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5. Editorial: Immune responses to MTB infection in people living with HIV.

Author

Anes, Elsa and Amogne, Wondwossen

Subjects
LATENT tuberculosis, EXTRAPULMONARY tuberculosis, LATENT infection, CELL metabolism, REGULATORY T cells
Abstract

The editorial discusses the immune responses to Mycobacterium tuberculosis (Mtb) infection in people living with HIV (PLWH). It highlights the distinct immune responses observed in individuals infected with Mtb, HIV, or both, and the implications for the development of tuberculosis (TB) in PLWH. The article also explores the impact of vitamin D deficiency on the risk of active TB in HIV-infected individuals and investigates the heterogeneity of granulocyte populations in PLWH. Additionally, it discusses the potential therapeutic role of exosomes in HIV-1 pathogenesis and the development of novel diagnostic tools and interventions for controlling infections in PLWH. [Extracted from the article]

Published
2024
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7. Cystatin F Depletion in Mycobacterium tuberculosis -Infected Macrophages Improves Cathepsin C/Granzyme B-Driven Cytotoxic Effects on HIV-Infected Cells during Coinfection.

Author

Mandal, Manoj, Pires, David, Calado, Marta, Azevedo-Pereira, José Miguel, and Anes, Elsa

Subjects
CYSTEINE proteinase inhibitors, MYCOBACTERIUM tuberculosis, PHAGOCYTES, MYCOBACTERIAL diseases, GRANZYMES
Abstract

Cystatin F (CstF) is a protease inhibitor of cysteine cathepsins, including those involved in activating the perforin/granzyme cytotoxic pathways. It is targeted at the endolysosomal pathway but can also be secreted to the extracellular milieu or endocytosed by bystander cells. CstF was shown to be significantly increased in tuberculous pleurisy, and during HIV coinfection, pleural fluids display high viral loads. In human macrophages, our previous results revealed a strong upregulation of CstF in phagocytes activated by interferon γ or after infection with Mycobacterium tuberculosis (Mtb). CstF manipulation using RNA silencing led to increased proteolytic activity of lysosomal cathepsins, improving Mtb intracellular killing. In the present work, we investigate the impact of CstF depletion in macrophages during the coinfection of Mtb-infected phagocytes with lymphocytes infected with HIV. The results indicate that decreasing the CstF released by phagocytes increases the major pro-granzyme convertase cathepsin C of cytotoxic immune cells from peripheral blood-derived lymphocytes. Consequently, an observed augmentation of the granzyme B cytolytic activity leads to a significant reduction in viral replication in HIV-infected CD4+ T-lymphocytes. Ultimately, this knowledge can be crucial for developing new therapeutic approaches to control both pathogens based on manipulating CstF. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Role of Type I Interferons during Mycobacterium tuberculosis and HIV Infections.

Author

Anes, Elsa, Azevedo-Pereira, José Miguel, and Pires, David

Subjects
*TYPE I interferons, *HIV infections, *MYCOBACTERIUM tuberculosis, *COMMUNICABLE diseases, *INTERFERONS
Abstract

Tuberculosis and AIDS remain two of the most relevant human infectious diseases. The pathogens that cause them, Mycobacterium tuberculosis (Mtb) and HIV, individually elicit an immune response that treads the line between beneficial and detrimental to the host. Co-infection further complexifies this response since the different cytokines acting on one infection might facilitate the dissemination of the other. In these responses, the role of type I interferons is often associated with antiviral mechanisms, while for bacteria such as Mtb, their importance and clinical relevance as a suitable target for manipulation are more controversial. In this article, we review the recent knowledge on how these interferons play distinct roles and sometimes have opposite consequences depending on the stage of the pathogenesis. We highlight the dichotomy between the acute and chronic infections displayed by both infections and how type I interferons contribute to an initial control of each infection individually, while their chronic induction, particularly during HIV infection, might facilitate Mtb primo-infection and progression to disease. We expect that further findings and their systematization will allow the definition of windows of opportunity for interferon manipulation according to the stage of infection, contributing to pathogen clearance and control of immunopathology. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Unravelling the triad of neuroinvasion, neurodissemination, and neuroinflammation of human immunodeficiency virus type 1 in the central nervous system.

