scholarly journals Lack of Platelet-Activating Factor Receptor Attenuates Experimental Food Allergy but Not Its Metabolic Alterations regarding Adipokine Levels

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Nathália Vieira Batista ◽  
Roberta Cristelli Fonseca ◽  
Denise Perez ◽  
Rafaela Vaz Sousa Pereira ◽  
Juliana de Lima Alves ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Food Allergy ◽  
Inflammatory Process ◽  
Platelet Activating Factor ◽  
Oral Challenge ◽  
Tissue Loss ◽  
Lack Of Information ◽  
Paf Receptor ◽  
Rolling Leukocytes

Platelet-activating factor (PAF) is known to be an important mediator of anaphylaxis. However, there is a lack of information in the literature about the role of PAF in food allergy. The aim of this work was to elucidate the participation of PAF during food allergy development and the consequent adipose tissue inflammation along with its alterations. Our data demonstrated that, both before oral challenge and after 7 days receiving ovalbumin (OVA) diet, OVA-sensitized mice lacking the PAF receptor (PAFR) showed a decreased level of anti-OVA IgE associated with attenuated allergic markers in comparison to wild type (WT) mice. Moreover, there was less body weight and adipose tissue loss in PAFR-deficient mice. However, some features of inflamed adipose tissue presented by sensitized PAFR-deficient and WT mice after oral challenge were similar, such as a higher rate of rolling leukocytes in this tissue and lower circulating levels of adipokines (resistin and adiponectin) in comparison to nonsensitized mice. Therefore, PAF signaling through PAFR is important for the allergic response to OVA but not for the adipokine alterations caused by this inflammatory process. Our work clarifies some effects of PAF during food allergy along with its role on the metabolic consequences of this inflammatory process.

scholarly journals Interleukin-1-induced leukocyte extravasation across rat mesenteric microvessels is mediated by platelet-activating factor

Blood ◽  
1995 ◽  
Vol 85 (9) ◽  
pp. 2553-2558 ◽  
Author(s):  
S Nourshargh ◽  
SW Larkin ◽  
A Das ◽  
TJ Williams
Keyword(s):  
Vessel Wall ◽  
Interleukin 1 ◽  
Platelet Activating Factor ◽  
Micron Diameter ◽  
Paf Receptor ◽  
Leukocyte Extravasation ◽  
Mesenteric Microvessels ◽  
Adherent Leukocytes

Although our understanding of the molecular interactions that mediate the adhesion of leukocytes to venular endothelial cells has greatly expanded, very little is known about the mechanisms that mediate the passage of leukocytes across the vessel wall in vivo. The aim of the present study was to investigate the role of endogenously formed platelet-activating factor (PAF) in the process of leukocyte extravasation induced by interleukin-1 (IL-1). To determine at which stage of emigration PAF was involved, we studied the behavior of leukocytes within rat mesenteric microvessels by intravital microscopy. Rats were injected intraperitoneally with saline, recombinant rat IL-1 beta (IL-1 beta), or the peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) 4 hours before the exteriorization of the mesenteric tissue. In animals treated with IL-1 beta there was a significant increase in the number of rolling and adherent leukocytes within venules (20- to 40-micron diameter) and in the number of extravasated leukocytes in the tissue. Pretreatment of rats with the PAF receptor antagonist UK-74,505 had no effect on the leukocyte responses of rolling and adhesion, but significantly inhibited the migration of the leukocytes across the vessel wall induced by IL-1 beta (76% inhibition). A structurally unrelated PAF antagonist, WEB-2170, produced the same effect (64% inhibition). However, in contrast, UK-74,505 had no effect on the leukocyte extravasation induced by FMLP, indicating selectivity for the response elicited by certain mediators. These results provide the first line of direct evidence for the involvement of endogenously formed PAF in the process of leukocyte extravasation induced by IL-1 in vivo.

