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1. Gut-Resident Lactobacillus Abundance Associates with IDO1 Inhibition and Th17 Dynamics in SIV-Infected Macaques

Author

Ivan Vujkovic-Cvijin, Louise A. Swainson, Simon N. Chu, Alexandra M. Ortiz, Clark A. Santee, Annalise Petriello, Richard M. Dunham, Douglas W. Fadrosh, Din L. Lin, Ali A. Faruqi, Yong Huang, Cristian Apetrei, Ivona Pandrea, Frederick M. Hecht, Christopher D. Pilcher, Nichole R. Klatt, Jason M. Brenchley, Susan V. Lynch, and Joseph M. McCune

Subjects
Biology (General), QH301-705.5
Abstract

Gut microbes can profoundly modulate mucosal barrier-promoting Th17 cells in mammals. A salient feature of HIV/simian immunodeficiency virus (SIV) immunopathogenesis is the loss of Th17 cells, which has been linked to increased activity of the immunomodulatory enzyme, indoleamine 2,3-dioxygenase 1 (IDO 1). The role of gut microbes in this system remains unknown, and the SIV-infected rhesus macaque provides a well-described model for HIV-associated Th17 loss and mucosal immune disruption. We observed a specific depletion of gut-resident Lactobacillus during acute and chronic SIV infection of rhesus macaques, which was also seen in early HIV-infected humans. This depletion in rhesus macaques correlated with increased IDO1 activity and Th17 loss. Macaques supplemented with a Lactobacillus-containing probiotic exhibited decreased IDO1 activity during chronic SIV infection. We propose that Lactobacillus species inhibit mammalian IDO1 and thus may help to preserve Th17 cells during pathogenic SIV infection, providing support for Lactobacillus species as modulators of mucosal immune homeostasis.

Published
2015
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2. Gut-Resident Lactobacillus Abundance Associates with IDO1 Inhibition and Th17 Dynamics in SIV-Infected Macaques

Author

Vujkovic-Cvijin, Ivan, Swainson, Louise A, Chu, Simon N, Ortiz, Alexandra M, Santee, Clark A, Petriello, Annalise, Dunham, Richard M, Fadrosh, Douglas W, Lin, Din L, Faruqi, Ali A, Huang, Yong, Apetrei, Cristian, Pandrea, Ivona, Hecht, Frederick M, Pilcher, Christopher D, Klatt, Nichole R, Brenchley, Jason M, Lynch, Susan V, and McCune, Joseph M

Subjects
Biological Sciences, HIV/AIDS, Infectious Diseases, Sexually Transmitted Infections, 1.1 Normal biological development and functioning, Infection, Good Health and Well Being, Animals, Female, HIV Infections, Indoleamine-Pyrrole 2, 3, -Dioxygenase, Intestinal Mucosa, Lactobacillus, Macaca mulatta, Simian Acquired Immunodeficiency Syndrome, Simian Immunodeficiency Virus, Th17 Cells, Simian immunodeficiency virus, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Gut microbes can profoundly modulate mucosal barrier-promoting Th17 cells in mammals. A salient feature of HIV/simian immunodeficiency virus (SIV) immunopathogenesis is the loss of Th17 cells, which has been linked to increased activity of the immunomodulatory enzyme, indoleamine 2,3-dioxygenase 1 (IDO 1). The role of gut microbes in this system remains unknown, and the SIV-infected rhesus macaque provides a well-described model for HIV-associated Th17 loss and mucosal immune disruption. We observed a specific depletion of gut-resident Lactobacillus during acute and chronic SIV infection of rhesus macaques, which was also seen in early HIV-infected humans. This depletion in rhesus macaques correlated with increased IDO1 activity and Th17 loss. Macaques supplemented with a Lactobacillus-containing probiotic exhibited decreased IDO1 activity during chronic SIV infection. We propose that Lactobacillus species inhibit mammalian IDO1 and thus may help to preserve Th17 cells during pathogenic SIV infection, providing support for Lactobacillus species as modulators of mucosal immune homeostasis.

