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Article ; Online: Gasdermin-D activation promotes NLRP3 activation and host resistance to Leishmania infection.

de Sá, Keyla S G / Amaral, Luana A / Rodrigues, Tamara S / Ishimoto, Adriene Y / de Andrade, Warrison A C / de Almeida, Leticia / Freitas-Castro, Felipe / Batah, Sabrina S / Oliveira, Sergio C / Pastorello, Mônica T / Fabro, Alexandre T / Zamboni, Dario S

Nature communications

2023 Volume 14, Issue 1, Page(s) 1049

Abstract: Intracellular parasites from the Leishmania genus cause Leishmaniasis, a disease affecting millions of people worldwide. NLRP3 inflammasome is key for disease outcome, but the molecular mechanisms upstream of the inflammasome activation are still unclear. ...

Abstract	Intracellular parasites from the Leishmania genus cause Leishmaniasis, a disease affecting millions of people worldwide. NLRP3 inflammasome is key for disease outcome, but the molecular mechanisms upstream of the inflammasome activation are still unclear. Here, we demonstrate that despite the absence of pyroptosis, Gasdermin-D (GSDMD) is active at the early stages of Leishmania infection in macrophages, allowing transient cell permeabilization, potassium efflux, and NLRP3 inflammasome activation. Further, GSDMD is processed into a non-canonical 25 kDa fragment. Gsdmd
MeSH term(s)	Humans ; Mice ; Animals ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Gasdermins ; Intracellular Signaling Peptides and Proteins/metabolism ; Leishmaniasis ; Leishmania/metabolism ; Pyroptosis/physiology
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Gasdermins ; Intracellular Signaling Peptides and Proteins ; Nlrp3 protein, mouse
Language	English
Publishing date	2023-02-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-36626-6
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Article ; Online: Transcriptomic analysis reveals that RasGEF1b deletion alters basal and LPS-induced expression of genes involved in chemotaxis and cytokine responses in macrophages.

Fernandes, Heliana B / de Oliveira, Isadora Mafra / Postler, Thomas S / Lima, Sérgio Q / Santos, Cícera A C / Oliveira, Michaelle S / Leão, Felipe B / Ghosh, Sankar / Souza, Maria C / Andrade, Warrison / Silva, Aristóbolo M

Scientific reports

2023 Volume 13, Issue 1, Page(s) 19614

Abstract: Ras guanine nucleotide exchange factor member 1b (RasGEF1b) of the RasGEF/CDC25 domain-containing family is preferentially expressed by macrophages. However, information is lacking about its role in macrophage function. In this study, we generated mice ... ...

Abstract	Ras guanine nucleotide exchange factor member 1b (RasGEF1b) of the RasGEF/CDC25 domain-containing family is preferentially expressed by macrophages. However, information is lacking about its role in macrophage function. In this study, we generated mice with ubiquitous deletion of Rasgef1b and used RNA-seq-based transcriptomics to compare the global gene expression in wild-type and knock-out primary bone-marrow-derived macrophages under basal conditions and after lipopolysaccharide (LPS) treatment. Transcriptional filtering identified several genes with significantly different transcript levels between wild-type and knock-out macrophages. In total, 49 and 37 differentially expressed genes were identified at baseline and in LPS-activated macrophages, respectively. Distinct biological processes were significantly linked to down-regulated genes at the basal condition only, and largely included chemotaxis, response to cytokines, and positive regulation of GTPase activity. Importantly, validation by RT-qPCR revealed that the expression of genes identified as down-regulated after LPS stimulation was also decreased in the knock-out cells under basal conditions. We used a luciferase-based reporter assay to showcase the capability of RasGEF1b in activating the Serpinb2 promoter. Notably, knockdown of RasGEF1b in RAW264.7 macrophages resulted in impaired transcriptional activation of the Serpinb2 promoter, both in constitutive and LPS-stimulated conditions. This study provides a small collection of genes that shows relative expression changes effected by the absence of RasGEF1b in macrophages. Thus, we present the first evidence that RasGEF1b mediates the regulation of both steady-state and signal-dependent expression of genes and propose that this GEF plays a role in the maintenance of the basal transcriptional level in macrophages.
MeSH term(s)	Animals ; Mice ; Chemotaxis ; Cytokines/genetics ; Cytokines/metabolism ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/metabolism ; Macrophages/metabolism ; Transcriptome
Chemical Substances	Cytokines ; Lipopolysaccharides ; RasGEF1B protein, mouse
Language	English
Publishing date	2023-11-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-47040-9
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Article ; Online: Transcriptomic analysis reveals that RasGEF1b deletion alters basal and LPS-induced expression of genes involved in chemotaxis and cytokine responses in macrophages