Molecular mechanisms involved in superoxide-induced leukocyte-endothelial cell interactions in vivo

1994 ◽  
Vol 266 (2) ◽  
pp. H637-H642 ◽  
Author(s):  
J. P. Gaboury ◽  
D. C. Anderson ◽  
P. Kubes
Keyword(s):  
Molecular Mechanisms ◽  
Leukocyte Adhesion ◽  
Platelet Activating Factor ◽  
Leukocyte Rolling ◽  
Rolling Velocity ◽  
Paf Receptor ◽  
Rolling Leukocytes ◽  
Adherent Leukocytes ◽  
Web 2086

Intravital microscopy was used to monitor leukocyte adherence, flux, rolling velocity, and number of rolling leukocytes (flux/velocity) in venules 25–40 microns in diameter. The superoxide-generating system, hypoxanthine and xanthine oxidase (HX/XO), was infused into the mesenteric circulation in untreated animals or in animals pretreated with either catalase (a hydrogen peroxide scavenger), WEB-2086 [a platelet-activating factor (PAF) receptor antagonist], or monoclonal antibodies directed against adhesion molecules CD18 (CL26) or P-selectin (PB1.3). HX/XO infusion caused a decrease in leukocyte rolling velocity and an increase in the number of rolling and adherent leukocytes. WEB-2086 prevented the increase in leukocyte adhesion and markedly increased leukocyte rolling velocity. PB1.3 abolished the HX/XO-associated rise in the flux of rolling leukocytes and proportionally decreased the number of adherent leukocytes. CL26 abolished HX/XO-induced leukocyte adhesion and also reduced the number of rolling leukocytes. In conclusion, P-selectin mediates the increased leukocyte flux induced by superoxide, whereas PAF and CD18 modulate leukocyte adhesion. PAF also reduces leukocyte rolling velocity, possibly as a result of CD18, but not P-selectin.

Insight into the role of dermal white adipose tissue loss in dermal fibrosis

2021 ◽  
Author(s):  
Si‐Yu Liu ◽  
Jun‐Jie Wu ◽  
Zhong‐Hua Chen ◽  
Ming‐Li Zou ◽  
Ying‐Ying Teng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Tissue Loss ◽  
Dermal Fibrosis ◽  
Insight Into

PAF receptor antagonist modulates neutrophil responses with thermal injury in vivo

2001 ◽  
Vol 281 (4) ◽  
pp. C1310-C1317 ◽  
Author(s):  
Nadeem Fazal ◽  
Walid M. Al-Ghoul ◽  
Mashkoor A. Choudhry ◽  
Mohammed M. Sayeed
Keyword(s):  
Receptor Antagonist ◽  
Burn Injury ◽  
Total Body Surface Area ◽  
Platelet Activating Factor ◽  
Skin Thickness ◽  
Reactive Oxygen Intermediate ◽  
Paf Receptor ◽  
Paf Receptor Antagonist

The role of platelet-activating factor (PAF) in Ca2+signaling and Ca2+-related enhancement of reactive oxygen intermediate (ROI) generation in neutrophils of burn-injured rats was ascertained by evaluating the effect of treatment of the rats with a PAF receptor antagonist. The treatment of rats with the antagonist also allowed us to evaluate the role of PAF in the priming of neutrophil ROI response with burn in vivo. A full skin thickness burn injury was produced in anesthetized rats by exposing 30% of total body surface area to 98°C water for 10 s. Sham and burn rats were killed 1 day later, and their blood was collected to obtain neutrophils. Fluorescence-activated cell sorter analysis was used to quantify ROI production by the neutrophils. Cytosolic-free Ca2+concentration ([Ca2+]i) imaging technique was employed to measure neutrophil [Ca2+]iin individual cells and microfluorometry for the assessment of [Ca2+]iresponses in suspensions of neutrophils. There was an overt enhancement of ROI generation by burn rat neutrophils. ROI release was accompanied by a marked elevation of [Ca2+]isignaling. The treatment of rats with PAF receptor antagonist before burn prevented the upregulation of both [Ca2+]iand ROI generation in neutrophils. These studies indicate that enhanced ROI production in neutrophils in the early stages after burn injury results from a PAF-mediated priming of the [Ca2+]isignaling pathways in vivo.

scholarly journals The Role of Adipose Tissue and Adipokines in Obesity-Related Inflammatory Diseases

