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6. Alcohol enhances type 1 interferon-α production and mortality in young mice infected with Mycobacterium tuberculosis

Author

Tripathi, Deepak, primary, Welch, Elwyn, additional, Cheekatla, Satyanarayana Swamy, additional, Radhakrishnan, Rajesh Kumar, additional, Venkatasubramanian, Sambasivan, additional, Paidipally, Padmaja, additional, Van, Abhinav, additional, Samten, Buka, additional, Devalraju, Kamakshi P., additional, Neela, Venkata Sanjeev Kumar, additional, Valluri, Vijaya Lakshmi, additional, Mason, Carol, additional, Nelson, Steve, additional, and Vankayalapati, Ramakrishna, additional

Published
2018
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7. ALCOHOL ENHANCES TYPE 1 INTERFERON-α AND MORTALITY OF YOUNG MICE INFECTED WITH Mycobacterium tuberculosis

Author

Tripathi, Deepak, primary, Welch, Elwyn, additional, Cheekatla, Satyanarayana Swamy, additional, Radhakrishnan, Rajesh Kumar, additional, Venkatasubramanian, Sambasivan, additional, Paidipally, Padmaja, additional, Van, Abhinav, additional, Tvinnereim, Amy R., additional, Samten, Buka, additional, Devalraju, Kamakshi P., additional, Neela, Venkata Sanjeev Kumar, additional, Valluri, Vijaya Lakshmi, additional, Mason, Carol, additional, Nelson, Steve, additional, and Vankayalapati, Ramakrishna, additional

Published
2018
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9. Tissue factor expression by myeloid cells contributes to protective immune response against Mycobacterium tuberculosis infection: Innate Immunity

Author

Venkatasubramanian, Sambasivan, Welch, Elwyn, Paidipally, Padmaja, Schechter, Melissa E., Idell, Steven, Tvinnereim, Amy R., Jeffers, Ann, Tucker, Torry, Raghunath, Anjana, Cheekatla, Satyanarayana, Vankayalapati, Ramakrishna, Mackman, Nizel, Tripathi, Deepak, and Andrade, Bruno B.

Abstract

Tissue Factor (TF) is a transmembrane glycoprotein that plays an essential role in hemostasis by activating coagulation. TF is also expressed by monocytes/macrophages as part of the innate immune response to infections. In the current study, we determined the role of TF expressed by myeloid cells during Mycobacterium tuberculosis (M. tb) infection by using mice lacking the TF gene in myeloid cells (TFΔ) and human monocyte derived macrophages (MDMs). We found that during M. tb infection, a deficiency of TF in myeloid cells was associated with reduced inducible nitric oxide synthase (iNOS) expression, enhanced arginase 1 (Arg1) expression, enhanced IL-10 production and reduced apoptosis in infected macrophages, which augmented M. tb growth. Our results demonstrate that a deficiency of TF in myeloid cells promotes M2 like phenotype in M .tb infected macrophages. A deficiency in TF expression by myeloid cells was also associated with reduced fibrin deposition and increased matrix metalloproteases (MMP)-2 and MMP-9 mediated inflammation in M. tb infected lungs. Our studies demonstrate that TF expressed by myeloid cells has newly recognized abilities to polarize macrophages and to regulate M. tb growth.

Published
2016
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13. NK-CD11c+ Cell Crosstalk in Diabetes Enhances IL-6-Mediated Inflammation during Mycobacterium tuberculosis Infection

Author

Cheekatla, Satyanarayana Swamy, primary, Tripathi, Deepak, additional, Venkatasubramanian, Sambasivan, additional, Nathella, Pavan Kumar, additional, Paidipally, Padmaja, additional, Ishibashi, Munenori, additional, Welch, Elwyn, additional, Tvinnereim, Amy R., additional, Ikebe, Mitsuo, additional, Valluri, Vijaya Lakshmi, additional, Babu, Subash, additional, Kornfeld, Hardy, additional, and Vankayalapati, Ramakrishna, additional

Published
2016
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14. Tissue factor expression by myeloid cells contributes to protective immune response againstMycobacterium tuberculosisinfection