Heliana B. Fernandes / Isadora Mafra de Oliveira / Thomas S. Postler / Sérgio Q. Lima / Cícera A. C. Santos / Michaelle S. Oliveira / Felipe B. Leão / Sankar Ghosh / Maria C. Souza / Warrison Andrade / Aristóbolo M. Silva

Scientific Reports, Vol 13, Iss 1, Pp 1-

2023 Volume 15

Abstract: Abstract Ras guanine nucleotide exchange factor member 1b (RasGEF1b) of the RasGEF/CDC25 domain-containing family is preferentially expressed by macrophages. However, information is lacking about its role in macrophage function. In this study, we ... ...

Abstract	Abstract Ras guanine nucleotide exchange factor member 1b (RasGEF1b) of the RasGEF/CDC25 domain-containing family is preferentially expressed by macrophages. However, information is lacking about its role in macrophage function. In this study, we generated mice with ubiquitous deletion of Rasgef1b and used RNA-seq-based transcriptomics to compare the global gene expression in wild-type and knock-out primary bone-marrow-derived macrophages under basal conditions and after lipopolysaccharide (LPS) treatment. Transcriptional filtering identified several genes with significantly different transcript levels between wild-type and knock-out macrophages. In total, 49 and 37 differentially expressed genes were identified at baseline and in LPS-activated macrophages, respectively. Distinct biological processes were significantly linked to down-regulated genes at the basal condition only, and largely included chemotaxis, response to cytokines, and positive regulation of GTPase activity. Importantly, validation by RT-qPCR revealed that the expression of genes identified as down-regulated after LPS stimulation was also decreased in the knock-out cells under basal conditions. We used a luciferase-based reporter assay to showcase the capability of RasGEF1b in activating the Serpinb2 promoter. Notably, knockdown of RasGEF1b in RAW264.7 macrophages resulted in impaired transcriptional activation of the Serpinb2 promoter, both in constitutive and LPS-stimulated conditions. This study provides a small collection of genes that shows relative expression changes effected by the absence of RasGEF1b in macrophages. Thus, we present the first evidence that RasGEF1b mediates the regulation of both steady-state and signal-dependent expression of genes and propose that this GEF plays a role in the maintenance of the basal transcriptional level in macrophages.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: NLRC4 biology in immunity and inflammation.

Andrade, Warrison A / Zamboni, Dario S

Journal of leukocyte biology

2020 Volume 108, Issue 4, Page(s) 1117–1127

Abstract: Inflammasomes are cytosolic multiprotein complexes that sense microbial infections or host cell damage, triggering cytokine production and a proinflammatory form of cell death, called pyroptosis. Whereas pyroptosis and cytokine production may often ... ...

