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Your search keyword '"Segueni, Noria"' showing total 14 results
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14 results on '"Segueni, Noria"'

3. The macrophage infectivity potentiator of Trypanosoma cruzi induces innate IFN-γ and TNF-α production by human neonatal and adult blood cells through TLR2/1 and TLR4.

Author

Djebbara, Sarra Ait, Mcheik, Saria, Percier, Pauline, Segueni, Noria, Poncelet, Antoine, and Truyens, Carine

Subjects
BLOOD cells, TRYPANOSOMA cruzi, CORD blood, KILLER cells, MYELOID cells
Abstract

We previously identified the recombinant (r) macrophage (M) infectivity (I) potentiator (P) of the protozoan parasite Trypanosoma cruzi (Tc) (rTcMIP) as an immuno-stimulatory protein that induces the release of IFN-γ, CCL2 and CCL3 by human cord blood cells. These cytokines and chemokines are important to direct a type 1 adaptive immune response. rTcMIP also increased the Ab response and favored the production of the Th1-related isotype IgG2a in mouse models of neonatal vaccination, indicating that rTcMIP could be used as a vaccine adjuvant to enhance T and B cell responses. In the present study, we used cord and adult blood cells, and isolated NK cells and human monocytes to investigate the pathways and to decipher the mechanism of action of the recombinant rTcMIP. We found that rTcMIP engaged TLR1/2 and TLR4 independently of CD14 and activated the MyD88, but not the TRIF, pathway to induce IFN-γ production by IL-15-primed NK cells, and TNF-α secretion by monocytes and myeloid dendritic cells. Our results also indicated that TNF-α boosted IFN-γ expression. Though cord blood cells displayed lower responses than adult cells, our results allow to consider rTcMIP as a potential pro-type 1 adjuvant that might be associated to vaccines administered in early life or later. [ABSTRACT FROM AUTHOR]

Published
2023
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6. Host-pathogen interactions during Mycobacterium tuberculosis infection : role of IL-36, TNF and IL-17/IL-22 pathways

Author

Segueni, Noria, Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Université d'Orléans, Valérie Quesniaux, and Bernhard Ryffel

Subjects
IL-17, IL-36, Anticorps, IL-22, TNF, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Mycobacterium tuberculosis, Antibodies
Abstract

Tuberculosis remains a major health problem in the world nowadays. The increasing incidence of resistant tuberculosis is associated with a poor diagnosis, reflecting important difficulties for total eradication. Understand host-pathogen interactions is crucial to establish new therapeutic strategies. This work first shows the limited contribution of IL-36 pathway during mycobacterial infection. These results suggest that IL-36 could be targeted for the treatment of psoriasis without a high risk of tuberculosis reactivation. We then demonstrate the differential role of TNF pathway among myeloid or lymphoid cells during M. tuberculosis infection, and our data support the development of immunomodulatory strategies to boost host immune response, thus helping to clear the infection. Moreover, we characterize a humanized murine model allowing the study of new anti-TNF candidates in the context of M. tuberculosis infection. Finally, we show that antibodies targeting IL-17 does not dampen host control of M. tuberculosis infection, unlike anti-TNF, and that IL-22 does not compensate absence of IL-17 for this control.; La tuberculose est encore aujourd’hui un problème de santé majeur et l’augmentation des cas de tuberculoses résistantes au niveau mondial, associé au dépistage et diagnostic insuffisants, suggère une éradication totale encore lointaine. La compréhension des relations hôte-pathogène est essentielle pour permettre d’établir de nouvelles stratégies thérapeutiques. Ces travaux de thèse ont mis en exergue la contribution limitée de la voie de signalisation IL-36, cytokine de la famille de l’IL-1, au cours de l’infection mycobactérienne. Ces données permettent d’envisager sérieusement l’IL-36 en tant que cible thérapeutique pour le psoriasis sans risquer la réactivation de tuberculose latente chez les patients. De plus, nous avons également démontré le rôle différentiel de la voie de signalisation TNF au sein de populations cellulaires spécifiques lors de l’infection par M. tuberculosis, et nos résultats apportent des connaissances solides pour envisager des stratégies immuno-modulatoires qui pourraient constituer l’avenir des traitements antituberculeux. D’autre part, nous avons caractérisé un modèle murin humanisé pour une étude facilitée des anticorps anti-TNF humains actuels. L’utilisation de ce modèle pourrait permettre, à termes, d’identifier et de valider de nouveaux candidats d’anticorps anti-TNF de deuxième génération. Enfin, nous avons montré que des anticorps neutralisants l’IL-17 ne perturbent pas la réponse immunitaire à la tuberculose, contrairement aux anticorps anti-TNF, et que l’absence de l’IL-17 n’est pas compensée par l’IL-22 puisque des animaux déficients pour ces deux voies de signalisation sont capables de contrôler l’infection.

