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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. 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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7. 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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8. 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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10. 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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11. 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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12. 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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