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At least 163 records · Page 9Linked to original sources
PubMed2000

[Evaluation of various antagonists of CGRP, a neuromediator implicated in the inflammatory mechanisms of nasal mucosa].

INTRODUCTION: This article presents a review of the literature addressing the role of different neuropeptides involved in neurogenic inflammation at the level of the nasal mucosa. DISCUSSION: Calcitonin gene-related peptide (CGRP) is a vasodilator peptide located in sensory C fibres. It plays an important role during neurogenic inflammation by controlling both tonicity and permeability of different vascular beds. Its release can be produced by capsaicin, bradykinin (BK) or histamine. In turn, CGRP appears to play an important role in modulating histamine-induced vascular responses. Different CGRP analogues are used to investigate the mechanisms of neurogenic inflammation. Some of them antagonise exogenous substances such as CGRP, capsaicin or bradykinin, attenuating the vasodilatation induced both in intensity and duration. They can contribute to the study of CGRP and its physiological involvement in neurogenic inflammation. Moreover, they may have therapeutic applications in the treatment of patients with nasal hyperreactivity.

Bradykinin↗
PubMedDate not supplied

[Autoimmune and inflammatory mechanisms of atherosclerosis development].

This paper contains the results of researches from the N.N.Anichkov laboratory of atherogenesis, the analysis of initial stages of,atherosclerosis made from the position of immune inflammation in the arterial wall. The leading role of mLDL, which are the main cholesterol carrier, in the development of immune inflammation in situ is shown.

Antigens↗
PubMed1990

[Inflammatory mechanisms in corneal ulceration].

A retrospective histologic and analytic study of 355 corneal ulcer specimens obtained from therapeutic keratoplasties indicated that, during active corneal dissolution, the polymorphonuclear white cells predominated at the site of stromal degradation. The presence of PMN cells in corneal tissue was harmful by releasing degradative lysosomal enzymes, thus playing an important role in the development of the corneal ulceration.

Cornea↗
PubMed1993

[Inflammatory mechanisms of atherosclerosis: pathogenic and etiologic inferences].

Inflammation is the reaction of a vascularized living tissue to local injury. At its chronic stage, inflammation displays 4 characteristic features that are all to be found in atherosclerotic plaques: lympho-monocytic infiltration; sclerosis; cellular proliferation; vascular proliferation. This view sheds new light and opens new avenues for research on atherosclerosis. That is true for pathogenesis which progressively integrates the mass of information that has accumulated about the cellular and molecular mechanisms of inflammation. That is also true fort the aetiology of atherosclerosis where the causal enigmas are approached with a more open mind, much wider than the traditional concepts of degeneration and overloading that have prevailed for so long. In the near future, some promising therapeutic clues should derive from this renewed approach of atherosclerosis.

Arteriosclerosis↗
PubMed2003

Inflammation and thrombosis.

Systemic inflammation is a potent prothrombotic stimulus. Inflammatory mechanisms upregulate procoagulant factors, downregulate natural anticoagulants and inhibit fibrinolytic activity. In addition to modulating plasma coagulation mechanisms, inflammatory mediators appear to increase platelet reactivity. In vivo, however, natural anticoagulants not only prevent thrombosis, but they also dampen inflammatory activity. Some insights into the evolution and linkages between inflammatory mechanisms and the coagulation/anticoagulation mechanisms have become evident from recent structural studies. This review will summarize the interactions between inflammation and coagulation.

Animals↗
PubMed1991

Immunoglobulin A: interaction with complement, phagocytic cells and endothelial cells.

Deposits of IgA together with complement (C) in different organs support the hypothesis that IgA can trigger inflammatory mechanisms. Some inflammatory mechanisms may be caused by activation of C and phagocytic cells. Therefore, it is essential to understand the interaction of IgA with C and phagocytic cells. Studies will be described demonstrating that polymeric human serum IgA is able to activate the alternative pathway of C and that the activating principle is located in the intact F(ab')2 portion of the molecule. Activation of C is dependent on the molecular composition of IgA, as derived from results obtained with rat monoclonal IgA antibodies. Furthermore, it is demonstrated that polymeric IgA (pIgA) and dimeric IgA (dIgA) are potent activators of C in a homologous rat model, whereas monomeric IgA (mIgA) has a very poor C-activating potential. The interaction of IgA with phagocytic cells induces phagocytosis and release of H2O2 by granulocytes, which may contribute to tissue damage. Little is known about the clearance mechanism of IgA. It is shown in this report that Kupffer cells and C play an important role in the clearance of IgA immune complexes (IC). Clearance of large-sized IgA IC occurs via different receptors present on Kupffer cells. Finally, a new aspect will be described: the interaction of IgA with endothelial cells. Rat liver endothelial cells are able to eliminate IgA IC from the circulation via specific receptors when no Kupffer cells are present. These observations may contribute to our knowledge on diseases such as IgA nephropathy and Henoch-Schönlein purpura. The studies summarized and presented here illustrate the inflammatory potential of IgA.

Animals↗
PubMed1996

[The acute inflammatory response. Mechanisms and therapeutic possibilities].

The paper reviews the events and mechanisms of the inflammatory response and the possibilities of modulation. The functions of several important inflammatory mediators and possible therapy related to these are summarized. The paper further describes the major events of the inflammatory response, primary and secondary mediators, the cellular origin of the mediators and possible regulatory mechanisms of the inflammatory response. The causes of inflammatory dysregulation are not clear in most cases and control of the inflammatory response will be improved, when the timing of and the relations between the mediators are clarified. Management of the dysregulated or autonomous inflammatory response may go beyond inhibition of mediators and include active support of depleted mediators. Interventions should start early in the acute process and be multimodal. Treatment of pain related to inflammatory conditions may be improved by more specific interventions at the level of the nociceptors.

Acute Disease↗