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Article ; Online: Advances on the Role and Applications of Interleukin-1 in Tuberculosis.

Silvério, Diogo / Gonçalves, Rute / Appelberg, Rui / Saraiva, Margarida

2021 Volume 12, Issue 6, Page(s) e0313421

Abstract: Interleukin-1 (IL-1) is a key player in the immune response to pathogens due to its role in promoting inflammation and recruiting immune cells to the site of infection. In tuberculosis (TB), tight regulation of IL-1 responses is critical to ensure host ... ...

Abstract	Interleukin-1 (IL-1) is a key player in the immune response to pathogens due to its role in promoting inflammation and recruiting immune cells to the site of infection. In tuberculosis (TB), tight regulation of IL-1 responses is critical to ensure host resistance to infection while preventing immune pathology. In the mouse model of Mycobacterium tuberculosis infection, both IL-1 absence and overproduction result in exacerbated disease and mortality. In humans, several polymorphisms in the
MeSH term(s)	Animals ; Antitubercular Agents/therapeutic use ; Genetic Predisposition to Disease ; Humans ; Interleukin-1/antagonists & inhibitors ; Interleukin-1/genetics ; Interleukin-1/immunology ; Mycobacterium tuberculosis/drug effects ; Mycobacterium tuberculosis/physiology ; Polymorphism, Genetic ; Tuberculosis/drug therapy ; Tuberculosis/genetics ; Tuberculosis/immunology ; Tuberculosis/microbiology
Chemical Substances	Antitubercular Agents ; Interleukin-1
Language	English
Publishing date	2021-11-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.03134-21
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Article: Neutrophils and intracellular pathogens: beyond phagocytosis and killing.

Appelberg, Rui

Trends in microbiology

2007 Volume 15, Issue 2, Page(s) 87–92

Abstract: Neutrophils are not simply scavenging phagocytes that clear extracellular spaces of rapidly proliferating microbes; they are also active in the control of infections by intracellular pathogens. Several mechanisms for nonphagocytic roles of neutrophils in ...

Abstract	Neutrophils are not simply scavenging phagocytes that clear extracellular spaces of rapidly proliferating microbes; they are also active in the control of infections by intracellular pathogens. Several mechanisms for nonphagocytic roles of neutrophils in protective immunity have been put forth over the years but further evidence has recently been accumulating at an increasing pace. In this review, I present the evidence that suggests neutrophils are involved in pathogen shuttling into the lymphoid tissues, in antigen presentation, and in early T cell recruitment and initiation of granuloma organization. Also, a clearer view on the antimicrobial molecules that can be acquired by macrophages to enhance their antimicrobial activity is now emerging. Finally, neutrophils can adversely affect immunity against certain parasites by causing immune deviation.
MeSH term(s)	Animals ; Bacterial Infections/immunology ; Biological Transport ; Cytoplasmic Granules/metabolism ; Humans ; Lymphoid Tissue/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Neutrophils/immunology ; Parasitic Diseases/immunology ; Phagocytosis
Language	English
Publishing date	2007-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1158963-2
ISSN	1878-4380 ; 0966-842X
ISSN (online)	1878-4380
ISSN	0966-842X
DOI	10.1016/j.tim.2006.11.009
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Article: Pathogenesis of Mycobacterium avium infection: typical responses to an atypical mycobacterium?

Appelberg, Rui

Immunologic research

2006 Volume 35, Issue 3, Page(s) 179–190

Abstract: Studying infections with Mycobacterium avium in mouse models has allowed the dissection of the antimycobacterial pathways of the mammalian host. Whereas the paradigm of cell-mediated immunity to intracellular pathogens has been confirmed, namely with ... ...