2010 ◽  
Vol 2010 ◽  
pp. 1-19 ◽  
Author(s):  
Carmela Rita Balistreri ◽  
Calogero Caruso ◽  
Giuseppina Candore
Keyword(s):  
Adipose Tissue ◽  
Immune Cells ◽  
Inflammatory Markers ◽  
Active Sites ◽  
Inflammatory Process ◽  
Inflammatory Diseases ◽  
Biological Effects ◽  
Rich Condition ◽  
Circulating Levels

Obesity is an energy-rich condition associated with overnutrition, which impairs systemic metabolic homeostasis and elicits stress. It also activates an inflammatory process in metabolically active sites, such as white adipose tissue, liver, and immune cells. As consequence, increased circulating levels of proinflammatory cytokines, hormone-like molecules, and other inflammatory markers are induced. This determines a chronic active inflammatory condition, associated with the development of the obesity-related inflammatory diseases. This paper describes the role of adipose tissue and the biological effects of many adipokines in these diseases.

scholarly journals Platelet-activating factor and human thyroid cancer

2005 ◽  
Vol 153 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Yves Denizot ◽  
Thierry Chianéa ◽  
François Labrousse ◽  
Véronique Truffinet ◽  
Manuela Delage ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Gland ◽  
Thyroid Carcinoma ◽  
Platelet Activating Factor ◽  
Human Thyroid ◽  
Papillary Thyroid ◽  
Benign Adenoma ◽  
Paf Receptor

Objective: Platelet-activating factor (PAF) is a pro-inflammatory and angiogenic lipid mediator involved in several types of cancer in humans. The levels of PAF, lyso-PAF (the PAF precursor), phospholipase A2 activity (PLA2, the enzymatic activity implicated in lyso-PAF formation) and acetylhydrolase activity (AHA, the PAF-degrading enzyme) were investigated in various diseased thyroid tissues. Subjects: Control and diseased tissue of patients with a hyperplastic goitre (n = 14), a benign adenoma (n = 12) and a papillary thyroid carcinoma (n = 15) were investigated. Results: PAF receptor transcripts were found in the human thyroid tissue. PAF, lyso-PAF, PLA2 and AHA were present in control thyroid tissues, their levels being significantly correlated with each other, suggesting tiny regulations of the PAF metabolic pathways inside the thyroid gland. PAF, lyso-PAF, PLA2 and AHA levels remained unchanged in diseased tissues of patients with a hyperplastic goitre, a benign adenoma and a papillary thyroid carcinoma. No difference was found between PAF, lyso-PAF, PLA2 and AHA levels with respect to the TNM tumour status and the histological sub-type of papillary thyroid carcinoma. No correlation was found between tissue PAF levels and those of vascular endothelial growth factor and basic fibroblast growth factor, two angiogenic growth factors involved in thyroid cancer and that mediate their effect through PAF release in breast and colorectal cancer. Conclusion: PAF, PAF receptor transcripts and the enzymatic activities implicated in PAF production and degradation are present in the thyroid gland. While the physiological role of PAF is presently unknown in thyroid physiology, this study highlights no evidence for a potentially important role of PAF during human thyroid cancer, a result that markedly differs from breast and colorectal ones.

scholarly journals Effect of platelet-activating factor on the growth of human erythroid and myeloid CD34+progenitors

1998 ◽  
Vol 7 (2) ◽  
pp. 99-103 ◽  
Author(s):  
F. Dupuis ◽  
N. Gachard ◽  
A. Allegraud ◽  
C. Dulery ◽  
V. Praloran ◽  
...  
Keyword(s):  
Liquid Medium ◽  
Conditioned Medium ◽  
Fetal Calf Serum ◽  
Calf Serum ◽  
Platelet Activating Factor ◽  
Biologically Active ◽  
Solid Culture ◽  
Paf Receptor ◽  
Semi Solid

