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Article ; Online: TRPV1 activation in human Langerhans cells and T cells inhibits mucosal HIV-1 infection via CGRP-dependent and independent mechanisms.

Mariotton, Jammy / Cohen, Emmanuel / Zhu, Aiwei / Auffray, Cédric / Barbosa Bomfim, Caio César / Barry Delongchamps, Nicolas / Zerbib, Marc / Bomsel, Morgane / Ganor, Yonatan

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 22, Page(s) e2302509120

Abstract: Upon its mucosal transmission, HIV type 1 (HIV-1) rapidly targets genital antigen-presenting Langerhans cells (LCs), which subsequently transfer infectious virus to ... ...

Abstract	Upon its mucosal transmission, HIV type 1 (HIV-1) rapidly targets genital antigen-presenting Langerhans cells (LCs), which subsequently transfer infectious virus to CD4
MeSH term(s)	Humans ; Calcitonin Gene-Related Peptide/pharmacology ; T-Lymphocytes/metabolism ; Langerhans Cells/metabolism ; Mucous Membrane/metabolism ; Capsaicin/pharmacology ; Pain/metabolism ; HIV Infections/metabolism ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism
Chemical Substances	Calcitonin Gene-Related Peptide (JHB2QIZ69Z) ; Capsaicin (S07O44R1ZM) ; TRPV Cation Channels ; TRPV1 protein, human
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2302509120
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Article ; Online: CGRP inhibits SARS-CoV-2 infection of bronchial epithelial cells and its pulmonary levels correlate with viral clearance in critical COVID-19 patients

Barbosa Bomfim, Caio Cesar / Genin, Hugo / Cottoignies-Callamarte, Andrea / Gallois-Montbrun, Sarah / Murigneux, Emilie / Sams, Anette / Rozenberg, Arielle R / Belouzard, Sandrine / Dubuisson, Jean / Kosminder, Olivier / Pene, Frederic / Terrier, Benjamin / Bomsel, Morgane / Ganor, Yonatan

bioRxiv

Abstract: Upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), patients with critical coronavirus disease 2019 (COVID-19) present with life-threatening respiratory distress, pulmonary damage and cytokine storm. One unexplored hub in ... ...

Abstract	Upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), patients with critical coronavirus disease 2019 (COVID-19) present with life-threatening respiratory distress, pulmonary damage and cytokine storm. One unexplored hub in COVID-19 is the neuropeptide calcitonin gene-related peptide (CGRP), which is highly abundant in the airways and could converge in multiple aspects of COVID-19-related pulmonary pathophysiology. Whether CGRP affects SARS-CoV-2 infection directly remains elusive. We show that in critical COVID-19 patients, CGRP is increased in both plasma and lungs. Importantly, CGRP pulmonary levels are elevated in early SARS-CoV-2-positive patients, and restore to baseline upon subsequent viral clearance in SARS-CoV-2-negative patients. We further show that CGRP and its stable analogue SAX directly inhibit infection of bronchial Calu-3 epithelial cells with SARS-CoV-2 Omicron and Alpha variants in a dose-dependent manner. Both pre- and post-infection treatment with GRRP and/or SAX is enough to block SARS-CoV-2 productive infection of Calu3 cells. CGRP-mediated inhibition occurs via activation of the CGRP receptor and involves down-regulation of SARS-CoV-2 entry receptors at the surface of Calu-3 cells. Together, we propose that increased pulmonary CGRP mediates beneficial viral clearance in critical COVID-19 patients, by directly inhibiting SARS-CoV-2 infection. Hence, CGRP-based interventions could be harnessed for management of COVID-19.
Keywords	covid19
Language	English
Publishing date	2024-01-06
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.01.05.574360
Database	COVID19

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Article ; Online: CGRP inhibits SARS-CoV-2 infection of bronchial epithelial cells and its pulmonary levels correlate with viral clearance in critical COVID-19 patients