Author

Venkatasubramanian, Sambasivan, primary, Tripathi, Deepak, additional, Tucker, Torry, additional, Paidipally, Padmaja, additional, Cheekatla, Satyanarayana, additional, Welch, Elwyn, additional, Raghunath, Anjana, additional, Jeffers, Ann, additional, Tvinnereim, Amy R., additional, Schechter, Melissa E, additional, Andrade, Bruno B, additional, Mackman, Nizel, additional, Idell, Steven, additional, and Vankayalapati, Ramakrishna, additional

Published
2015
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16. A Rho GDP dissociation inhibitor produced by apoptotic T cells inhibits growth of Mycobacterium tuberculosis (INC2P.415)

Author

Venkatasubramanian, Sambasivan, primary, Dhiman, Rohan, additional, Paidipally, Padmaja, additional, Cheekatla, Satyanarayana, additional, Tripathi, Deepak, additional, Welch, Elwyn, additional, Tvinnereim, Amy, additional, Jones, Brenda, additional, Theodorescu, Dan, additional, Barnes, Peter, additional, and Vankayalapati, Ramakrishna, additional

Published
2015
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20. A Rho GDP Dissociation Inhibitor Produced by Apoptotic T-Cells Inhibits Growth of Mycobacterium tuberculosis

Author

Venkatasubramanian, Sambasivan, primary, Dhiman, Rohan, additional, Paidipally, Padmaja, additional, Cheekatla, Satyanarayana S., additional, Tripathi, Deepak, additional, Welch, Elwyn, additional, Tvinnereim, Amy R., additional, Jones, Brenda, additional, Theodorescu, Dan, additional, Barnes, Peter F., additional, and Vankayalapati, Ramakrishna, additional

Published
2015
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21. Tissue factor expression by myeloid cells contributes to protective immune response against Mycobacterium tuberculosis infection.

Author

Venkatasubramanian, Sambasivan, Tripathi, Deepak, Tucker, Torry, Paidipally, Padmaja, Cheekatla, Satyanarayana, Welch, Elwyn, Raghunath, Anjana, Jeffers, Ann, Tvinnereim, Amy R., Schechter, Melissa E, Andrade, Bruno B, Mackman, Nizel, Idell, Steven, and Vankayalapati, Ramakrishna

Abstract

Tissue factor (TF) is a transmembrane glycoprotein that plays an essential role in hemostasis by activating coagulation. TF is also expressed by monocytes/macrophages as part of the innate immune response to infections. In the current study, we determined the role of TF expressed by myeloid cells during Mycobacterium tuberculosis ( M. tb) infection by using mice lacking the TF gene in myeloid cells (TFΔ) and human monocyte derived macrophages (MDMs). We found that during M. tb infection, a deficiency of TF in myeloid cells was associated with reduced inducible nitric oxide synthase (iNOS) expression, enhanced arginase 1 (Arg1) expression, enhanced IL-10 production and reduced apoptosis in infected macrophages, which augmented M. tb growth. Our results demonstrate that a deficiency of TF in myeloid cells promotes M2-like phenotype in M .tb infected macrophages. A deficiency in TF expression by myeloid cells was also associated with reduced fibrin deposition and increased matrix metalloproteases (MMP)-2 and MMP-9 mediated inflammation in M. tb infected lungs. Our studies demonstrate that TF expressed by myeloid cells has newly recognized abilities to polarize macrophages and to regulate M. tb growth. [ABSTRACT FROM AUTHOR]

Published
2016
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23. IL-21 Receptor Signaling Is Essential for Optimal CD4+ T Cell Function and Control of Mycobacterium tuberculosis Infection in Mice.