Abstract	Studying infections with Mycobacterium avium in mouse models has allowed the dissection of the antimycobacterial pathways of the mammalian host. Whereas the paradigm of cell-mediated immunity to intracellular pathogens has been confirmed, namely with regard to the pivotal roles of CD4+ T cells, macrophages, and the IL12-IFNgamma cytokine axis, atypical features have been uncovered such as the resistance to NO, the involvement of minor players in the induction of type 1 protective immunity (such as TLR2, CD40, and CD30), and the development of immunopathology during the infection with highly virulent strains such as the development of caseous necrosis of granulomas or the progressive emergence of severe lymphopenia.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Macrophages/immunology ; Macrophages/microbiology ; Mice ; Mycobacterium Infections, Nontuberculous/immunology ; Mycobacterium avium/immunology ; Mycobacterium avium Complex/immunology ; Tuberculosis/immunology ; Tuberculosis/veterinary
Language	English
Publishing date	2006
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632857-x
ISSN	1559-0755 ; 0257-277X
ISSN (online)	1559-0755
ISSN	0257-277X
DOI	10.1385/IR:35:3:179
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Zs.A 1755: Show issues

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Article: Macrophage nutriprive antimicrobial mechanisms.

Appelberg, Rui

Journal of leukocyte biology

2006 Volume 79, Issue 6, Page(s) 1117–1128

Abstract: In addition to oxidative and antibiotic mechanisms of antimicrobial activity, macrophages are able to deprive intracellular pathogens of required nutrients. Thus, microbial killing may not rely only in the toxic environment the microbe reaches but also ... ...

Abstract	In addition to oxidative and antibiotic mechanisms of antimicrobial activity, macrophages are able to deprive intracellular pathogens of required nutrients. Thus, microbial killing may not rely only in the toxic environment the microbe reaches but also may result from the scarcity of nutrients in the cellular compartment it occupies. Here, we analyze evidence for such nutriprive (from the latin privare, to deprive of nutrients), antimicrobial mechanisms. Although the direct analysis of nutrient availability is most often not feasible, indirect evidence of lack of nutrients in the microbial organelles has been inferred from the study of mutants, the analysis of gene expression, and the consequences of changing the intracellular location of the pathogen. We propose that according to the microbe and its survival strategy, different mechanisms to impede access to nutrients may be constitutively present or may be induced by cytokines and other pathways. Thus, membrane transporters may remove nutrients from vacuolar compartments, and enzymes may degrade some growth factors. A series of diverse compounds may sequester other molecules required for microbial growth, as exemplified by the action of iron chelators. Modulation of vesicular trafficking may prevent the fusion of certain vesicles containing nutrients with those containing the pathogen, counteracting the evasion strategies of the pathogen. The understanding of these mechanisms will certainly help in designing new therapeutic and prophylactic approaches to preventing infectious diseases.
MeSH term(s)	Amino Acids/metabolism ; Animals ; Bacteria/growth & development ; Bacteria/metabolism ; Bacterial Infections/physiopathology ; Biological Transport ; Cholesterol/metabolism ; Cytoplasmic Vesicles/physiology ; Eukaryota/genetics ; Eukaryota/metabolism ; Eukaryotic Cells/metabolism ; Eukaryotic Cells/microbiology ; Eukaryotic Cells/parasitology ; Heterocyclic Compounds/metabolism ; Host-Parasite Interactions ; Humans ; Interferon-gamma/pharmacology ; Interferon-gamma/physiology ; Intracellular Fluid/metabolism ; Iron/metabolism ; Macrophage Activation/drug effects ; Macrophages/physiology ; Mice ; Phagocytosis ; Phosphates/metabolism ; Protozoan Infections/physiopathology ; Trace Elements/metabolism ; Vacuoles/physiology
Chemical Substances	Amino Acids ; Heterocyclic Compounds ; Phosphates ; Trace Elements ; Interferon-gamma (82115-62-6) ; Cholesterol (97C5T2UQ7J) ; Iron (E1UOL152H7)
Language	English
Publishing date	2006-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0206079
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Article ; Online: Systems-level temporal immune-metabolic profile in Crimean-Congo hemorrhagic fever virus infection.