Barbosa Bomfim, Caio César / Genin, Hugo / Cottoignies-Callamarte, Andréa / Gallois-Montbrun, Sarah / Murigneux, Emilie / Sams, Anette / Rosenberg, Arielle R / Belouzard, Sandrine / Dubuisson, Jean / Kosminder, Olivier / Pène, Frédéric / Terrier, Benjamin / Bomsel, Morgane / Ganor, Yonatan

bioRxiv

Abstract	Upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), patients with critical coronavirus disease 2019 (COVID-19) present with life-threatening respiratory distress, pulmonary damage and cytokine storm. One unexplored hub in COVID-19 is the neuropeptide calcitonin gene-related peptide (CGRP), which is highly abundant in the airways and could converge in multiple aspects of COVID-19-related pulmonary pathophysiology. Whether CGRP affects SARS-CoV-2 infection directly remains elusive. We show that in critical COVID-19 patients, CGRP is increased in both plasma and lungs. Importantly, CGRP pulmonary levels are elevated in early SARS-CoV-2-positive patients, and restore to baseline upon subsequent viral clearance in SARS-CoV-2-negative patients. We further show that CGRP and its stable analogue SAX directly inhibit infection of bronchial Calu-3 epithelial cells with SARS-CoV-2 Omicron and Alpha variants in a dose-dependent manner. Both pre- and post-infection treatment with GRRP and/or SAX is enough to block SARS-CoV-2 productive infection of Calu3 cells. CGRP-mediated inhibition occurs via activation of the CGRP receptor and involves down-regulation of SARS-CoV-2 entry receptors at the surface of Calu-3 cells. Together, we propose that increased pulmonary CGRP mediates beneficial viral clearance in critical COVID-19 patients, by directly inhibiting SARS-CoV-2 infection. Hence, CGRP-based interventions could be harnessed for management of COVID-19.
Keywords	covid19
Language	English
Publishing date	2024-01-06
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.01.05.574360
Database	COVID19

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Article ; Online: GPX4 regulates cellular necrosis and host resistance in Mycobacterium tuberculosis infection.

Amaral, Eduardo P / Foreman, Taylor W / Namasivayam, Sivaranjani / Hilligan, Kerry L / Kauffman, Keith D / Barbosa Bomfim, Caio Cesar / Costa, Diego L / Barreto-Duarte, Beatriz / Gurgel-Rocha, Clarissa / Santana, Monique Freire / Cordeiro-Santos, Marcelo / Du Bruyn, Elsa / Riou, Catherine / Aberman, Kate / Wilkinson, Robert John / Barber, Daniel L / Mayer-Barber, Katrin D / Andrade, Bruno B / Sher, Alan

The Journal of experimental medicine

2022 Volume 219, Issue 11

Abstract: Cellular necrosis during Mycobacterium tuberculosis (Mtb) infection promotes both immunopathology and bacterial dissemination. Glutathione peroxidase-4 (Gpx4) is an enzyme that plays a critical role in preventing iron-dependent lipid peroxidation- ... ...

Abstract	Cellular necrosis during Mycobacterium tuberculosis (Mtb) infection promotes both immunopathology and bacterial dissemination. Glutathione peroxidase-4 (Gpx4) is an enzyme that plays a critical role in preventing iron-dependent lipid peroxidation-mediated cell death (ferroptosis), a process previously implicated in the necrotic pathology seen in Mtb-infected mice. Here, we document altered GPX4 expression, glutathione levels, and lipid peroxidation in patients with active tuberculosis and assess the role of this pathway in mice genetically deficient in or overexpressing Gpx4. We found that Gpx4-deficient mice infected with Mtb display substantially increased lung necrosis and bacterial burdens, while transgenic mice overexpressing the enzyme show decreased bacterial loads and necrosis. Moreover, Gpx4-deficient macrophages exhibited enhanced necrosis upon Mtb infection in vitro, an outcome suppressed by the lipid peroxidation inhibitor, ferrostatin-1. These findings provide support for the role of ferroptosis in Mtb-induced necrosis and implicate the Gpx4/GSH axis as a target for host-directed therapy of tuberculosis.
MeSH term(s)	Animals ; Ferroptosis ; Glutathione/metabolism ; Glutathione Peroxidase/metabolism ; Lipid Peroxidation ; Mice ; Mice, Transgenic ; Necrosis ; Phospholipid Hydroperoxide Glutathione Peroxidase ; Tuberculosis/immunology ; Tuberculosis/metabolism
Chemical Substances	Phospholipid Hydroperoxide Glutathione Peroxidase (EC 1.11.1.12) ; Glutathione Peroxidase (EC 1.11.1.9) ; selenium-independent glutathione peroxidase (EC 1.11.1.9) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2022-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20220504
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Zs.MG 45: Show issues

