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Article ; Online: Editorial: The Skin Immune Response to Infectious Agents.

Conceição-Silva, Fatima / Morgado, Fernanda N / Pinheiro, Roberta O / Tacchini-Cottier, Fabienne

2022 Volume 12, Page(s) 810059

MeSH term(s)	Animals ; Disease Susceptibility/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity ; Skin Diseases, Infectious/etiology ; Skin Diseases, Infectious/metabolism ; Skin Physiological Phenomena/immunology
Language	English
Publishing date	2022-01-12
Publishing country	Switzerland
Document type	Editorial ; Introductory Journal Article ; 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.2021.810059
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Article ; Online: The red flags of ulnar neuropathy in leprosy.

Jardim, Márcia / Vital, Robson T / Illarramendi, Ximena / Hacker, Mariana / Junqueira, Beatriz / Pitta, Izabela J R / Pinheiro, Roberta O / Sarno, Euzenir N

PloS one

2021 Volume 16, Issue 11, Page(s) e0259804

Abstract: The diagnosis of pure neural leprosy is more challenging because patients share characteristics with other common pathologies, such as ulnar compression, which should be taken into consideration for differential diagnosis. In this study, we identify ... ...

Abstract	The diagnosis of pure neural leprosy is more challenging because patients share characteristics with other common pathologies, such as ulnar compression, which should be taken into consideration for differential diagnosis. In this study, we identify ulnar nerve conduction characteristics to aid in the differential diagnosis of ulnar neuropathy (UN) in leprosy and that of non-leprosy etiology. In addition, we include putative markers to better understand the inflammatory process that may occur in the nerve. Data were extracted from a database of people affected by leprosy (leprosy group) diagnosed with UN at leprosy diagnosis. A non-leprosy group of patients diagnosed with mechanical neuropathy (compressive, traumatic) was also included. Both groups were submitted to clinical, neurological, neurophysiological and immunological studies. Nerve enlargement and sensory impairment were significantly higher in leprosy patients than in patients with compressive UN. Bilateral impairment was significantly higher in the leprosy group than in the non-leprosy group. Leprosy reactions were associated to focal demyelinating lesions at the elbow and to temporal dispersion (TD). Clinical signs such as sensory impairment, nerve enlargement and bilateral ulnar nerve injury associated with eletrodiagnostic criteria such as demyelinating finds, specifically temporal dispersion, could be tools to help us decided on the best conduct in patients with elbow ulnar neuropathy and specifically decide if we should perform a nerve biopsy for diagnosis of pure neural leprosy.
MeSH term(s)	Adolescent ; Adult ; Aged ; Biomarkers ; Brazil/epidemiology ; Cross-Sectional Studies ; Data Management ; Databases, Factual ; Diagnosis, Differential ; Elbow Joint ; Female ; Humans ; Leprosy/diagnosis ; Leprosy/metabolism ; Leprosy, Tuberculoid ; Male ; Middle Aged ; Neural Conduction ; Ulnar Nerve/metabolism ; Ulnar Neuropathies/diagnosis ; Ulnar Neuropathies/physiopathology
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-11-19
Publishing country	United States
Document type	Journal Article ; Observational Study
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0259804
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Article ; Online: Oligomeric α-Synuclein induces skin degeneration in reconstructed human epidermis.

Oliveira, Júlia T / Dakic, Vanja / Vitória, Gabriela / Pedrosa, Carolina da S G / Mendes, Mayara / Aragão, Luiz Guilherme H S / Cardim-Pires, Thyago R / Lelièvre, Damien / Furtado, Daniel Rodrigues / Pinheiro, Roberta O / Foguel, Débora / Breton, Lionel / Bouez, Charbel / De Vecchi, Rodrigo / Guimarães, Marília Zaluar P / Rehen, Stevens

Neurobiology of aging

2022 Volume 113, Page(s) 108–117

Abstract: Aged and photoaged skin exhibit fine wrinkles that are signs of epidermal inflammation and degeneration. It has been shown that healthy elderly skin expresses amyloidogenic proteins, including α-Synuclein, which are known to oligomerize and trigger ... ...