Ambikan, Anoop T / Elaldi, Nazif / Svensson-Akusjärvi, Sara / Bagci, Binnur / Pektas, Ayse Nur / Hewson, Roger / Bagci, Gokhan / Arasli, Mehmet / Appelberg, Sofia / Mardinoglu, Adil / Sood, Vikas / Végvári, Ákos / Benfeitas, Rui / Gupta, Soham / Cetin, Ilhan / Mirazimi, Ali / Neogi, Ujjwal

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

2023 Volume 120, Issue 37, Page(s) e2304722120

Abstract: Crimean-Congo hemorrhagic fever (CCHF) caused by CCHF virus (CCHFV) is one of the epidemic-prone diseases prioritized by the World Health Organisation as public health emergency with an urgent need for accelerated research. The trajectory of host ... ...

Abstract	Crimean-Congo hemorrhagic fever (CCHF) caused by CCHF virus (CCHFV) is one of the epidemic-prone diseases prioritized by the World Health Organisation as public health emergency with an urgent need for accelerated research. The trajectory of host response against CCHFV is multifarious and remains unknown. Here, we reported the temporal spectrum of pathogenesis following the CCHFV infection using genome-wide blood transcriptomics analysis followed by advanced systems biology analysis, temporal immune-pathogenic alterations, and context-specific progressive and postinfection genome-scale metabolic models (GSMM) on samples collected during the acute (T0), early convalescent (T1), and convalescent-phase (T2). The interplay between the retinoic acid-inducible gene-I-like/nucleotide-binding oligomerization domain-like receptor and tumor necrosis factor signaling governed the trajectory of antiviral immune responses. The rearrangement of intracellular metabolic fluxes toward the amino acid metabolism and metabolic shift toward oxidative phosphorylation and fatty acid oxidation during acute CCHFV infection determine the pathogenicity. The upregulation of the tricarboxylic acid cycle during CCHFV infection, compared to the noninfected healthy control and between the severity groups, indicated an increased energy demand and cellular stress. The upregulation of glycolysis and pyruvate metabolism potentiated energy generation through alternative pathways associated with the severity of the infection. The downregulation of metabolic processes at the convalescent phase identified by blood cell transcriptomics and single-cell type proteomics of five immune cells (CD4
MeSH term(s)	Humans ; Hemorrhagic Fever Virus, Crimean-Congo ; Hemorrhagic Fever, Crimean ; CD8-Positive T-Lymphocytes ; Up-Regulation ; Metabolome
Language	English
Publishing date	2023-09-05
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.2304722120
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Zs.A 1148: Show issues

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Article ; Online: Antimicrobial peptides as novel anti-tuberculosis therapeutics.

Silva, João P / Appelberg, Rui / Gama, Francisco Miguel

Biotechnology advances

2016 Volume 34, Issue 5, Page(s) 924–940

Abstract: Tuberculosis (TB), a disease caused by the human pathogen Mycobacterium tuberculosis, has recently joined HIV/AIDS as the world's deadliest infectious disease, affecting around 9.6 million people worldwide in 2014. Of those, about 1.2 million died from ... ...

Abstract	Tuberculosis (TB), a disease caused by the human pathogen Mycobacterium tuberculosis, has recently joined HIV/AIDS as the world's deadliest infectious disease, affecting around 9.6 million people worldwide in 2014. Of those, about 1.2 million died from the disease. Resistance acquisition to existing antibiotics, with the subsequent emergence of Multi-Drug Resistant mycobacteria strains, together with an increasing economic burden, has urged the development of new anti-TB drugs. In this scope, antimicrobial peptides (AMPs), which are small, cationic and amphipathic peptides that make part of the innate immune system, now arise as promising candidates for TB treatment. In this review, we analyze the potential of AMPs for this application. We address the mechanisms of action, advantages and disadvantages over conventional antibiotics and how problems associated with its use may be overcome to boost their therapeutic potential. Additionally, we address the challenges of translational development from benchside to bedside, evaluate the current development pipeline and analyze the expected global impact from a socio-economic standpoint. The quest for more efficient and more compliant anti-TB drugs, associated with the great therapeutic potential of emerging AMPs and the rising peptide market, provide an optimal environment for the emergence of AMPs as promising therapies. Still, their pharmacological properties need to be enhanced and manufacturing-associated issues need to be addressed.
Language	English
Publishing date	2016-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	47165-3
ISSN	1873-1899 ; 0734-9750
ISSN (online)	1873-1899
ISSN	0734-9750
DOI	10.1016/j.biotechadv.2016.05.007
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Zs.A 3730: Show issues