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Article ; Online: T cell-specific P2RX7 favors lung parenchymal CD4

Santiago-Carvalho, Igor / Almeida-Santos, Gislane / Macedo, Bruna Gois / Barbosa-Bomfim, Caio Cesar / Almeida, Fabricio Moreira / Pinheiro Cione, Marcos Vinícios / Vardam-Kaur, Trupti / Masuda, Mia / Van Dijk, Sarah / Melo, Bruno Marcel / Silva do Nascimento, Rogério / da Conceição Souza, Rebeka / Peixoto-Rangel, Alba Lucínia / Coutinho-Silva, Robson / Hirata, Mario Hiroyuki / Alves-Filho, José Carlos / Álvarez, José Maria / Lassounskaia, Elena / Borges da Silva, Henrique /

D'Império-Lima, Maria Regina

Cell reports

2023 Volume 42, Issue 11, Page(s) 113448

Abstract: ... ...

Abstract	CD4
MeSH term(s)	Animals ; Humans ; Mice ; CD4-Positive T-Lymphocytes ; Influenza, Human/metabolism ; Lung/pathology ; Receptors, Chemokine/metabolism ; Tuberculosis/pathology
Chemical Substances	Receptors, Chemokine ; P2rx7 protein, mouse
Language	English
Publishing date	2023-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113448
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Article ; Online: Inhibiting Adenosine Receptor Signaling Promotes Accumulation of Effector CD4+ T Cells in the Lung Parenchyma During Severe Tuberculosis.

Amaral, Eduardo P / Machado de Salles, Érika / Barbosa Bomfim, Caio Cesar / Salgado, Rafael Moysés / Almeida, Fabrício M / de Souza, Paula Carolina / Alvarez, José Maria / Hirata, Mario H / Lasunskaia, Elena B / D'Império-Lima, Maria Regina

The Journal of infectious diseases

2019 Volume 219, Issue 6, Page(s) 964–974

Abstract: Background: Tuberculous pneumonia, necrotic granulomatous lesions, and bacterial dissemination characterize severe forms of mycobacterial infection.: Methods: To evaluate the pulmonary CD4+ T-cell response during severe tuberculosis, C57BL/6 mice ... ...

Abstract	Background: Tuberculous pneumonia, necrotic granulomatous lesions, and bacterial dissemination characterize severe forms of mycobacterial infection. Methods: To evaluate the pulmonary CD4+ T-cell response during severe tuberculosis, C57BL/6 mice were infected with approximately 100 bacilli of 3 hypervirulent mycobacterial isolates (Mycobacterium tuberculosis strain Beijing 1471 and Mycobacterium bovis strains B2 and MP287/03) or the H37Rv M tuberculosis strain as reference for mycobacterial virulence. Because high expression of both CD39 and CD73 ectonucleotidases was detected on parenchymal CD4+ T cells, we investigated whether CD4+ T-cell suppression in the context of severe disease was due to the extracellular adenosine accumulation that resulted from tissue damage. Results: Lowest expression of CD69, which is an activation marker implicated in maintaining cells in tissues, was observed in lungs from mice displaying the most severe pulmonary pathology. Reduced interferon (IFN)γ-producing CD4+ T cells were also found in the lung of these mice. Intranasal administration of the adenosine receptor antagonist caffeine substantially enhanced the frequency and number of parenchymal CD4+ T cells as well as both CD69 expression and IFNγ production. Conclusions: These results indicate that adenosine, which may be generated by extracellular adenosine triphosphate degradation, impairs the parenchymal CD4+ T-cell response and contributes to the development of severe tuberculosis.
MeSH term(s)	5'-Nucleotidase/metabolism ; Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; CD4-Positive T-Lymphocytes/pathology ; Caffeine/pharmacology ; Interferon-gamma/metabolism ; Lectins, C-Type/metabolism ; Lung/microbiology ; Lung/pathology ; Mice, Inbred C57BL ; Mycobacterium bovis/pathogenicity ; Mycobacterium tuberculosis/pathogenicity ; Purinergic P1 Receptor Antagonists/pharmacology ; Receptors, Purinergic P1/metabolism ; Signal Transduction ; Tuberculosis, Pulmonary/microbiology ; Tuberculosis, Pulmonary/pathology
Chemical Substances	Antigens, CD ; Antigens, Differentiation, T-Lymphocyte ; CD69 antigen ; Lectins, C-Type ; Purinergic P1 Receptor Antagonists ; Receptors, Purinergic P1 ; Caffeine (3G6A5W338E) ; Interferon-gamma (82115-62-6) ; 5'-Nucleotidase (EC 3.1.3.5)
Language	English
Publishing date	2019-06-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiy586
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Zs.MO 445: Show issues

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Article ; Online: Harmful Effects of Granulocytic Myeloid-Derived Suppressor Cells on Tuberculosis Caused by Hypervirulent Mycobacteria.