Abstract	Aged and photoaged skin exhibit fine wrinkles that are signs of epidermal inflammation and degeneration. It has been shown that healthy elderly skin expresses amyloidogenic proteins, including α-Synuclein, which are known to oligomerize and trigger inflammation and neurodegeneration. However, little is known about their putative role in skin physiology and sensitivity. To unravel this possible role, we investigated the impact of oligomeric α-Synuclein (Oα-Syn) in 2D and 3D keratinocyte human models. Exogenous Oα-Syn caused degeneration of reconstructed human epidermis (RHE) by diminishing proliferation and thickness of the stratum basale. Oα-Syn also increased NF-kB nuclear translocation in keratinocytes and triggered inflammation in the RHE, by increasing expression of interleukin-1β and tumor necrosis factor-alpha, and the release of tumor necrosis factor-alpha in a time-dependent manner. Dexamethasone and an IL-1β inhibitor partially diminished RHE degeneration caused by Oα-Syn. These findings suggest that Oα-Syn induces epidermal inflammation and decreases keratinocyte proliferation, and therefore might contribute to epidermal degeneration observed in human skin aging.
MeSH term(s)	Aged ; Epidermis/metabolism ; Epidermis/pathology ; Humans ; Inflammation/metabolism ; Keratinocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; alpha-Synuclein
Language	English
Publishing date	2022-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2022.02.010
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Article ; Online: Mycobacterium leprae induces a tolerogenic profile in monocyte-derived dendritic cells via TLR2 induction of IDO.

Oliveira, Jéssica A P / Gandini, Mariana / Sales, Jorgenilce S / Fujimori, Sérgio K / Barbosa, Mayara G M / Frutuoso, Valber S / Moraes, Milton O / Sarno, Euzenir N / Pessolani, Maria C V / Pinheiro, Roberta O

Journal of leukocyte biology

2020 Volume 110, Issue 1, Page(s) 167–176

Abstract: The enzyme IDO-1 is involved in the first stage of tryptophan catabolism and has been described in both microbicidal and tolerogenic microenvironments. Previous data from our group have shown that IDO-1 is differentially regulated in the distinctive ... ...

Abstract	The enzyme IDO-1 is involved in the first stage of tryptophan catabolism and has been described in both microbicidal and tolerogenic microenvironments. Previous data from our group have shown that IDO-1 is differentially regulated in the distinctive clinical forms of leprosy. The present study aims to investigate the mechanisms associated with IDO-1 expression and activity in human monocyte-derived dendritic cells (mDCs) after stimulation with irradiated Mycobacterium leprae and its fractions. M. leprae and its fractions induced the expression and activity of IDO-1 in human mDCs. Among the stimuli studied, irradiated M. leprae and its membrane fraction (MLMA) induced the production of proinflammatory cytokines TNF and IL-6 whereas irradiated M. leprae and its cytosol fraction (MLSA) induced an increase in IL-10. We investigated if TLR2 activation was necessary for IDO-1 induction in mDCs. We observed that in cultures treated with a neutralizing anti-TLR2 antibody, there was a decrease in IDO-1 activity and expression induced by M. leprae and MLMA. The same effect was observed when we used a MyD88 inhibitor. Our data demonstrate that coculture of mDCs with autologous lymphocytes induced an increase in regulatory T (Treg) cell frequency in MLSA-stimulated cultures, showing that M. leprae constituents may play opposite roles that may possibly be related to the dubious effect of IDO-1 in the different clinical forms of disease. Our data show that M. leprae and its fractions are able to differentially modulate the activity and functionality of IDO-1 in mDCs by a pathway that involves TLR2, suggesting that this enzyme may play an important role in leprosy immunopathogenesis.
MeSH term(s)	Biomarkers ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Flow Cytometry ; Humans ; Immune Tolerance ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Leprosy/etiology ; Leprosy/metabolism ; Leprosy/pathology ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Mycobacterium leprae/immunology ; Toll-Like Receptor 2/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Biomarkers ; IDO1 protein, human ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; TLR2 protein, human ; Toll-Like Receptor 2 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2020-10-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.4A0320-188R
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Article ; Online: DNA Sensing via TLR-9 Constitutes a Major Innate Immunity Pathway Activated during Erythema Nodosum Leprosum.

