this personal series of patients, subpectoral placement of the prosthesis has significantly reduced but not eliminated the occurrence of capsule contracture without sacrificing a normal breast appearance.