Published
2015

7. Controlled Mycobacterium tuberculosis infection in mice under treatment with anti-IL-17A or IL-17F antibodies, in contrast to TNFα neutralization

Author

Segueni, Noria, primary, Tritto, Elaine, additional, Bourigault, Marie-Laure, additional, Rose, Stéphanie, additional, Erard, François, additional, Le Bert, Marc, additional, Jacobs, Muazzam, additional, Di Padova, Franco, additional, Stiehl, Daniel P., additional, Moulin, Pierre, additional, Brees, Dominique, additional, Chibout, Salah-Dine, additional, Ryffel, Bernhard, additional, Kammüller, Michael, additional, and Quesniaux, Valerie F., additional

Published
2016
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9. Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection.

Author

Segueni, Noria, primary, Benmerzoug, Sulayman, additional, Rose, Stéphanie, additional, Gauthier, Amandine, additional, Bourigault, Marie-Laure, additional, Reverchon, Flora, additional, Philippeau, Amandine, additional, Erard, François, additional, Le Bert, Marc, additional, Bouscayrol, Hélène, additional, Wachter, Thierry, additional, Garcia, Irène, additional, Kollias, George, additional, Jacobs, Muazzam, additional, Ryffel, Bernhard, additional, and Quesniaux, Valerie F.J., additional

Published
2016
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10. Control of Mycobacterial Infections in Mice Expressing Human Tumor Necrosis Factor (TNF) but Not Mouse TNF

Author

Olleros, Maria L., primary, Chavez-Galan, Leslie, additional, Segueni, Noria, additional, Bourigault, Marie L., additional, Vesin, Dominique, additional, Kruglov, Andrey A., additional, Drutskaya, Marina S., additional, Bisig, Ruth, additional, Ehlers, Stefan, additional, Aly, Sahar, additional, Walter, Kerstin, additional, Kuprash, Dmitry V., additional, Chouchkova, Miliana, additional, Kozlov, Sergei V., additional, Erard, François, additional, Ryffel, Bernard, additional, Quesniaux, Valérie F. J., additional, Nedospasov, Sergei A., additional, and Garcia, Irene, additional

Published
2015
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12. Relative contribution of IL‐1α, IL‐1β and TNF to the host response to Mycobacterium tuberculosis and attenuated M. bovis BCG

Author

Bourigault, Marie‐Laure, primary, Segueni, Noria, additional, Rose, Stéphanie, additional, Court, Nathalie, additional, Vacher, Rachel, additional, Vasseur, Virginie, additional, Erard, François, additional, Le Bert, Marc, additional, Garcia, Irene, additional, Iwakura, Yoichiro, additional, Jacobs, Muazzam, additional, Ryffel, Bernhard, additional, and Quesniaux, Valerie F. J., additional

Published
2013
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13. Tumor Necrosis Factor and Its Receptors Are Crucial to Control Mycobacterium bovisBacillus Calmette-Guerin Pleural Infection in a Murine Model