Dias, André A / Silva, Camila O / Santos, João Pedro S / Batista-Silva, Leonardo R / Acosta, Chyntia Carolina D / Fontes, Amanda N B / Pinheiro, Roberta O / Lara, Flávio A / Machado, Alice M / Nery, José Augusto C / Sarno, Euzenir N / Pereira, Geraldo M B / Pessolani, Maria Cristina V

Journal of immunology (Baltimore, Md. : 1950)

2016 Volume 197, Issue 5, Page(s) 1905–1913

Abstract: The chronic course of lepromatous leprosy may be interrupted by acute inflammatory episodes known as erythema nodosum leprosum (ENL). Despite its being a major cause of peripheral nerve damage in leprosy patients, the immunopathogenesis of ENL remains ... ...

Abstract	The chronic course of lepromatous leprosy may be interrupted by acute inflammatory episodes known as erythema nodosum leprosum (ENL). Despite its being a major cause of peripheral nerve damage in leprosy patients, the immunopathogenesis of ENL remains ill-defined. Recognized by distinct families of germline-encoded pattern recognition receptors, endogenous and pathogen-derived nucleic acids are highly immunostimulatory molecules that play a major role in the host defense against infections, autoimmunity, and autoinflammation. The aim of this work was to investigate whether DNA sensing via TLR-9 constitutes a major inflammatory pathway during ENL. Flow cytometry and immunohistochemistry analysis showed significantly higher TLR-9 expression in ENL when compared with nonreactional lepromatous patients, both locally in the skin lesions and in circulating mononuclear cells. The levels of endogenous and pathogen-derived TLR-9 ligands in the circulation of ENL patients were also higher. Furthermore, PBMCs isolated from the ENL patients secreted higher levels of TNF, IL-6, and IL-1β in response to a TLR-9 agonist than those of the nonreactional patients and healthy individuals. Finally, E6446, a TLR-9 synthetic antagonist, was able to significantly inhibit the secretion of proinflammatory cytokines by ENL PBMCs in response to Mycobacterium leprae lysate. Our data strongly indicate that DNA sensing via TLR-9 constitutes a major innate immunity pathway involved in the pathogenesis and evolution of ENL. Thus, the use of TLR-9 antagonists emerges as a potential alternative to more effectively treat ENL aiming to prevent the development of nerve injuries and deformities in leprosy.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; DNA/metabolism ; Erythema Nodosum/immunology ; Erythema Nodosum/microbiology ; Female ; Flow Cytometry ; Humans ; Immunity, Innate ; Leprosy, Lepromatous/immunology ; Leprosy, Lepromatous/microbiology ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/microbiology ; Male ; Middle Aged ; Mycobacterium leprae/chemistry ; Mycobacterium leprae/immunology ; Signal Transduction ; Toll-Like Receptor 9/immunology ; Toll-Like Receptor 9/metabolism ; Young Adult
Chemical Substances	TLR9 protein, human ; Toll-Like Receptor 9 ; DNA (9007-49-2)
Language	English
Publishing date	2016-09-01
Publishing country	United States
Document type	Journal Article
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.1600042
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Article ; Online: Pterocarpanquinone LQB-118 induces apoptosis in Leishmania (Viannia) braziliensis and controls lesions in infected hamsters.

Costa, Luciana / Pinheiro, Roberta O / Dutra, Patrícia M L / Santos, Rosiane F / Cunha-Júnior, Edézio F / Torres-Santos, Eduardo C / da Silva, Alcides J M / Costa, Paulo R R / Da-Silva, Silvia A G

PloS one

2014 Volume 9, Issue 10, Page(s) e109672

Abstract: Previous results demonstrate that the hybrid synthetic pterocarpanquinone LQB-118 presents antileishmanial activity against Leishmania amazonensis in a mouse model. The aim of the present study was to use a hamster model to investigate whether LQB-118 ... ...