Published
2015

3. Gut-Resident Lactobacillus Abundance Associates with IDO1 Inhibition and Th17 Dynamics in SIV-Infected Macaques

Author

Joseph M. McCune, Ivona Pandrea, Clark A. Santee, Yong Huang, Cristian Apetrei, Nichole R. Klatt, Louise A. Swainson, Annalise Petriello, Jason M. Brenchley, Susan V. Lynch, Douglas Fadrosh, Frederick Hecht, Simon Chu, Richard M. Dunham, Ivan Vujkovic-Cvijin, Din L. Lin, Alexandra M. Ortiz, Christopher D. Pilcher, and Ali A. Faruqi

Subjects
animal diseases, Medical Physiology, Simian Acquired Immunodeficiency Syndrome, HIV Infections, medicine.disease_cause, Indoleamine-Pyrrole 2, General Biochemistry, Genetics and Molecular Biology, Article, law.invention, Microbiology, Probiotic, Immune system, Intestinal mucosa, law, Lactobacillus, medicine, Animals, Indoleamine-Pyrrole 2,3,-Dioxygenase, Immune homeostasis, Intestinal Mucosa, lcsh:QH301-705.5, chemistry.chemical_classification, biology, Simian immunodeficiency virus, virus diseases, biology.organism_classification, Macaca mulatta, Rhesus macaque, Enzyme, Infectious Diseases, Good Health and Well Being, lcsh:Biology (General), chemistry, Immunology, Dioxygenase, HIV/AIDS, Th17 Cells, Female, Simian Immunodeficiency Virus, Biochemistry and Cell Biology, Infection, Biotechnology
Abstract

SummaryGut microbes can profoundly modulate mucosal barrier-promoting Th17 cells in mammals. A salient feature of HIV/simian immunodeficiency virus (SIV) immunopathogenesis is the loss of Th17 cells, which has been linked to increased activity of the immunomodulatory enzyme, indoleamine 2,3-dioxygenase 1 (IDO 1). The role of gut microbes in this system remains unknown, and the SIV-infected rhesus macaque provides a well-described model for HIV-associated Th17 loss and mucosal immune disruption. We observed a specific depletion of gut-resident Lactobacillus during acute and chronic SIV infection of rhesus macaques, which was also seen in early HIV-infected humans. This depletion in rhesus macaques correlated with increased IDO1 activity and Th17 loss. Macaques supplemented with a Lactobacillus-containing probiotic exhibited decreased IDO1 activity during chronic SIV infection. We propose that Lactobacillus species inhibit mammalian IDO1 and thus may help to preserve Th17 cells during pathogenic SIV infection, providing support for Lactobacillus species as modulators of mucosal immune homeostasis.

Published
2015

4. Gut-Resident LactobacillusAbundance Associates with IDO1 Inhibition and Th17 Dynamics in SIV-Infected Macaques

Author

Vujkovic-Cvijin, Ivan, Swainson, Louise A., Chu, Simon N., Ortiz, Alexandra M., Santee, Clark A., Petriello, Annalise, Dunham, Richard M., Fadrosh, Douglas W., Lin, Din L., Faruqi, Ali A., Huang, Yong, Apetrei, Cristian, Pandrea, Ivona, Hecht, Frederick M., Pilcher, Christopher D., Klatt, Nichole R., Brenchley, Jason M., Lynch, Susan V., and McCune, Joseph M.

Abstract

Gut microbes can profoundly modulate mucosal barrier-promoting Th17 cells in mammals. A salient feature of HIV/simian immunodeficiency virus (SIV) immunopathogenesis is the loss of Th17 cells, which has been linked to increased activity of the immunomodulatory enzyme, indoleamine 2,3-dioxygenase 1 (IDO 1). The role of gut microbes in this system remains unknown, and the SIV-infected rhesus macaque provides a well-described model for HIV-associated Th17 loss and mucosal immune disruption. We observed a specific depletion of gut-resident Lactobacillusduring acute and chronic SIV infection of rhesus macaques, which was also seen in early HIV-infected humans. This depletion in rhesus macaques correlated with increased IDO1 activity and Th17 loss. Macaques supplemented with a Lactobacillus-containing probiotic exhibited decreased IDO1 activity during chronic SIV infection. We propose that Lactobacillusspecies inhibit mammalian IDO1 and thus may help to preserve Th17 cells during pathogenic SIV infection, providing support for Lactobacillusspecies as modulators of mucosal immune homeostasis.

Published
2015
Full Text
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