Abstract	Inflammasomes are cytosolic multiprotein complexes that sense microbial infections or host cell damage, triggering cytokine production and a proinflammatory form of cell death, called pyroptosis. Whereas pyroptosis and cytokine production may often promote host resistance to infections, uncontrolled inflammasome activation leads to autoinflammatory diseases in humans. Among the multiple inflammasomes described, the neuronal apoptosis inhibitory protein/nucleotide-binding domain leucine-rich repeat-containing protein family caspase activation and recruitment domain-containing protein 4 (NLRC4) inflammasome emerged as a critical component for the restriction of bacterial infections. Accordingly, our understanding of this inflammasome advanced remarkably over the last 10 yr, expanding our knowledge about ligand-receptor interaction; cryo-EM structure; and downstream effectors and substrates, such as gasdermin-D, caspase-1, caspase-8, and caspase-7. In this review, we discuss recent advances on the biology of the NLRC4 inflammasome, in terms of structure and activation mechanisms, importance in bacterial and nonbacterial diseases, and the identification of NLRC4 gain-of-function mutations leading to NLRC4-associated autoinflammatory diseases in humans.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Bacterial Infections/immunology ; Bacterial Infections/pathology ; CARD Signaling Adaptor Proteins/immunology ; Calcium-Binding Proteins/immunology ; Caspase 1/immunology ; Caspase 7 ; Caspase 8/immunology ; Humans ; Inflammasomes/immunology ; Intracellular Signaling Peptides and Proteins/immunology ; Phosphate-Binding Proteins/immunology
Chemical Substances	CARD Signaling Adaptor Proteins ; Calcium-Binding Proteins ; GSDMD protein, human ; Inflammasomes ; Intracellular Signaling Peptides and Proteins ; NLRC4 protein, human ; Phosphate-Binding Proteins ; CASP7 protein, human (EC 3.4.22.-) ; CASP8 protein, human (EC 3.4.22.-) ; Caspase 7 (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2020-06-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.3MR0420-573R
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Article ; Online: Lipid droplet accumulation occurs early following Salmonella infection and contributes to intracellular bacterial survival and replication.

Kiarely Souza, Ellen / Pereira-Dutra, Filipe S / Rajão, Matheus A / Ferraro-Moreira, Felipe / Goltara-Gomes, Taynná C / Cunha-Fernandes, Tamires / Santos, Julia da Cunha / Prestes, Elisa B / Andrade, Warrison A / Zamboni, Dario S / Bozza, Marcelo T / Bozza, Patrícia T

Molecular microbiology

2021 Volume 117, Issue 2, Page(s) 293–306

Abstract: Salmonellosis is a public health problem caused by Salmonella sp., a highly adapted facultative intracellular pathogen. After internalization, Salmonella sp. Manipulates several host processes, mainly through the activation of the type III secretion ... ...

Abstract	Salmonellosis is a public health problem caused by Salmonella sp., a highly adapted facultative intracellular pathogen. After internalization, Salmonella sp. Manipulates several host processes, mainly through the activation of the type III secretion system (T3SS), including modification of host lipid metabolism and lipid droplet (LD) accumulation. LDs are dynamic and complex lipid-rich organelles involved in several cellular processes. The present study investigated the mechanism involved in LD biogenesis in Salmonella-infected macrophages and its role in bacterial pathogenicity. Here, we reported that S. Typhimurium induced a rapid time-dependent increase of LD formation in macrophages. The LD biogenesis was demonstrated to depend on Salmonella's viability and SPI1-related T3SS activity, with the participation of Toll-Like Receptor (TLR) signaling. We also observed that LD accumulation occurs through TLR2-dependent signaling and is counter-regulated by TLR4. Last, the pharmacologic modulation of LD formation by inhibiting diacylglycerol O-acyltransferase 1 (DGAT1) and cytosolic phospholipase A2 (cPLA2) significantly reduced the intracellular bacterial proliferation and impaired the prostaglandin E2 (PGE
MeSH term(s)	Humans ; Lipid Droplets/metabolism ; Lipid Metabolism/physiology ; Macrophages/microbiology ; Salmonella Infections ; Type III Secretion Systems/metabolism
Chemical Substances	Type III Secretion Systems
Language	English
Publishing date	2021-12-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/mmi.14844
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Article ; Online: Identification of immunomodulatory drugs that inhibit multiple inflammasomes and impair SARS-CoV-2 infection.