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Article ; Online: TNF-Mediated Compensatory Immunity to

Resende, Mariana / Cardoso, Marcos S / Fróis-Martins, Ricardo / Borges, Margarida / Jordan, Michael B / Castro, António Gil / Appelberg, Rui

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 203, Issue 9, Page(s) 2451–2458

Abstract: Granuloma formation is a hallmark of several infectious diseases, including those caused ... ...

Abstract	Granuloma formation is a hallmark of several infectious diseases, including those caused by
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/physiology ; Granuloma/etiology ; Interferon-gamma/physiology ; Macrophage Activation/immunology ; Mice ; Mice, Inbred C57BL ; Mycobacterium avium/immunology ; Signal Transduction ; Tumor Necrosis Factor-alpha/physiology
Chemical Substances	Tumor Necrosis Factor-alpha ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2019-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1801594
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Article ; Online: IFNγ and iNOS-Mediated Alterations in the Bone Marrow and Thymus and Its Impact on

Barreira-Silva, Palmira / Melo-Miranda, Rita / Nobrega, Claudia / Roque, Susana / Serre-Miranda, Cláudia / Borges, Margarida / Armada, Gisela / de Sá Calçada, Daniela / Behar, Samuel M / Appelberg, Rui / Correia-Neves, Margarida

Frontiers in immunology

2021 Volume 12, Page(s) 696415

Abstract: Disseminated infection with the high virulence strain ... ...

Abstract	Disseminated infection with the high virulence strain of
MeSH term(s)	Animals ; Apoptosis ; Atrophy ; Bone Marrow/pathology ; Bone Marrow Transplantation ; Cell Differentiation ; DNA-Binding Proteins/deficiency ; Female ; Interferon-gamma/physiology ; Lymphoid Progenitor Cells/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mycobacterium avium ; Nitric Oxide/physiology ; Nitric Oxide Synthase Type II/physiology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/pathology ; Thymocytes/pathology ; Thymus Gland/pathology ; Thymus Gland/transplantation ; Tuberculosis/immunology ; Tuberculosis/pathology
Chemical Substances	DNA-Binding Proteins ; Rag2 protein, mouse ; Nitric Oxide (31C4KY9ESH) ; Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2021-12-20
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.696415
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Article ; Online: Multi-omics insights into host-viral response and pathogenesis in Crimean-Congo hemorrhagic fever viruses for novel therapeutic target.

Neogi, Ujjwal / Elaldi, Nazif / Appelberg, Sofia / Ambikan, Anoop / Kennedy, Emma / Dowall, Stuart / Bagci, Binnur K / Gupta, Soham / Rodriguez, Jimmy E / Svensson-Akusjärvi, Sara / Monteil, Vanessa / Vegvari, Akos / Benfeitas, Rui / Banerjea, Akhil / Weber, Friedemann / Hewson, Roger / Mirazimi, Ali

eLife

2022 Volume 11

Abstract: The pathogenesis and host-viral interactions of the Crimean-Congo hemorrhagic fever orthonairovirus (CCHFV) are convoluted and not well evaluated. Application of the multi-omics system biology approaches, including biological network analysis in ... ...

