1,721,363 research outputs found
Annexin 1 and neutrophil apoptosis
No full textANXA1 (annexin 1), a member of the 'annexin' family of calcium- and phospholipid-binding proteins, was originally identified as an endogenous mediator of the anti-inflammatory actions of glucocorticoids. However, this protein exerts multiple inhibitory effects on the host inflammatory response, including a preferential regulation of the adhesion step of blood-borne neutrophil within the microenvironment of an inflamed vasculature. It is now emerging that ANXA1 is endowed with other roles, since the protein is abundant in inflammatory exudates as it is produced and released by the extravasated neutrophil. In the present paper, we review the novel proapoptotic effect of ANXA1 and discuss its potential with respect to the pathophysiology of inflammation and leucocyte recruitment
The melanocortin peptide HP228 displays protective effects in acute models of inflammation and organ damage
No full textAnti-inflammatory role of the murine formyl-peptide receptor 2: ligand-specific effects on leukocyte responses and experimental inflammation.Dufton N, Hannon R, Brancaleone V, Dalli J, Patel HB, Gray M, D'Acquisto F, Buckingham JC, Perretti M, Flower RJ.
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Activation of the annexin A1 pathway underlies the protective effects exerted by estrogen in polymorphonuclear leukocytes
No full textFormyl-peptide receptor is not involved in the protection afforded by annexin 1 in murine acute myocardial infarct
No full textGenetic Ablation Of The Fpr1 Gene Prevents Emphysema In Mice Chronically Exposed To Cigarette Smoke
No full textINTRODUCTION: Cigarette smoke (CS) is the main causative factor of COPD in man. Morphological features of COPD including emphysema
and chronic bronchitis associated with mucus hypersecretion can be induced in mice by chronic CS exposure. The peptide fMLP
(N-formyl-L-methionyl-L-leucyl-L-phenylalanine) is an active component of cigarette smoke (CS). fMLP interacts on the neutrophil and
macrophage membranes with a high-affinity receptor subtype (FPR) and with a low-affinity subtype FPRL1 promoting a chemotactic
response, superoxide anion production and degranulation. fMLP-receptors are found to be increased in the lavage fluids from cigarette
smokers and subjects with COPD. To date, the role of FPRs in COPD remains poorly understood. We examined whether FPR contributes to
lung damage induced by CS, by comparing the response of FPR knockout (Fpr1-/-) mice with that of wild-type (WT) C57 Bl/6 mice.
METHODS and RESULTS: After chronic exposure to CS (3 cigarettes/day, 5 days/week for 7 months) WT mice showed significant foci of
emphysema disseminated throughout the lung parenchyma with a significant increase of the mean linear intercept (+ 21 %) and a
decrease of the internal surface area (– 13 %). Air-control groups and smoke exposed Fpr1-/- mice showed no areas of emphysema.
Acute smoke exposure (5 cigarettes/day, for 3 days) caused in WT mice a 3,7 fold and a 1,3 fold increase in BALF neutrophils and
macrophages, respectively. Fpr1 ablation in mice prevented after CS exposure the increase of neutrophils and macrophages by 73 and
42%, respectively. CONCLUSIONS: This study supports a role for FPR signalling in the development of CS-induced emphysema
Annexin A1 interaction with the FPR2/ALX receptor: identification of distinct domains and downstream associated signaling.
No full textGoing Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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