Kinetics of Endogenous Leukotriene B4 and E4 Production Following Injection of the Chemotactic Peptide FMLP in the Rabbit

Celardo, Antonio; Dell’Elba, Giuseppe; Manarini, Stefano; Evangelista, Virgilio; Gaetano, Giovanni de; Cerletti, Chiara

doi:10.1016/s0090-6980(97)00146-9

Cited by 4 publications

(7 citation statements)

References 21 publications

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“…35–37 Notably, the metabolite N-acetyl-leukotriene E4 (N-acetyl LTE 4 ) had the highest relative abundance in the TDF group, which was markedly and positively linked with a number of pathophysiological characteristics, including inflammation, asthma, and thrombosis. 38…”

Section: Resultsmentioning

confidence: 99%

Lactobacillus rhamnosusGG attenuates tenofovir disoproxil fumarate-induced bone loss in male miceviagut-microbiota-dependent anti-inflammation

Líu

et al. 2019

Therapeutic Advances in Chronic Disease

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Background: Although antiretroviral agents trigger bone loss in human immunodeficiency virus patients, tenofovir disoproxil fumarate (TDF) induces more severe bone damage, such as osteoporosis. While, the mechanisms are unclear, probiotic supplements may be effective against osteoporosis. Methods: C57BL6/J mice were administered with Lactobacillus rhamnosus GG (LGG)+TDF, TDF, and zoledronic acid+TDF, respectively. Bone morphometry and biomechanics were evaluated using microcomputed tomography, bone slicing, and flexural tests. The lymphocyte, proinflammatory cytokines, and intestinal permeability levels were detected using enzyme-linked immunosorbent assays, quantitative real-time polymerase chain reaction, and flow cytometry. The gut microbiota composition and metabolomics were analyzed using 16S recombinant deoxyribonucleic acid pyrosequencing and ultra-performance liquid-chromatography–quadrupole time-of-flight mass spectrometry. Results: LGG administered orally induced marked increases in trabecular bone microarchitecture, cortical bone volume, and biomechanical properties in the LGG+TDF group compared with that in the TDF-only group. Moreover, LGG treatment increased intestinal barrier integrity, expanded regulatory T cells, decreased Th17 cells, and downregulated osteoclastogenesis-related cytokines in the bone marrow, spleen, and gut. Furthermore, LGG reconstructed the gut microbiota and changed the metabolite composition, especially lysophosphatidylcholine levels. However, the amount of N-acetyl-leukotriene E4 was the highest in the TDF-only group. Conclusion: LGG reconstructed the community structure of the gut microbiota, promoted the expression of lysophosphatidylcholines, and improved intestinal integrity to suppress the TDF-induced inflammatory response, which resulted in attenuation of TDF-induced bone loss in mice. LGG probiotics may be a safe and effective strategy to prevent and treat TDF-induced osteoporosis.

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Section: Resultsmentioning

confidence: 99%

Lactobacillus rhamnosusGG attenuates tenofovir disoproxil fumarate-induced bone loss in male miceviagut-microbiota-dependent anti-inflammation

Líu

et al. 2019

Therapeutic Advances in Chronic Disease

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“…For measurement of LTs, blood was incubated with γ‐glutamyl transferase and leucine‐amino peptidase (0.2 U mL −1 each) in order to transform cysteinyl‐LTs to LTE4. The blood was extracted and LTB4 and LTE4 were quantified by HPLC as described [15,16]. Briefly, the extracted residue was reconstituted in the mobile phase (methanol/acetic acid 0.1%, pH 6.5, in deionized water/acetonitrile 60 : 35 : 5 v/v/v) and the analysis performed by isocratic elution at flow rate of 0.5 mL min −1 .…”

Section: Methodsmentioning

confidence: 99%

“…The compounds were detected at 280 nm, with retention times of 23.8 and 27.2 min for LTB4 and LTE4, respectively. The basal levels of LTB4 and LTE4 in the rabbit blood, undetectable by the HPLC‐UV detector, were measured in the HPLC‐collected fractions by specific enzyme immunoassay (EIA) (Cayman Chemicals, Ann Arbor, MI, USA) and corresponded to 0.2 ± 0.1 and 0.3 ± 0.1 nmol L −1 , respectively (mean ± SEM, n = 5) [15,16]. TxB2 was measured in plasma, by radioimmunoassay using a specific antibody [17] kindly provided by Dr G. Ciabattoni, University of Chieti, Chieti, Italy.…”