We have assessed the effect of platelet-activating factor (PAF), a biologically active phospholipid present in the human marrow, on the growth of human marrow and blood CD34+progenitors. While the metabolization rate of PAF by CD34+cells is low (weak acetylhydrolase and acylation processes) it is readily catabolized by the acetylhydrolase activity present in the growth medium (10% fetal calf serum + 10% 5637-conditioned medium). Treatment of marrow CD34+cells with the non-metabolizable PAF agonist C-PAF (1 nM to 100 nM) immediately before semi-solid culture significantly(p<0.01)decreased the number of BFU-E but not of CFU-GM colonies. Treatment of marrow or blood CD34+cells with C-PAF (10-100 nM) for 3 days in liquid medium before semi-solid culture significantly(p<0.01)decreased the number of BFUE and CFU-GM colonies. Treatment of blood CD34+cells with the two PAF receptor antagonists CV 3988 and BN 52021 (1 μ M) had no significant effect on the number of BFU-E and CFU-GM colonies suggesting no role of endogenous PAF in these processes. These results show that exogenous PAF downregulates human erythropoiesis and myelopoiesis, a result that might be of importance during inflammatory states.

scholarly journals Platelets trigger perivascular mast cell degranulation to cause inflammatory responses and tissue injury

2020 ◽  
Vol 6 (12) ◽  
pp. eaay6314 ◽  
Author(s):  
Jörn Karhausen ◽  
Hae Woong Choi ◽  
Krishna Rao Maddipati ◽  
Joseph P. Mathew ◽  
Qing Ma ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Platelet Activation ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Platelet Activating Factor ◽  
Organ Injury ◽  
Paf Receptor ◽  
Platelet Aggregates ◽  
Systemic Responses

Platelet responses have been associated with end-organ injury and mortality following complex insults such as cardiac surgery, but how platelets contribute to these pathologies remains unclear. Our studies originated from the observation of microvascular platelet retention in a rat cardiac surgery model. Ensuing work supported the proximity of platelet aggregates with perivascular mast cells (MCs) and demonstrated that platelet activation triggered systemic MC activation. We then identified platelet activating factor (PAF) as the platelet-derived mediator stimulating MCs and, using chimeric animals with platelets defective in PAF generation or MCs lacking PAF receptor, defined the role of this platelet-MC interaction for vascular leakage, shock, and tissue inflammation. In application of these findings, we demonstrated that inhibition of platelet activation in modeled cardiac surgery blunted MC-dependent inflammation and tissue injury. Together, our work identifies a previously undefined mechanism of inflammatory augmentation, in which platelets trigger local and systemic responses through activation of perivascular MCs.

Hypoxia induces endothelial cells to increase their adherence for neutrophils: role of PAF

1992 ◽  
Vol 263 (3) ◽  
pp. H956-H962 ◽  
Author(s):  
K. A. Milhoan ◽  
T. A. Lane ◽  
C. M. Bloor
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Myocardial Ischemia ◽  
Platelet Activating Factor ◽  
Conditioned Media ◽  
Polymorphonuclear Neutrophils ◽  
Cell Monolayers ◽  
Paf Receptor ◽  
Paf Receptor Antagonist

We investigated the interactions of polymorphonuclear neutrophils (PMN) and endothelial cells in myocardial ischemia using a hypoxia model. We exposed porcine aortic (PAEC) and porcine coronary microvessel (PCMEC) endothelial cells to 2% O2 for 2 h (PO2 = 53 mmHg) and measured the adherence of unstimulated neutrophils (PMN) to both control and hypoxia-conditioned endothelial cell monolayers. Hypoxia conditioning increased PMN adherence to PAEC and PCMEC by 51 and 101%, respectively, above control levels. The increase in PMN adhesion to PAEC was associated with a threefold increase in endothelial cell-associated platelet-activating factor (PAF) compared with control PAEC. The conditioned media from PAEC exposed to hypoxia also contained sixfold more PAF than control conditioned media, and it activated PMN to become adherent to untreated PAEC. The hypoxia-induced PAEC adhesion response was inhibited by preincubating PMN with the specific PAF receptor antagonist, L-659,989. We conclude that PAF is produced by cultured endothelial cells in response to hypoxia and that PAF generation is chiefly responsible for the increased adherence properties of hypoxia-conditioned endothelial cells. This response may play a major role in regulating PMN margination during myocardial ischemia.

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