Author

Chavez-Galan, Leslie, Vesin, Dominique, Segueni, Noria, Prasad, Pritha, Buser-Llinares, Raphaële, Blaser, Guillaume, Pache, Jean-Claude, Ryffel, Bernhard, Quesniaux, Valérie F.J., and Garcia, Irene

Abstract

Tumor necrosis factor (TNF) is crucial to control Mycobacterium tuberculosisinfection, which remains a leading cause of morbidity and mortality worldwide. TNF blockade compromises host immunity and may cause reactivation of latent infection, resulting in overt pulmonary, pleural, and extrapulmonary tuberculosis. Herein, we investigate the roles of TNF and TNF receptors in the control of Mycobacterium bovisbacillus Calmette-Guerin (BCG) pleural infection in a murine model. As controls, wild-type mice and those with a defective CCR5, a receptor that is crucial for control of viral infection but not for tuberculosis, were used. BCG-induced pleural infection was uncontrolled and progressive in absence of TNF or TNF receptor 1 (TNFR1)/TNFR2 (TNFR1R2) with increased inflammatory cell recruitment and bacterial load in the pleural cavity, and heightened levels of pleural and serum proinflammatory cytokines and chemokines, compared to wild-type control mice. The visceral pleura was thickened with chronic inflammation, which was prominent in TNF−/−and TNFR1R2−/−mice. The parietal pleural of TNF−/−and TNFR1R2−/−mice exhibited abundant inflammatory nodules containing mycobacteria, and these mice developed nonresolving inflammation and succumbed from disseminated BCG infection. By contrast, CCR5−/−mice survived and controlled pleural BCG infection as wild-type control mice. In conclusion, BCG-induced pleurisy was uncontrolled in the absence of TNF or TNF receptors with exacerbated inflammatory response, impaired bacterial clearance, and defective mesothelium repair, suggesting a critical role of TNF to control mycobacterial pleurisy.

Published
2016
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14. The macrophage infectivity potentiator of Trypanosoma cruzi induces innate IFN-γ and TNF-α production by human neonatal and adult blood cells through TLR2/1 and TLR4.

Author

Ait Djebbara S, Mcheik S, Percier P, Segueni N, Poncelet A, and Truyens C

Subjects
Animals, Mice, Infant, Newborn, Humans, Adult, Toll-Like Receptor 4, Tumor Necrosis Factor-alpha, Macrophages, Interferon-gamma, Killer Cells, Natural, Toll-Like Receptor 2, Trypanosoma cruzi
Abstract

We previously identified the recombinant (r) macrophage (M) infectivity (I) potentiator (P) of the protozoan parasite Trypanosoma cruzi (Tc) (rTcMIP) as an immuno-stimulatory protein that induces the release of IFN-γ, CCL2 and CCL3 by human cord blood cells. These cytokines and chemokines are important to direct a type 1 adaptive immune response. rTcMIP also increased the Ab response and favored the production of the Th1-related isotype IgG2a in mouse models of neonatal vaccination, indicating that rTcMIP could be used as a vaccine adjuvant to enhance T and B cell responses. In the present study, we used cord and adult blood cells, and isolated NK cells and human monocytes to investigate the pathways and to decipher the mechanism of action of the recombinant rTcMIP. We found that rTcMIP engaged TLR1/2 and TLR4 independently of CD14 and activated the MyD88, but not the TRIF, pathway to induce IFN-γ production by IL-15-primed NK cells, and TNF-α secretion by monocytes and myeloid dendritic cells. Our results also indicated that TNF-α boosted IFN-γ expression. Though cord blood cells displayed lower responses than adult cells, our results allow to consider rTcMIP as a potential pro-type 1 adjuvant that might be associated to vaccines administered in early life or later., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Ait Djebbara, Mcheik, Percier, Segueni, Poncelet and Truyens.)

Published
2023
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