Abstract	The pathogenesis and host-viral interactions of the Crimean-Congo hemorrhagic fever orthonairovirus (CCHFV) are convoluted and not well evaluated. Application of the multi-omics system biology approaches, including biological network analysis in elucidating the complex host-viral response, interrogates the viral pathogenesis. The present study aimed to fingerprint the system-level alterations during acute CCHFV-infection and the cellular immune responses during productive CCHFV-replication in vitro. We used system-wide network-based system biology analysis of peripheral blood mononuclear cells (PBMCs) from a longitudinal cohort of CCHF patients during the acute phase of infection and after one year of recovery (convalescent phase) followed by untargeted quantitative proteomics analysis of the most permissive CCHFV-infected Huh7 and SW13 cells. In the RNAseq analysis of the PBMCs, comparing the acute and convalescent-phase, we observed system-level host's metabolic reprogramming towards central carbon and energy metabolism (CCEM) with distinct upregulation of oxidative phosphorylation (OXPHOS) during CCHFV-infection. Upon application of network-based system biology methods, negative coordination of the biological signaling systems like FOXO/Notch axis and Akt/mTOR/HIF-1 signaling with metabolic pathways during CCHFV-infection were observed. The temporal quantitative proteomics in Huh7 showed a dynamic change in the CCEM over time and concordant with the cross-sectional proteomics in SW13 cells. By blocking the two key CCEM pathways, glycolysis and glutaminolysis, viral replication was inhibited in vitro. Activation of key interferon stimulating genes during infection suggested the role of type I and II interferon-mediated antiviral mechanisms both at the system level and during progressive replication.
MeSH term(s)	Antiviral Agents/therapeutic use ; Cross-Sectional Studies ; Hemorrhagic Fever Virus, Crimean-Congo/genetics ; Hemorrhagic Fever, Crimean ; Humans ; Interferons ; Leukocytes, Mononuclear
Chemical Substances	Antiviral Agents ; Interferons (9008-11-1)
Language	English
Publishing date	2022-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.76071
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Article ; Online: Myeloid HIF-1α regulates pulmonary inflammation during experimental Mycobacterium tuberculosis infection.

Resende, Mariana / Ferreira, Catarina M / Barbosa, Ana Margarida / Cardoso, Marcos S / Sousa, Jeremy / Saraiva, Margarida / Castro, António G / Appelberg, Rui / Torrado, Egídio

Immunology

2019 Volume 159, Issue 1, Page(s) 121–129

Abstract: The transcription factor hypoxia-inducible factor-1 alpha (HIF-1α) is a key regulator of the response and function of myeloid cells in hypoxic and inflammatory microenvironments. To define the role of HIF-1α in tuberculosis, the progression of aerosol ... ...

Abstract	The transcription factor hypoxia-inducible factor-1 alpha (HIF-1α) is a key regulator of the response and function of myeloid cells in hypoxic and inflammatory microenvironments. To define the role of HIF-1α in tuberculosis, the progression of aerosol Mycobacterium tuberculosis infection was analysed in mice deficient in HIF-1α in the myeloid lineage (mHIF-1α
MeSH term(s)	Animals ; Bacterial Load ; Cells, Cultured ; Disease Models, Animal ; Disease Progression ; Host-Pathogen Interactions ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Lung/immunology ; Lung/metabolism ; Lung/microbiology ; Mice, Inbred C57BL ; Mice, Knockout ; Mycobacterium tuberculosis/growth & development ; Mycobacterium tuberculosis/immunology ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Myeloid Cells/microbiology ; Pneumonia/genetics ; Pneumonia/immunology ; Pneumonia/metabolism ; Pneumonia/microbiology ; Signal Transduction ; Tuberculosis, Pulmonary/genetics ; Tuberculosis, Pulmonary/immunology ; Tuberculosis, Pulmonary/metabolism ; Tuberculosis, Pulmonary/microbiology
Chemical Substances	Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2019-11-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.13131
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