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Titolo:
Inosine monophosphate and aspirin-triggered 15-epi-lipoxin A(4) act in concert to regulate neutrophil trafficking: Additive actions of two new endogenous anti-inflammatory mediators
Autore:
Wada, K; Qiu, FH; Stahl, GL; Serhan, CN;
Indirizzi:
Harvard Univ, Brigham & Womens Hosp, Sch Med,Ctr Expt therapeut & ReperfusInjury, Dept Anesthesiol Perioperat & Pain Med, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 ioperat & Pain Med, Boston, MA 02115 USA
Titolo Testata:
JOURNAL OF HEMATOTHERAPY & STEM CELL RESEARCH
fascicolo: 1, volume: 10, anno: 2001,
pagine: 75 - 79
SICI:
1525-8165(200102)10:1<75:IMAA1A>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-VIVO; STABLE ANALOGS; RECRUITMENT; MECHANISMS; NETWORKS; INJURY; LXA(4); ALPHA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: Serhan, CN Harvard Univ, Brigham & Womens Hosp, Sch Med,Ctr Expt therapeut& ReperfusInjury, Dept Anesthesiol Perioperat & Pain Med, Boston, MA 02115USA Harvard Univ Boston MA USA 02115 ain Med, Boston, MA 02115 USA
Citazione:
K. Wada et al., "Inosine monophosphate and aspirin-triggered 15-epi-lipoxin A(4) act in concert to regulate neutrophil trafficking: Additive actions of two new endogenous anti-inflammatory mediators", J HEMATH ST, 10(1), 2001, pp. 75-79

Abstract

Regulation of neutrophil (PMN) trafficking by soluble mediators is a critical component in the outcome of host defense, inflammation resolution, and neutrophil-mediated tissue injury. Elucidation of the endogenous mediators that protect tissues from excess leukocyte traffic and aberrant PMN activation that can lead to tissue damage and chronic inflammation is of considerable interest, especially the endogenous mechanisms of anti-inflammation. Tothis end, we recently uncovered two new classes of mediators: inosine monophosphate (IMP) and aspirin-triggered 15(R)-epimers of native lipoxin A(4). Here, we examined the combined actions of both classes of compounds in regulating key events in neutrophil trafficking. Neutrophil rolling in mouse microvessels was inhibited by both IMP or 5S,6R,15R-trihydroxy-7,9,13-trans-11-cis-eicosatetraenoic acid (15-epi-LXA(4)) in a concentration- dependent fashion. When combined, IMP (300 nM) and 15-epi-LX (10 nM) demonstrated additive inhibition of neutrophil rolling in microvessels. IMP and 15-epi-LX also significantly inhibited tumor necrosis factor-alpha (TNF-alpha)-inducedneutrophil accumulation into the mouse air pouch in a dose-dependent manner. Again, the combination of low dose IMP (10 mug) and LX analog (5 mug) gave additive inhibition of neutrophil accumulation in this model. These results demonstrate the inhibition of neutrophil trafficking in two separate models by two different classes of small endogenous molecules. The additive inhibition by IMP and aspirin-triggered LX may represent key pathways that protect and resolve inflammatory responses that could be harnessed for treatment.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 00:20:39