Barbosa Bomfim, Caio César / Pinheiro Amaral, Eduardo / Santiago-Carvalho, Igor / Almeida Santos, Gislane / Machado Salles, Érika / Hastreiter, Araceli Aparecida / Silva do Nascimento, Rogério / Almeida, Fabrício M / Lopes Biá Ventura Simão, Thatiana / Linhares Rezende, Andreza / Hiroyuki Hirata, Mario / Ambrósio Fock, Ricardo / Álvarez, José Maria / Lasunskaia, Elena B / D'Império Lima, Maria Regina

The Journal of infectious diseases

2020 Volume 223, Issue 3, Page(s) 494–507

Abstract: Background: The role of myeloid-derived suppressor cells (MDSCs) in patients with severe tuberculosis who suffer from uncontrolled pulmonary inflammation caused by hypervirulent mycobacterial infection remains unclear.: Methods: This issue was ... ...

Abstract	Background: The role of myeloid-derived suppressor cells (MDSCs) in patients with severe tuberculosis who suffer from uncontrolled pulmonary inflammation caused by hypervirulent mycobacterial infection remains unclear. Methods: This issue was addressed using C57BL/6 mice infected with highly virulent Mycobacterium bovis strain MP287/03. Results: CD11b+GR1int population increased in the bone marrow, blood and lungs during advanced disease. Pulmonary CD11b+GR1int (Ly6GintLy6Cint) cells showed granularity similar to neutrophils and expressed immature myeloid cell markers. These immature neutrophils harbored intracellular bacilli and were preferentially located in the alveoli. T-cell suppression occurred concomitantly with CD11b+GR1int cell accumulation in the lungs. Furthermore, lung and bone marrow GR1+ cells suppressed both T-cell proliferation and interferon γ production in vitro. Anti-GR1 therapy given when MDSCs infiltrated the lungs prevented expansion and fusion of primary pulmonary lesions and the development of intragranulomatous caseous necrosis, along with increased mouse survival and partial recovery of T-cell function. Lung bacterial load was reduced by anti-GR1 treatment, but mycobacteria released from the depleted cells proliferated extracellularly in the alveoli, forming cords and clumps. Conclusions: Granulocytic MDSCs massively infiltrate the lungs during infection with hypervirulent mycobacteria, promoting bacterial growth and the development of inflammatory and necrotic lesions, and are promising targets for host-directed therapies.
MeSH term(s)	Animals ; Antigens, Ly ; Bone Marrow ; CD11b Antigen ; Cell Proliferation ; Disease Models, Animal ; Granulocytes/immunology ; Immunomodulation ; Lung/metabolism ; Lung/pathology ; Mice ; Mice, Inbred C57BL ; Mycobacterium bovis/pathogenicity ; Myeloid Cells ; Myeloid-Derived Suppressor Cells/immunology ; Myeloid-Derived Suppressor Cells/pathology ; Neutrophils ; Tuberculosis/pathology
Chemical Substances	Antigens, Ly ; CD11b Antigen ; Itgam protein, mouse ; Ly6G antigen, mouse
Language	English
Publishing date	2020-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiaa708
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Article ; Online: Human CD40 ligand deficiency dysregulates the macrophage transcriptome causing functional defects that are improved by exogenous IFN-γ.

