The involvement of platelet activating factor in endotoxin‐induced pulmonary platelet recruitment in the guinea‐pig

Beijer, Lena; Botting, Jack Howard; Crook, Paul; Oyekan, Adebayo; Page, Clive; Rylander, Ragnar

doi:10.1111/j.1476-5381.1987.tb11384.x

Cited by 36 publications

(10 citation statements)

References 27 publications

(24 reference statements)

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“…When conscious guinea pigs were exposed to an aerosol of endotoxin (25-100 pg ml-l), pretreatment with the hetrazepinoic PAF antagonist brotizolam (0.5-1 mgikg i.v.) inhibited the endotoxin-induced pulmonary platelet recruitment in a dose-related manner [133,134]. Thoracic accumulation of "lIndium-labeled platelets was followed for 150 min, being maximal at this time point.…”

mentioning

confidence: 99%

Hetrazepines as antagonists of platelet activating factor

Weber

Heuer

1989

Medicinal Research Reviews

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mentioning

confidence: 99%

Hetrazepines as antagonists of platelet activating factor

Weber

Heuer

1989

Medicinal Research Reviews

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“…PAF itself or combining with LPS can promote platelet activation and recruitment and worsen endotoxin-induced lung injury [29], [30]. Our study has showed that plasma PAF levels were significantly elevated in LPS-challenged F508del mice compared the wildtype mice.…”

Section: Discussionmentioning

confidence: 74%

Lipoxin A4 and Platelet Activating Factor Are Involved in E. coli or LPS-Induced Lung Inflammation in CFTR-Deficient Mice

Yang

et al. 2014

PLoS ONE

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CFTR (cystic fibrosis transmembrane conductance regulator) is expressed by both neutrophils and platelets. Lack of functional CFTR could lead to severe lung infection and inflammation. Here, we found that mutation of CFTR (F508del) or inhibition of CFTR in mice led to more severe thrombocytopenia, alveolar neutrocytosis and bacteriosis, and lower lipoxin A4/MIP-2 (macrophage inhibitory protein-2) or lipoxin A4/neutrophil ratios in the BAL (bronchoalveolar lavage) during acute E. coli pneumonia. In vitro, inhibition of CFTR promotes MIP-2 production in LPS-stimulated neutrophils; however, lipoxin A4 could dose-dependently suppress this effect. In LPS-induced acute lung inflammation, blockade of PSGL-1 (P-selectin glycoprotein ligand-1) or P-selectin, antagonism of PAF by WEB2086, or correction of mutated CFTR trafficking by KM11060 could significantly increase plasma lipoxin A4 levels in F508del relevant to wildtype mice. Concurrently, F508del mice had higher plasma platelet activating factor (PAF) levels and PAF-AH activity compared to wildtype under LPS challenge. Inhibiting hydrolysis of PAF by a specific PAF-AH (PAF-acetylhydrolase) inhibitor, MAFP, could worsen LPS-induced lung inflammation in F508del mice compared to vehicle treated F508del group. Particularly, depletion of platelets in F508del mice could significantly decrease plasma lipoxin A4 and PAF-AH activity and deteriorate LPS-induced lung inflammation compared to control F508del mice. Taken together, lipoxin A4 and PAF are involved in E. coli or LPS-induced lung inflammation in CFTR-deficient mice, suggesting that lipoxin A4 and PAF might be therapeutic targets for ameliorating CFTR-deficiency deteriorated lung inflammation.

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“…A previous study showed that PAF can stimulate mononuclear cells of peripheral blood leading to the release of TNF-α and IL-6 in viral infection [36]. PAF itself or combined with LPS can promote platelet activation and recruitment and worsen endotoxin-induced injury [37,38]. Therefore, PAF and cytokines potentiate each other's effects in vivo to modulate the immune response [39].…”

Section: Discussionmentioning

confidence: 99%

Serum cytokines and clinical features in patients with fever and thrombocytopenia syndrome

Chen

Lin

Fan

et al. 2019

Clinica Chimica Acta

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A B S T R A C TPurpose: To explore the clinical, microbiological and immunological features of patients with fever and thrombocytopenia. Methods: Patients with unexplained fever and thrombocytopenia were enrolled. Viruses were detected using real-time PCR, and bacteria were measured by culturing methods. Serum cytokines, platelet antibody IgG (PA-IgG) and Helicobacter pylori (HP) were detected using ELISA. Results: Pathogens were detected in 74.68% of patients, which included single fungal/viral/bacterial infection and multiple infection. The pathogens could not be unidentified in 25.32% of cases. Cytokines including Interleukin (IL)-6, IL-10, interferon-γ(IFN-γ), platelet activating factor (PAF) and PA-IgG were significantly higher in patients as compared to healthy controls (P < .01 or P < .05). Principal component analyses extracted four groups of parameters that have a strong positive predicting value, revealing that disease status evaluation would be more accurate if we combined the platelet parameters and inflammatory biomarkers. While event-free survival (EFS) that indicates the time of platelet elevated after therapy was the highest in patients with single bacterial or fungal infection, EFS was affected by the levels of cytokines and PA-IgG. Conclusions: Differences in immune function may be the main factors affecting the prognosis of patients with fever and thrombocytopenia, while treatment based on precise etiological diagnosis is important for therapeutic efficacy.

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The involvement of platelet activating factor in endotoxin‐induced pulmonary platelet recruitment in the guinea‐pig

Cited by 36 publications

References 27 publications

Hetrazepines as antagonists of platelet activating factor

Hetrazepines as antagonists of platelet activating factor

Lipoxin A4 and Platelet Activating Factor Are Involved in E. coli or LPS-Induced Lung Inflammation in CFTR-Deficient Mice

Serum cytokines and clinical features in patients with fever and thrombocytopenia syndrome

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