Author

Cheekatla, Satyanarayana Swamy, Tripathi, Deepak, Venkatasubramanian, Sambasivan, Paidipally, Padmaja, Welch, Elwyn, Tvinnereim, Amy R., Nurieva, Roza, and Vankayalapati, Ramakrishna

Subjects
*INTERLEUKIN-21, *MYCOBACTERIUM tuberculosis, *TUBERCULOSIS, *T cells, *CYTOKINES
Abstract

In this study, we determined the role of IL-21R signaling in Mycobacterium tuberculosis infection, using IL-21R knockout (KO) mice. A total of 50% of M. tuberculosis H37Rv--infected IL-21R KO mice died in 6 mo compared with no deaths in infected wild type (WT) mice. M. tuberculosis--infected IL-21R KO mice had enhanced bacterial burden and reduced infiltration of Ag-specific T cells in lungs compared with M. tuberculosis--infected WT mice. Ag-specific T cells from the lungs of M. tuberculosis--infected IL-21R KO mice had increased expression of T cell inhibitory receptors, reduced expression of chemokine receptors, proliferated less, and produced less IFN-γ, compared with Ag-specific T cells from the lungs of M. tuberculosis--infected WT mice. T cells from M. tuberculosis--infected IL-21R KO mice were unable to induce optimal macrophage responses to M. tuberculosis. This may be due to a decrease in the Ag-specific T cell population. We also found that IL-21R signaling is associated with reduced expression of a transcriptional factor Eomesodermin and enhanced functional capacity of Ag-specific T cells of M. tuberculosis--infected mice. The sum of our findings suggests that IL-21R signaling is essential for the optimal control of M. tuberculosis infection. [ABSTRACT FROM AUTHOR]

Published
2017
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24. Letters.

Author

Crews, Timothy G., Cook, Kip D., and Welch, Elwyn B.

Subjects
*LETTERS to the editor, *SAME-sex marriage, *BLACK athletes, *SLAVERY, *ELECTIONS
Abstract

Several letters to the editor are presented including "Saving Grace" in the September/October 2006 issue, "Will Gay Marriage Be a Wedge Issue in the Elections?" in the September/October 2006 issue and the of the book "Forty Million Dollar Slaves: The Rise, Fall and Redemption of the Black Athlete."

Published
2006

25. IL-21 Receptor Signaling Is Essential for Optimal CD4 + T Cell Function and Control of Mycobacterium tuberculosis Infection in Mice.

Author

Cheekatla SS, Tripathi D, Venkatasubramanian S, Paidipally P, Welch E, Tvinnereim AR, Nurieva R, and Vankayalapati R

Subjects
Animals, Cell Proliferation, Cells, Cultured, Female, Humans, Interferon-gamma metabolism, Lung microbiology, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, Interleukin-21 genetics, Signal Transduction, T-Box Domain Proteins genetics, T-Box Domain Proteins metabolism, CD4-Positive T-Lymphocytes immunology, Lung immunology, Macrophages immunology, Mycobacterium tuberculosis immunology, Receptors, Interleukin-21 metabolism, Tuberculosis immunology
Abstract

In this study, we determined the role of IL-21R signaling in Mycobacterium tuberculosis infection, using IL-21R knockout (KO) mice. A total of 50% of M. tuberculosis H37Rv - infected IL-21R KO mice died in 6 mo compared with no deaths in infected wild type (WT) mice. M. tuberculosis - infected IL-21R KO mice had enhanced bacterial burden and reduced infiltration of Ag-specific T cells in lungs compared with M. tuberculosis - infected WT mice. Ag-specific T cells from the lungs of M. tuberculosis - infected IL-21R KO mice had increased expression of T cell inhibitory receptors, reduced expression of chemokine receptors, proliferated less, and produced less IFN- γ, compared with Ag-specific T cells from the lungs of M. tuberculosis - infected WT mice. T cells from M. tuberculosis - infected IL-21R KO mice were unable to induce optimal macrophage responses to M. tuberculosis. This may be due to a decrease in the Ag-specific T cell population. We also found that IL-21R signaling is associated with reduced expression of a transcriptional factor Eomesodermin and enhanced functional capacity of Ag-specific T cells of M. tuberculosis - infected mice. The sum of our findings suggests that IL-21R signaling is essential for the optimal control of M. tuberculosis infection., (Copyright © 2017 by The American Association of Immunologists, Inc.)

Published
2017
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