Abstract	Previous results demonstrate that the hybrid synthetic pterocarpanquinone LQB-118 presents antileishmanial activity against Leishmania amazonensis in a mouse model. The aim of the present study was to use a hamster model to investigate whether LQB-118 presents antileishmanial activity against Leishmania (Viannia) braziliensis, which is the major Leishmania species related to American tegumentary leishmaniasis. The in vitro antileishmanial activity of LQB-118 on L. braziliensis was tested on the promastigote and intracellular amastigote forms. The cell death induced by LQB-118 in the L. braziliensis promastigotes was analyzed using an annexin V-FITC/PI kit, the oxidative stress was evaluated by 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) and the ATP content by luminescence. In situ labeling of DNA fragments by terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to investigate apoptosis in the intracellular amastigotes. L. braziliensis-infected hamsters were treated from the seventh day of infection with LQB-118 administered intralesionally (26 µg/kg/day, three times a week) or orally (4,3 mg/kg/day, five times a week) for eight weeks. LQB-118 was active against the L. braziliensis promastigotes and intracellular amastigotes, producing IC50 (50% inhibitory concentration) values of 3,4±0,1 and 7,5±0,8 µM, respectively. LQB-118 induced promastigote phosphatidylserine externalization accompanied by increased reactive oxygen species production and ATP depletion. Intracellular amastigote DNA fragmentation was also observed, without affecting the viability of macrophages. The treatment of L. braziliensis-infected hamsters with LQB-118, either orally or intralesionally, was effective in the control of lesion size, parasite load and increase intradermal reaction to parasite antigen. Taken together, these results show that the antileishmanial effect of LQB-118 extends to L. braziliensis in the hamster model, involves the induction of parasite apoptosis and shows promising therapeutic option by oral or local routes in leishmaniasis.
MeSH term(s)	Animals ; Antiprotozoal Agents/pharmacology ; Apoptosis/drug effects ; Cricetinae ; Female ; Leishmania braziliensis/drug effects ; Leishmaniasis, Cutaneous/parasitology ; Leishmaniasis, Cutaneous/pathology ; Macrophages/drug effects ; Macrophages/parasitology ; Membrane Potential, Mitochondrial/drug effects ; Mesocricetus ; Naphthoquinones/pharmacology ; Phosphatidylserines/metabolism ; Pterocarpans/pharmacology
Chemical Substances	Antiprotozoal Agents ; LQB 118 ; Naphthoquinones ; Phosphatidylserines ; Pterocarpans
Language	English
Publishing date	2014-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0109672
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Article: The T-cell anergy induced by Leishmania amazonensis antigens is related with defective antigen presentation and apoptosis.

Pinheiro, Roberta O / Pinto, Eduardo F / Benedito, Alessandra B / Lopes, Ulisses G / Rossi-Bergmann, Bartira

Anais da Academia Brasileira de Ciencias

2004 Volume 76, Issue 3, Page(s) 519–527

Abstract: Leishmania amazonensis is the main agent of diffuse cutaneous leishmaniasis, a disease associated with anergic immune responses. In this study we show that the crude antigen of Leishmania amazonensis (LaAg) but not L. braziliensis promastigotes (LbAg) ... ...

Abstract	Leishmania amazonensis is the main agent of diffuse cutaneous leishmaniasis, a disease associated with anergic immune responses. In this study we show that the crude antigen of Leishmania amazonensis (LaAg) but not L. braziliensis promastigotes (LbAg) contains substances that suppress mitogenic and spontaneous proliferative responses of T cells. The suppressive substances in LaAg are thermoresistant (100 degrees C/1h) and partially dependent on protease activity. T cell anergy was not due to a decreased production of growth factors as it was not reverted by addition of exogenous IL-2, IL-4, IFN-gamma or IL-12. LaAg did not inhibit anti-CD3-induced T cell activation, suggesting that anergy was due to a defect in antigen presentation. It was also not due to cell necrosis, but was accompanied by expressive DNA fragmentation in lymph node cells, indicative of apoptosis. Although pre-incubation of macrophages with LaAg prevented their capacity to present antigens, this effect was not due to apoptosis of the former. These results suggest that the T cell anergy found in diffuse leishmaniasis may be the result of parasite antigen-driven apoptosis of those cells following defective antigen presentation.
MeSH term(s)	Animals ; Antigens, Protozoan/immunology ; Apoptosis/immunology ; Clonal Anergy/immunology ; Leishmania/immunology ; Leishmaniasis, Diffuse Cutaneous/immunology ; Leishmaniasis, Diffuse Cutaneous/parasitology ; Lymph Nodes/cytology ; Lymph Nodes/immunology ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/immunology
Chemical Substances	Antigens, Protozoan
Language	English
Publishing date	2004-08-23
Publishing country	Brazil
Document type	Journal Article
ZDB-ID	2046885-4
ISSN	1678-2690 ; 0001-3765
ISSN (online)	1678-2690
ISSN	0001-3765
DOI	10.1590/s0001-37652004000300006
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Article ; Online: CD163 favors Mycobacterium leprae survival and persistence by promoting anti-inflammatory pathways in lepromatous macrophages.