Section: Methodsmentioning

confidence: 99%

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TxA2-mediated myocardial ischemia as a consequence of an acute lung inflammatory reaction in the rabbit

Evangelista

Dell’Elba

Celardo

et al. 2003

Journal of Thrombosis and Haemostasis

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Summary. Epidemiological studies link acute infection of the respiratory tract to a transient increased risk of acute myocardial infarction. The underlying mechanisms remain unknown. We hypothesized that vasoactive mediators produced by inflammatory cells in the lungs and drained in the coronary circulation may trigger acute myocardial ischemia. To test this hypothesis we used an experimental model in the rabbit. Injection of the bacterial‐derived peptide N‐formyl‐Met‐Leu‐Phe (or N‐formyl‐Methionyl‐Leucyl‐Phenylalanine)(fMLP) in the jugular vein induced massive recruitment of both polymorphonuclear leukocytes (PMN) and platelets in the microcirculation of the lungs, accompanied by rapid and marked increase of leukotriene B4, cysteinyl leukotrienes and thromboxane (Tx) A2 in the aortic blood. In all animals, fMLP evoked ischemic electrocardiographic changes: within the first minute of infusion a profound depression of the ST segment and inversion of the T wave were observed. Mean aortic pressure and heart rate fell to 64.0 ± 6.9 and 83.5 ± 3.1% of the basal levels at 3 and 10 min, respectively. All these alterations were transient. Aspirin, prevented electrocardiographic ischemic changes, reverted bradycardia and hypotension but did not significantly modify either PMN or platelet recruitment nor leukotriene synthesis. Ridogrel, a Tx‐synthase and receptor inhibitor, prevented ECG alterations and bradycardia, but did not prevent and even worsened hypotension; it blocked platelet, but not PMN, sequestration. Pretreatment of animals with intravenous high dose of aspirin prevented ridogrel‐dependent hypotension and platelet inhibition, suggesting that PGI2 contributes to the effects of Tx‐synthase and receptor inhibitor. In hypercholesterolemic rabbits, ECG alterations persisted longer than in normal controls. In summary, our results indicate that acute activation of PMN and platelets in the lungs provokes transient myocardial ischemia, in normal animals that is exacerbated in hypercholesterolemic rabbits. TxA2 appears to be the major mediator of this phenomenon. Moreover the data suggest that a balance between TxA2 and PGI2 plays a pivotal role in platelet activation and recruitment in our model.

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“…Involvement of low-affinity subtype of fMLP receptor in the anti-alopecia effect is suggested, since the dose is far much higher than those for various effects of fMLP ( $ 10 mg per kg) (Bureau et al, 1989;Celardo et al, 1997). Although fMLP receptor subtypes in rat have never been identified, formylpeptide receptor (FPR) and FPR like-1 receptor (FPRL1R) are known as high-and low-affinity receptor subtypes, respectively, in human (Le et al, 2002).…”

Section: Fprl1 Receptor Agonist Peptides Prevent Etoposide-induced Almentioning

confidence: 99%

FPRL1 Receptor Agonist Peptides Prevent Etoposide-Induced Alopecia in Neonatal Rats

Tsuruki

Ito

Takaha

et al. 2004

Journal of Investigative Dermatology

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Kinetics of Endogenous Leukotriene B4 and E4 Production Following Injection of the Chemotactic Peptide FMLP in the Rabbit

Cited by 4 publications

References 21 publications

Lactobacillus rhamnosusGG attenuates tenofovir disoproxil fumarate-induced bone loss in male miceviagut-microbiota-dependent anti-inflammation

Lactobacillus rhamnosusGG attenuates tenofovir disoproxil fumarate-induced bone loss in male miceviagut-microbiota-dependent anti-inflammation

TxA2-mediated myocardial ischemia as a consequence of an acute lung inflammatory reaction in the rabbit

FPRL1 Receptor Agonist Peptides Prevent Etoposide-Induced Alopecia in Neonatal Rats

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