Cabral-Marques, Otavio / Ramos, Rodrigo Nalio / Schimke, Lena F / Khan, Taj Ali / Amaral, Eduardo Pinheiro / Barbosa Bomfim, Caio César / Junior, Osvaldo Reis / França, Tabata Takahashi / Arslanian, Christina / Carola Correia Lima, Joanna Darck / Weber, Cristina Worm / Ferreira, Janaíra Fernandes / Tavares, Fabiola Scancetti / Sun, Jing / D'Imperio Lima, Maria Regina / Seelaender, Marília / Garcia Calich, Vera Lucia / Marzagão Barbuto, José Alexandre / Costa-Carvalho, Beatriz Tavares /

Riemekasten, Gabriela / Seminario, Gisela / Bezrodnik, Liliana / Notarangelo, Luigi / Torgerson, Troy R / Ochs, Hans D / Condino-Neto, Antonio

The Journal of allergy and clinical immunology

2017 Volume 139, Issue 3, Page(s) 900–912.e7

Abstract: Background: CD40 ligand (CD40L) deficiency predisposes to opportunistic infections, including those caused by fungi and intracellular bacteria. Studies of CD40L-deficient patients reveal the critical role of CD40L-CD40 interaction for the function of T, ...

Abstract	Background: CD40 ligand (CD40L) deficiency predisposes to opportunistic infections, including those caused by fungi and intracellular bacteria. Studies of CD40L-deficient patients reveal the critical role of CD40L-CD40 interaction for the function of T, B, and dendritic cells. However, the consequences of CD40L deficiency on macrophage function remain to be investigated. Objectives: We sought to determine the effect of CD40L absence on monocyte-derived macrophage responses. Methods: After observing the improvement of refractory disseminated mycobacterial infection in a CD40L-deficient patient by recombinant human IFN-γ (rhIFN-γ) adjuvant therapy, we investigated macrophage functions from CD40L-deficient patients. We analyzed the killing activity, oxidative burst, cytokine production, and in vitro effects of rhIFN-γ and soluble CD40 ligand (sCD40L) treatment on macrophages. In addition, the effect of CD40L absence on the macrophage transcriptome before and after rhIFN-γ treatment was studied. Results: Macrophages from CD40L-deficient patients exhibited defective fungicidal activity and reduced oxidative burst, both of which improved in the presence of rhIFN-γ but not sCD40L. In contrast, rhIFN-γ and sCD40L ameliorate impaired production of inflammatory cytokines. Furthermore, rhIFN-γ reversed defective control of Mycobacterium tuberculosis proliferation by patients' macrophages. The absence of CD40L dysregulated the macrophage transcriptome, which was improved by rhIFN-γ. Additionally, rhIFN-γ increased expression levels of pattern recognition receptors, such as Toll-like receptors 1 and 2, dectin 1, and dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin in macrophages from both control subjects and patients. Conclusion: Absence of CD40L impairs macrophage development and function. In addition, the improvement of macrophage immune responses by IFN-γ suggests this cytokine as a potential therapeutic option for patients with CD40L deficiency.
MeSH term(s)	Adolescent ; Adult ; CD40 Ligand/deficiency ; Cells, Cultured ; Child ; Child, Preschool ; Humans ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology ; Immunologic Deficiency Syndromes/metabolism ; Interferon-gamma/pharmacology ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/physiology ; Male ; Monocytes/cytology ; Mycobacterium tuberculosis ; Phagocytosis ; Transcriptome/drug effects ; Young Adult
Chemical Substances	CD40 Ligand (147205-72-9) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2017-03
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2016.07.018
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Article ; Online: TRPV1 activation in human Langerhans cells and T cells inhibits mucosal HIV-1 infection via CGRP-dependent and independent mechanisms.

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Article ; Online: CGRP inhibits SARS-CoV-2 infection of bronchial epithelial cells and its pulmonary levels correlate with viral clearance in critical COVID-19 patients

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Article ; Online: CGRP inhibits SARS-CoV-2 infection of bronchial epithelial cells and its pulmonary levels correlate with viral clearance in critical COVID-19 patients

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Article ; Online: GPX4 regulates cellular necrosis and host resistance in Mycobacterium tuberculosis infection.

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Article ; Online: T cell-specific P2RX7 favors lung parenchymal CD4

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Article ; Online: Inhibiting Adenosine Receptor Signaling Promotes Accumulation of Effector CD4+ T Cells in the Lung Parenchyma During Severe Tuberculosis.

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Article ; Online: Harmful Effects of Granulocytic Myeloid-Derived Suppressor Cells on Tuberculosis Caused by Hypervirulent Mycobacteria.

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Article ; Online: Human CD40 ligand deficiency dysregulates the macrophage transcriptome causing functional defects that are improved by exogenous IFN-γ.

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