Moura, Danielle F / de Mattos, Katherine A / Amadeu, Thaís P / Andrade, Priscila R / Sales, Jorgenilce S / Schmitz, Verônica / Nery, José Augusto C / Pinheiro, Roberta O / Sarno, Euzenir N

European journal of immunology

2012 Volume 42, Issue 11, Page(s) 2925–2936

Abstract: Lepromatous macrophages possess a regulatory phenotype that contributes to the immunosuppression observed in leprosy. CD163, a scavenger receptor that recognizes hemoglobin-haptoglobin complexes, is expressed at higher levels in lepromatous cells, ... ...

Abstract	Lepromatous macrophages possess a regulatory phenotype that contributes to the immunosuppression observed in leprosy. CD163, a scavenger receptor that recognizes hemoglobin-haptoglobin complexes, is expressed at higher levels in lepromatous cells, although its functional role in leprosy is not yet established. We herein demonstrate that human lepromatous lesions are microenvironments rich in IDO⁺CD163⁺. Cells isolated from these lesions were CD68⁺IDO⁺CD163⁺ while higher levels of sCD163 in lepromatous sera positively correlated with IL-10 levels and IDO activity. Different Myco-bacterium leprae (ML) concentrations in healthy monocytes likewise revealed a positive correlation between increased concentrations of the mycobacteria and IDO, CD209, and CD163 expression. The regulatory phenotype in ML-stimulated monocytes was accompanied by increased TNF, IL-10, and TGF-β levels whereas IL-10 blockade reduced ML-induced CD163 expression. The CD163 blockade reduced ML uptake in human monocytes. ML uptake was higher in HEK293 cells transfected with the cDNA for CD163 than in untransfected cells. Simultaneously, increased CD163 expression in lepromatous cells seemed to be dependent on ML uptake, and contributed to augmented iron storage in lepromatous macrophages. Altogether, these results suggest that ML-induced CD163 expression modulates the host cell phenotype to create a favorable environment for myco-bacterial entry and survival.
MeSH term(s)	Antigens, CD/genetics ; Antigens, CD/immunology ; Antigens, Differentiation, Myelomonocytic/genetics ; Antigens, Differentiation, Myelomonocytic/immunology ; Biopsy ; Flow Cytometry ; Humans ; Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology ; Interleukin-10/immunology ; Leprosy, Lepromatous/immunology ; Leprosy, Lepromatous/microbiology ; Leprosy, Lepromatous/pathology ; Macrophages/immunology ; Macrophages/microbiology ; Mycobacterium leprae/immunology ; RNA, Messenger/chemistry ; RNA, Messenger/genetics ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/immunology ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD163 antigen ; IDO1 protein, human ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; RNA, Messenger ; Receptors, Cell Surface ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2012-09-14
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201142198
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Article ; Online: The T-cell anergy induced by Leishmania amazonensis antigens is related with defective antigen presentation and apoptosis

Pinheiro Roberta O. / Pinto Eduardo F. / Benedito Alessandra B. / Lopes Ulisses G. / Rossi-Bergmann Bartira

