Éditeur(s) : Port-au-Prince, Impr. de L’Abeille, 1904 Port-au-Prince, Impr. de L’Abeille, 1904
Résumé : 2b-L/E- 1904
HLL Dep HAI 353C F04; Hollis 004565407

LLMC31873

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : [S.l. : s.n.], 1946 (Port-au-Prince, Haïti : Imprimerie de l’Etat [S.l. : s.n.], 1946 (Port-au-Prince, Haïti : Imprimerie de l’Etat
Résumé : 4-tr-Trouillot, etc.
Law Dep HAI 961 TRO, Hollis 001399594

LLMC31882

Éditeur(s) : HAL CCSD
Résumé : Macrophages (MΦ), well-known to play a key role in immune response, also respond to environmental toxic chemicals such as diesel exhaust particles (DEP), an air pollutant recently classified as carcinogenic to humans. MΦ are heterogeneous and plastic cells which activate according to their microenvironment into either an M1 subtype (so called classically activated or pro-inflammatory) under IFNγ and LPS stimulation or an M2 subtype (so called alternatively activated or anti-inflammatory) under IL-4 and/or IL-13 stimulation. However, potential effects of DEPs on M1/M2 MΦ polarization remain poorly documented. First, we characterized the expression marker of in vitro M-CSF-differentiated MΦ from human monocytes and activated into the M1 or M2 subtypes. Our main results show that M-CSF-generated MΦ considered as anti-inflammatory are actually able to switch to an M1 phenotype after IFNγ/LPS stimulation. Furthermore, the markers identified in this study were used to assess the impact of organic extracts of DEP (DEPe) on MΦ polarization and more generally on their physiology. DEPe alter some M1 and M2 markers expressed by polarized MΦ, without causing the overall inhibition of the M1 and M2 polarization process or the switch to a different phenotype. This phenotype alteration is associated with a decrease in the LPS-dependent inflammatory response in M1 MΦ and the chemotactic capacities in M2 MΦ. DEPe decrease the secretion of some cytokines and chemokines such as IL-6, IL-12p40 and CCL18 via AhR and/or Nrf2 activation. At the same time, we show that M1 and M2 MΦ in response to DEPe are able to secrete a sufficient level of a pro-fibrotic growth factor, the platelet derived growth factor B (PDGF-B) via AhR activation, leading to stimulation of lung fibroblast proliferation. Finally, these works show that DEPe have immunotoxic properties with regards to the physiology of human in vitro polarized MΦ. This immunotoxicity may then contribute to the deleterious effects of these urban environmental contaminants on human health.
Les macrophages (MΦ), des cellules clefs de la réponse immunitaire peuvent répondre à des contaminants environnementaux comme les particules diesel (DEP), des polluants atmosphériques récemment classés cancérigènes pour l'Homme. Les MΦ sont des cellules hétérogènes et plastiques qui s'activent en fonction de leur microenvironnement soit en MΦ M1 (dits classiquement activés ou pro-inflammatoires) sous l'effet de l'INFγ et du LPS soit en MΦ M2 (dits alternativement activés ou réparateurs) sous l'effet de l'IL-4 et/ou de l'IL-13. Les effets des DEP sur la polarisation M1/M2 des MΦ restent peu documentés. Nous avons dans un premier temps caractérisé l'expression des marqueurs des MΦ différenciés in vitro en présence de M-CSF à partir de monocytes humains et polarisés en sous-type M1 ou M2. Nos principaux résultats montrent que les MΦ différenciés au M-CSF considérés comme des MΦ anti-inflammatoires, sont en réalité capables de s'activer vers un phénotype M1 après une stimulation au LPS/IFNγ. De plus, les marqueurs mis en évidence au cours de ce travail ont permis d'évaluer l'impact d'extraits organiques de DEP (DEPe) sur la polarisation des MΦ et plus généralement sur leur physiologie. Les DEPe altèrent l'expression de certains marqueurs M1 et M2 des MΦ, sans toutefois provoquer d'inhibition globale des processus de polarisation M1 et M2 ou de transition d'un phénotype vers un autre. Cette altération du phénotype est associée à une diminution de la réponse inflammatoire LPS-dépendante dans les MΦ M1 et des capacités chimiotactiques des MΦ M2. Les DEPe diminuent la sécrétion de certaines cytokines et chimiokines comme l'IL-6, l'IL-12p40 et le CCL18 via l'activation d'AhR et/ou de Nrf2. Parallèlement, nous montrons que les MΦ M1 et M2 exposés aux DEPe sécrètent le platelet deried growth factor B (PDGF-B), un facteur de croissance profibrosant, via l'activation d'AhR en quantité suffisante pour stimuler la prolifération de fibroblastes pulmonaires. Au total, ces travaux démontrent que les DEP possèdent des propriétés immunotoxiques vis-à-vis de la physiologie des macrophages humains polarisés in vitro. Cette immunotoxicité pourrait participer aux effets délétères de ces contaminants environnementaux urbains sur la santé humaine.
https://tel.archives-ouvertes.fr/tel-01188679