Author

Calado, Marta, Ferreira, Rita, Pires, David, Santos‐Costa, Quirina, Anes, Elsa, Brites, Dora, and Azevedo‐Pereira, José Miguel

Abstract

Since the identification of human immunodeficiency virus type 1 (HIV‐1) in 1983, many improvements have been made to control viral replication in the peripheral blood and to treat opportunistic infections. This has increased life expectancy but also the incidence of age‐related central nervous system (CNS) disorders and HIV‐associated neurodegeneration/neurocognitive impairment and depression collectively referred to as HIV‐associated neurocognitive disorders (HAND). HAND encompasses a spectrum of different clinical presentations ranging from milder forms such as asymptomatic neurocognitive impairment or mild neurocognitive disorder to a severe HIV‐associated dementia (HAD). Although control of viral replication and suppression of plasma viral load with combination antiretroviral therapy has reduced the incidence of HAD, it has not reversed milder forms of HAND. The objective of this review, is to describe the mechanisms by which HIV‐1 invades and disseminates in the CNS, a crucial event leading to HAND. The review will present the evidence that underlies the relationship between HIV infection and HAND. Additionally, recent findings explaining the role of neuroinflammation in the pathogenesis of HAND will be discussed, along with prospects for treatment and control. [ABSTRACT FROM AUTHOR]

Published
2024
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28. Liposomal Delivery of Newly Identified Prophage Lysins in a Pseudomonas aeruginosa Model

Author

Morais, Diana, primary, Tanoeiro, Luís, additional, Marques, Andreia, additional, Gonçalves, Tiago, additional, Duarte, Aida, additional, Matos, António, additional, Vital, Joana, additional, Cruz, Maria, additional, Carvalheiro, Manuela, additional, Anes, Elsa, additional, Vítor, Jorge, additional, Gaspar, Maria, additional, and Vale, Filipa, additional

Published
2022
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33. Modulation of Cystatin C in Human Macrophages Improves Anti-Mycobacterial Immune Responses to Mycobacterium tuberculosis Infection and Coinfection With HIV

Author

Pires, David, primary, Calado, Marta, additional, Velez, Tomás, additional, Mandal, Manoj, additional, Catalão, Maria João, additional, Neyrolles, Olivier, additional, Lugo-Villarino, Geanncarlo, additional, Vérollet, Christel, additional, Azevedo-Pereira, José Miguel, additional, and Anes, Elsa, additional

Published
2021
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43. Acting on Actin During Bacterial Infection

Author

Anes, Elsa

Subjects
Science / Life Sciences / Cell Biology
Abstract

Bacterial resistance to antibiotics is becoming a major threat to public health. It is imperative to find new therapeutic interventions to fight pathogens. Thus, deciphering host-pathogen interactions may allow defining targets for new strategies for effective treatments of infectious diseases. This chapter focuses on the bacterial manipulation of the host cell actin cytoskeleton. We discuss three infectious processes. The first is pathogen establishment of infection/invasion, explaining cellular uptake pathways that rely on actin, such as phagocytosis and macropinocytosis. The second process focus on the establishment of a replication niche, a process that subverts cytoskeletal functions associated with membrane trafficking namely phagosome maturation and cellular innate immune responses. Finally, pathogen dissemination is an emerging field that microfilaments have shown to participate: pathogen motility through the cytoplasm and from cell-to-cell or on the outer surface of the plasma membrane mimicking a receptor tyrosine kinase signaling pathway that helps the projection of pathogens to neighboring cells. It also establishes a connection with the innate immunity related with induction of cell signaling to inflammation, inflammasome activation, and programmed cell death. These studies revealed several potential targets related to actin cytoskeleton manipulation to design new therapeutic strategies for bacterial infections.

Published
2017

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