PAF increases phagocytic capacity and superoxide anion production in equine alveolar macrophages and blood neutrophils

Muehlmann, Luís Alexandre; Michelotto, Pedro Vicente; Nunes, Everson Araújo; Grando, Fernanda Cristine Ceccon; Silva, Fabiana Tieme da; Nishiyama, Anita

doi:10.1016/j.rvsc.2011.07.008

Cited by 12 publications

(11 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have highlighted the necessity of PAF receptor activation in deactivation of ultraviolet B (UVB) induced suppression of hypersensitivity responses [ 23 ]. In addition, PAF administration to equine alveolar macrophages increased phagocytic capacity and superoxide anion production [ 24 ]. Moreover, during immunological defence, PAF can play an immunomodulatory role including monocyte or macrophage degranulation, cytokine release, phagocytosis, and cell adhesion [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Macrophage Derived Platelet Activating Factor Implicated in the Resolution Phase of Gouty Inflammation

Yagnik

2014

International Journal of Inflammation

View full text Add to dashboard Cite

Human blood derived in vitro differentiated monocytes or macrophages are a population of cells which have been investigated over the years to determine the role these cells play in the resolution phase of gout. Macrophages are able to phagocytose monosodium urate monohydrate (MSU) crystals without releasing inflammatory factors. This study analysed macrophage platelet activating factor secretion and its possible role in the pathway of gout resolution. Analysis of sunatants from in vitro differentiated macrophages stimulated with MSU crystals revealed the secretion of platelet activating factor (PAF) 1.54 ± 0.10 mean ± SEM; ng/mL per 106 cells. This secretion was absent in immature monocytes treated similarly. When these monocytes were pretreated with recombinant human PAF-acetylhydrolase (rhuPAF-AH) and MSU crystals resulted in TNFα suppression. Addition of WEB2086, a platelet activating factor (PAF) antagonist, to differentiated macrophages with MSU crystals unmasked TNFα secretion 0.7 ± 0.06 mean ± SEM; ng/mL per 106 cells. This study identifies a role for PAF and the PAF receptor antagonist in the pathway by which macrophages ingest MSU crystals and resolve the concomitant inflammation.

show abstract

Section: Introductionmentioning

confidence: 99%

Macrophage Derived Platelet Activating Factor Implicated in the Resolution Phase of Gouty Inflammation

Yagnik

2014

International Journal of Inflammation

View full text Add to dashboard Cite

show abstract

“…PAF C-16 can activate monocytes/macrophages by binding to PAFR (Simon et al, 1994) and stimulate the production of inflammatory mediators such as TNF-α, IL-1α and β, reactive oxygen intermediate (ROI) and reactive nitrogen intermediate (RNI) species (Hartung et al, 1983;Bonavida et al, 1989;Poubelle et al, 1991;Muehlmann et al, 2012), and thus may play a protective role during infection. We have recently shown that PAF C-16 and its analogs have direct inhibitory effect on the growth of mycobacteria (Riaz et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Dissecting the Mechanism of Intracellular Mycobacterium smegmatis Growth Inhibition by Platelet Activating Factor C-16

et al. 2020

View full text Add to dashboard Cite

Mycobacterium tuberculosis (M.tb) infection results in approximately 1.3 million human deaths each year. M.tb resides primarily inside macrophages, and maintains persistent infection. In response to infection and inflammation, platelet activating factor C-16 (PAF C-16), a phospholipid compound, is released by various cells including neutophils and monocytes. We have recently shown that PAF C-16 can directly inhibit the growth of two representative non-pathogenic mycobacteria, Mycobacterium bovis BCG and Mycobacterium smegmatis (M. smegmatis), by damaging the bacterial cell membrane. Here, we have examined the effect of PAF C-16 on M. smegmatis residing within macrophages, and identified mechanisms involved in their growth inhibitory function. Our results demonstrated that exogenous PAF C-16 inhibited the growth of M. smegmatis inside phagocytic cells of monocytic cell line, THP-1; this effect was partially blocked by PAF receptor antagonists, suggesting the involvement of PAF receptor-mediated signaling pathways. Arachidonic acid, a downstream metabolite of PAF C-16 signaling pathway, directly inhibited the growth of M. smegmatis in vitro. Moreover, the inhibition of phospholipase C and phospholipase A 2 activities, involved in PAF C-16 signaling pathway, increased survival of intracellular M. smegmatis. Interestingly, we also observed that inhibition of inducible nitric oxide synthase (iNOS) enzyme and antibody-mediated neutralization of TNF-α partially mitigated the intracellular growth inhibitory effect of PAF C-16. Use of a number of PAF C-16 structural analogs, including Lyso-PAF, 2-O-methyl PAF, PAF C-18 and Hexanolamino PAF, revealed that the presence of acetyl group (CH 3 CO) at sn-2 position of the glycerol backbone of PAF is important for the intracellular growth inhibition activity against M. smegmatis. Taken together, these results suggest that exogenous PAF C-16 treatment inhibits intracellular M. smegmatis growth, at least partially, in a nitric oxide and TNF-α dependent manner.

show abstract

“…Another similarity between COVID-19 and PAF is that they are both connected to Kawasaki-like disease in children [25]. PAF has been also found to increase phagocytic capacity in equine alveolar macrophages [26] and its levels are increased in acute pulmonary disease [27], pulmonary hypertension [28] and sepsis [29].…”

Section: Introductionmentioning

confidence: 93%

Micronutrients, Non-Nutrients and Mediterranean Diet: A Potential Protective Role Against COVID-19 through Modulation of PAF Actions and Metabolism

Detopoulou¹,

Demopoulos²,

Antonopoulou³

2020

Preprint

View full text Add to dashboard Cite

The new coronavirus disease 2019 (COVID-19) pandemic is an emerging situation with high rates of morbidity and mortality, in the pathophysiology of which inflammation and thrombosis are implicated. The disease is directly connected to the nutritional status of patients and a well-balanced diet is recommended by official sources. Recently, the role of platelet activating factor (PAF) was suggested in the pathogenesis of COVID-19. In the present review several micronutrients (vitamin A, vitamin C, vitamin E, vitamin D, selenium, omega-3 fatty acids, minerals), phytonutrients and Mediterranean diet compounds (olive oil, fish, honey, plant foods) with potential anti-COVID activity are presented. We further underline that the well-known anti-inflammatory and anti-thrombotic actions of the investigated nutrients and/ or holistic dietary schemes, such as the Mediterranean diet, are also mediated through PAF. In conclusion, although there is no single food to prevent coronavirus, the aim is to follow a healthy diet containing PAF inhibitors in order to target both inflammation and thrombosis and try to avoid or/and reduce the deleterious effects of the COVID-19 epidemic.

show abstract

PAF increases phagocytic capacity and superoxide anion production in equine alveolar macrophages and blood neutrophils

Cited by 12 publications

References 17 publications

Macrophage Derived Platelet Activating Factor Implicated in the Resolution Phase of Gouty Inflammation

Macrophage Derived Platelet Activating Factor Implicated in the Resolution Phase of Gouty Inflammation

Dissecting the Mechanism of Intracellular Mycobacterium smegmatis Growth Inhibition by Platelet Activating Factor C-16

Micronutrients, Non-Nutrients and Mediterranean Diet: A Potential Protective Role Against COVID-19 through Modulation of PAF Actions and Metabolism

Contact Info

Product

Resources

About