NNT : 2015REN1S011
tel-01188679
https://tel.archives-ouvertes.fr/tel-01188679
https://tel.archives-ouvertes.fr/tel-01188679/document
https://tel.archives-ouvertes.fr/tel-01188679/file/JAGUIN_Marie.pdf

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince : Impr. nationale, 1903 Port-au-Prince : Impr. nationale, 1903
Résumé : 2a-L/E- 1903
LL Dep HAI 372 FO3; Hollis 004434799

LLMC31861

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Cap Haïtien, Chez l’auteur; Paris, V. Giard & E. Brière, 1901. Cap Haïtien, Chez l’auteur; Paris, V. Giard & E. Brière, 1901.
Résumé : 4-tr-Chaum.-1901
HLL Dep HAI 380C F01; Hollis 004570401

LLMC31876

Éditeur(s) : HAL CCSD Public Library of Science
Résumé : International audience
Macrophages (MΦ), well-known to play an important role in immune response, also respond to environmental toxic chemicals such as diesel exhaust particles (DEP). Potential effects of DEPs towards MΦ polarization, a key hall-mark of MΦ physiology, remain however poorly documented. This study was therefore designed to evaluate the effects of a reference DEP extract (DEPe) on human MΦ polarization. Human blood monocytes-derived MΦ were incubated with IFNγ+LPS or IL-4 to obtain M1 and M2 subtypes, respectively; a 24 h exposure of polarizing MΦ to 10 μg/ml DEPe was found to impair expression of some macrophagic M1 and M2 markers, without however overall inhibition of M1 and M2 polarization processes. Notably, DEPe treatment increased the secretion of the M1 marker IL-8 and the M2 marker IL-10 in both MΦ subtypes, whereas it reduced lipopolysaccharide-induced IL-6 and IL-12p40 secretion in M1 MΦ. In M2 MΦ, DEPe exposure led to a reduction of CD200R expression and of CCL17, CCL18 and CCL22 secretion, associated with a lower chemotaxis of CCR4-positive cells. DEPe activated the Nrf2 and AhR pathways and induced expression of their reference target genes such as Hmox-1 and cytochrome P-4501B1 in M1 and M2 MΦ. Nrf2 or AhR silencing through RNA interference prevented DEPe-related down-regulation of IL-6. AhR silencing also inhibited the down-secretion of IL-12p40 and CCL18 in M1- and M2-DEPe-exposed MΦ, respectively. DEPs are therefore likely to alter expression of some M1 and M2 markers in an AhR- and Nrf2-dependent manner; such regulations may contribute to deleterious immune effects of atmospheric DEP.
ISSN: 1932-6203

hal-01122723
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01122723
PUBMED : 25710172
DOI : 10.1371/journal.pone.0116560

Éditeur(s) : Port-au-Prince [1906?]-1914 Port-au-Prince [1906?]-1914
Résumé : 2b-L/E- 1906-14
HLL Dep HAI 497 F06

LLMC31886

Éditeur(s) : Port-au-Prince, Imprimerie nationale, 1930. Port-au-Prince, Imprimerie nationale, 1930.
Résumé : 2a-L/E- 1930
Law dep.HAI 352,3 F30; Hollis 004565365

LLMC31866

Éditeur(s) : Paris, Marescq jeune, 1901. Paris, Marescq jeune, 1901.
Résumé : 4-tr-Dube-1901
HLL Dep. HAI 961 DUB; Hollis 004455252

LLMC31881

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Lung diseases are aggravated by exposure to diesel exhaust particles (DEPs) found in air pollution. Macrophages are thought to play a crucial role in lung immune response to these pollutants, even if the mechanisms involved remain incompletely characterized. In the present study, we demonstrated that classically and alternative human macrophages (MΦ) exhibited increased secretion of PDGF-B in response to DEP extract (DEPe). This occurred via aryl hydrocarbon receptor (AhR)-activation because DEPe-induced PDGF-B overexpression was abrogated after AhR expression knock-down by RNA interference, in both M1 and M2 polarizing MΦ. In addition, TCDD and benzo(a)pyrene, two potent AhR ligands, also significantly increased mRNA expression of PDGF-B in M1 MΦ, whereas some weak ligands of AhR did not. We next evaluated the impact of conditioned media (CM) from MΦ culture exposed to DEPe or of recombinant PDGF-B onto lung fibroblast proliferation. The tyrosine kinase inhibitor, AG1295, prevents phosphorylations of PDGF-Rβ, AKT and ERK1/2 and the proliferation of MRC5 fibroblasts induced by recombinant PDGF-B and by CM from M1 polarizing MΦ, strongly suggesting that the PDGF-BB secreted by DEPe-exposed MΦ is sufficient to activate the PDGF-Rβ pathway of human lung fibroblasts. In conclusion, we demonstrated that human MΦ, whatever their polarization status, secrete PDGF-B in response to DEPe and that PDGF-B is a target gene of AhR. Therefore, induction of PDGF-B by DEP may participate in the deleterious effects towards human health triggered by such environmental urban contaminants.
ISSN: 0041-008X

hal-01146840
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01146840
DOI : 10.1016/j.taap.2015.04.007
PUBMED : 25896968