Jet exhaust particles alter human dendritic cell maturation
ABSTRACT Among combustion-derived air pollutants, little is known about jet kerosene characteristics and effects.
Particles yielded by experimental kerosene combustion in a jet engine were characterized with electron microscopy and X-ray energy dispersive spectroscopy. Immature human monocyte-derived dendritic cells were exposed for 18 h to 10, 25 or 100 μg/mL jet exhaust particles and/or Escherichia coli-derived endotoxin. Antigen-presenting and costimulation molecules (HLA DR, CD40, CD80, CD86, CD11c), tumor necrosis factor-α and interleukin-10 production were measured.
The primary particles of jet exhaust are spherical (9.9 nm), carbonaceous and exert an adjuvant effect on human monocyte-derived dendritic cell maturation in vitro. Concomitant particle and endotoxin stimulation induced a high cytokine production with low antigen-presenting molecules; particle contact prior to endotoxin contact led to an opposite phenotype. Finally, low cytokine production and high costimulation molecules were present when particle adjunction followed endotoxin contact.
Jet exhaust particles act as adjuvants to endotoxin-induced dendritic cell maturation, suggesting possible implications for human health and a role for the time pattern of infectious and pollutant interplay.
- SourceAvailable from: Joana Vitte
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- "Les mastocytes participent à l'immunité innée et adaptative en tant que cellules sentinelles aux fonctions variées : défense antimicrobienne et antiparasitaire, présentation d'antigène, induction et régulation des réponses lymphocytaires T    . La plupart de ces activités du mastocyte sont de description très récente , expliquant son entrée tardive dans le club des phagocytes mononucléés   . Actuellement, le rôle le plus important du mastocyte en pratique médicale reste la phase effectrice de la réponse allergique : dégranulation massive et brutale avec libération de médiateurs préformés vasoactifs, proinflammatoires et nociceptifs, induite par l'interaction des immunoglobulines (Ig) E, portées par les récepteurs membranaires RFceI (récepteurs de forte affinité pour le fragment constant des IgE), avec l'allergène multivalent correspondant . "
ABSTRACT: Mast cells are immune cells of an hematopoietic origin which mature in peripheral tissues. While they participate in both innate and adoptive immunity as sentinel cells, their major role in medical practice is actually to be found in the effector stage of the allergic response:massive and brutal degranulation leads to the liberation of pre-formed vasoactive, pro-inflammatory and harmful mediators, this event being induced by the interaction of the immunoglobulin E present on RFcɛI membrane receptors with the corresponding multivalent allergen. The preformed mediators of the immediate reaction are stored in the large secretory granules of mast cells. Formation of these granules requires the cooperation of endocytic and secretory pathways, with the biochemical feature of a significant production of proteoglycans which stabilize and protect the granular contents. Degranulatioin induced via IgE and RFcɛI involves translocation of the cytoplasmic granules toward the plasma membrane followed by exocytosis. The general mechanism of vesicular fusion appears to depend on a unique molecular schema: SNARE proteins present on the membranes undergoing fusion form a molecular bridge which keeps the two membranes contiguous; Sec1/Munc18 proteins (SM) control the formation of the SNARE complex and cooperate with it to induce membrane fusion. Entrance of synaptotagmin, a generally vesicular protein which functions as a calcium detector, into the SNARE complex allows the regulation by calcium to begin. The arrival of a complexin stabilizes the SNARE complex while at the same time preventing it from going on to membrane fusion. Here we propose to review current information concerning the mast cell degranulation phenomenon and its regulation.Revue Française d'Allergologie 06/2012; 52(4):340–344. DOI:10.1016/j.reval.2012.04.001 · 0.35 Impact Factor
- "En effet, la particule elle-même semble avoir un effet nul ou très faible sur les cellules sentinelle ; ses effets biologiques sont dus aux molécules actives transportées par la particule, dont la structure est sphérique, avec des feuillets concentriques [13,27]. La pollution particulaire comprend également les déchets de combustion des avions, dont la structure et le comportement vis-à-vis des DC sont très proches des données sur les particules diesel  "
Article: Cofacteurs de la pollinose[Show abstract] [Hide abstract]
ABSTRACT: Pollinosis, the generic name of pollen-induced allergies, classically involves the ORL (rhinitis and/or conjunctivitis) and pulmonary (asthma) fields, but also cutaneous reactions (eczema, urticaria and types of edema) may also occur. The pathophysiology of pollinosis, a multi-factorial illness, is not completely understood. The outcome of the host-pollen interaction is influenced by endogenous factors (genetic susceptibility as reflected by abnormal functional responses of the different cellular populations involved, the status of the tissue barriers, and the global status of the immune defense mechanism) and exogenous factors (properties of the pollen grains, the influence of gaseous and/or particulate pollutants, and the influence of commensal or pathogenic microorganisms). At the sub-cellular level, mitochondria have recently been shown to play a role in the pathophysiology of pollinosis, both as sources of energy for mast cell degranulation and during pro-allergic signaling through reactive oxygen species. We will review certain immunological, genetic and environmental aspects which are today essential for the diagnosis and management of pollinosis.Revue Française d'Allergologie 04/2012; 52(3):189–193. DOI:10.1016/j.reval.2012.01.017 · 0.35 Impact Factor
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ABSTRACT: PURPOSE OF REVIEW: This overview highlights recent experimental and epidemiological evidence for the programming effects of outdoor air pollution exposures during early development on lung function and chronic respiratory disorders, such as asthma and related allergic disorders. RECENT FINDINGS: Air pollutants may impact anatomy and/or physiological functioning of the lung and interrelated systems. Programming effects may result from pollutant-induced shifts in a number of molecular, cellular, and physiological states and their interacting systems. Specific key regulatory systems susceptible to programming may influence lung development and vulnerability to respiratory diseases, including both central and peripheral components of neuroendocrine pathways and autonomic nervous system (ANS) functioning which, in turn, influence the immune system. Starting in utero, environmental factors, including air pollutants, may permanently organize these systems toward trajectories of enhanced pediatric (e.g., asthma, allergy) as well as adult disease risk (e.g., chronic obstructive pulmonary disease). Evidence supports a central role of oxidative stress in the toxic effects of air pollution. Additional research suggests xenobiotic metabolism and subcellular components, such as mitochondria are targets of ambient air pollution and play a role in asthma and allergy programming. Mechanisms operating at the level of the placenta are being elucidated. Epigenetic mechanisms may be at the roots of adaptive developmental programming. SUMMARY: Optimal coordinated functioning of many complex processes and their networks of interaction are necessary for normal lung development and the maintenance of respiratory health. Outdoor air pollution may play an important role in early programming of respiratory health and is potentially amenable to intervention.Current opinion in pediatrics 02/2013; 25(2). DOI:10.1097/MOP.0b013e32835e78cc · 2.74 Impact Factor