Anais da Academia Brasileira de Ciências, Vol 76, Iss 3, Pp 519-

2004 Volume 527

Abstract	Leishmania amazonensis is the main agent of diffuse cutaneous leishmaniasis, a disease associated with anergic immune responses. In this study we show that the crude antigen of Leishmania amazonensis (LaAg) but not L. braziliensis promastigotes (LbAg) contains substances that suppress mitogenic and spontaneous proliferative responses of T cells. The suppressive substances in LaAg are thermoresistant (100ºC/1h) and partially dependent on protease activity. T cell anergy was not due to a decreased production of growth factors as it was not reverted by addition of exogenous IL-2, IL-4, IFN-gamma or IL-12. LaAg did not inhibit anti-CD3-induced T cell activation, suggesting that anergy was due to a defect in antigen presentation. It was also not due to cell necrosis, but was accompanied by expressive DNA fragmentation in lymph node cells, indicative of apoptosis. Although pre-incubation of macrophages with LaAg prevented their capacity to present antigens, this effect was not due to apoptosis of the former. These results suggest that the T cell anergy found in diffuse leishmaniasis may be the result of parasite antigen-driven apoptosis of those cells following defective antigen presentation.
Keywords	Leishmania ; anergy ; apoptosis ; Science ; Q
Subject code	610
Language	English
Publishing date	2004-01-01T00:00:00Z
Publisher	Academia Brasileira de Ciências
Document type	Article ; Online
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Article ; Online: TLR6-driven lipid droplets in Mycobacterium leprae-infected Schwann cells: immunoinflammatory platforms associated with bacterial persistence.

Mattos, Katherine A / Oliveira, Viviane G C / D'Avila, Heloisa / Rodrigues, Luciana S / Pinheiro, Roberta O / Sarno, Euzenir N / Pessolani, Maria Cristina V / Bozza, Patricia T

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 187, Issue 5, Page(s) 2548–2558

Abstract: The mechanisms responsible for nerve injury in leprosy need further elucidation. We recently demonstrated that the foamy phenotype of Mycobacterium leprae-infected Schwann cells (SCs) observed in nerves of multibacillary patients results from the ... ...

Abstract	The mechanisms responsible for nerve injury in leprosy need further elucidation. We recently demonstrated that the foamy phenotype of Mycobacterium leprae-infected Schwann cells (SCs) observed in nerves of multibacillary patients results from the capacity of M. leprae to induce and recruit lipid droplets (LDs; also known as lipid bodies) to bacterial-containing phagosomes. In this study, we analyzed the parameters that govern LD biogenesis by M. leprae in SCs and how this contributes to the innate immune response elicited by M. leprae. Our observations indicated that LD formation requires the uptake of live bacteria and depends on host cell cytoskeleton rearrangement and vesicular trafficking. TLR6 deletion, but not TLR2, completely abolished the induction of LDs by M. leprae, as well as inhibited the bacterial uptake in SCs. M. leprae-induced LD biogenesis correlated with increased PGE(2) and IL-10 secretion, as well as reduced IL-12 and NO production in M. leprae-infected SCs. Analysis of nerves from lepromatous leprosy patients showed colocalization of M. leprae, LDs, and cyclooxygenase-2 in SCs, indicating that LDs are sites for PGE(2) synthesis in vivo. LD biogenesis Inhibition by the fatty acid synthase inhibitor C-75 abolished the effect of M. leprae on SC production of immunoinflammatory mediators and enhanced the mycobacterial-killing ability of SCs. Altogether, our data indicated a critical role for TLR6-dependent signaling in M. leprae-SC interactions, favoring phagocytosis and subsequent signaling for induction of LD biogenesis in infected cells. Moreover, our observations reinforced the role of LDs favoring mycobacterial survival and persistence in the nerve. These findings give further support to a critical role for LDs in M. leprae pathogenesis in the nerve.
MeSH term(s)	Animals ; Humans ; Immunohistochemistry ; Inclusion Bodies/immunology ; Inclusion Bodies/metabolism ; Inclusion Bodies/pathology ; Inflammation/immunology ; Inflammation/microbiology ; Inflammation/pathology ; Leprosy/immunology ; Leprosy/pathology ; Lipid Metabolism/physiology ; Lipids/immunology ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Mycobacterium leprae/immunology ; Schwann Cells/immunology ; Schwann Cells/microbiology ; Schwann Cells/pathology ; Toll-Like Receptor 6/immunology ; Toll-Like Receptor 6/metabolism
Chemical Substances	Lipids ; TLR6 protein, human ; Toll-Like Receptor 6
Language	English
Publishing date	2011-09-01
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.1101344
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