de Almeida, Letícia / da Silva, Alexandre L N / Rodrigues, Tamara S / Oliveira, Samuel / Ishimoto, Adriene Y / Seribelli, Amanda A / Becerra, Amanda / Andrade, Warrison A / Ataide, Marco A / Caetano, Camila C S / de Sá, Keyla S G / Pelisson, Natália / Martins, Ronaldo B / de Paula Souza, Juliano / Arruda, Eurico / Batah, Sabrina S / Castro, Ricardo / Frantz, Fabiani G / Cunha, Fernando Q /

Cunha, Thiago M / Fabro, Alexandre T / Cunha, Larissa D / Louzada-Junior, Paulo / de Oliveira, Rene D R / Zamboni, Dario S

Science advances

2022 Volume 8, Issue 37, Page(s) eabo5400

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces mild or asymptomatic COVID-19 in most cases, but some patients develop an excessive inflammatory process that can be fatal. As the NLRP3 inflammasome and additional inflammasomes are ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces mild or asymptomatic COVID-19 in most cases, but some patients develop an excessive inflammatory process that can be fatal. As the NLRP3 inflammasome and additional inflammasomes are implicated in disease aggravation, drug repositioning to target inflammasomes emerges as a strategy to treat COVID-19. Here, we performed a high-throughput screening using a 2560 small-molecule compound library and identified FDA-approved drugs that function as pan-inflammasome inhibitors. Our best hit, niclosamide (NIC), effectively inhibits both inflammasome activation and SARS-CoV-2 replication. Mechanistically, induction of autophagy by NIC partially accounts for inhibition of NLRP3 and AIM2 inflammasomes, but NIC-mediated inhibition of NAIP/NLRC4 inflammasome are autophagy independent. NIC potently inhibited inflammasome activation in human monocytes infected in vitro, in PBMCs from patients with COVID-19, and in vivo in a mouse model of SARS-CoV-2 infection. This study provides relevant information regarding the immunomodulatory functions of this promising drug for COVID-19 treatment.
MeSH term(s)	Animals ; Humans ; Immunomodulating Agents ; Inflammasomes ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein ; SARS-CoV-2 ; COVID-19 Drug Treatment
Chemical Substances	Immunomodulating Agents ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2022-09-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abo5400
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Article ; Online: Inflammasome-dependent Mechanisms Involved in Sensing and Restriction of Bacterial Replication.

Andrade, Warrison A / Zamboni, Dario S

Current issues in molecular biology

2017 Volume 25, Page(s) 99–132

Abstract: Inflammasomes are multiprotein platforms assembled in the cytosol in response to pathogens and cell stress. Inflammasomes are recognized by their important role on defenses against bacterial infections and have been also implicated in a range of human ... ...

Abstract	Inflammasomes are multiprotein platforms assembled in the cytosol in response to pathogens and cell stress. Inflammasomes are recognized by their important role on defenses against bacterial infections and have been also implicated in a range of human inflammatory disorders. Intracellular sensors such as NLRP1, NLRP3, NLRC4, AIM2 and Pyrin induce assembly of inflammasomes, while caspase-11 induces the non-canonical pathway for activation of the NLRP3 inflammasome. The formation of the inflammasome leads to caspase-1 activation that triggers pyroptosis and activation of interleukin-1β (IL-1β) and IL-18. Pyroptotic cell death and cytokines production are involved in restriction of bacterial replication by limiting the replication niche of intracellular bacteria and by inducing inflammatory responses. In this review we focus on the mechanisms mediated by inflammasome activation that leads to inflammatory responses and restriction of bacterial infection.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/immunology ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/immunology ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/immunology ; Caspase 1/genetics ; Caspase 1/immunology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/immunology ; Gene Expression Regulation ; Gram-Negative Bacteria/growth & development ; Gram-Negative Bacteria/immunology ; Gram-Positive Bacteria/growth & development ; Gram-Positive Bacteria/immunology ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Inflammasomes/immunology ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; NLR Proteins ; Pyrin/genetics ; Pyrin/immunology ; Pyroptosis/genetics ; Pyroptosis/immunology ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/microbiology
Chemical Substances	AIM2 protein, human ; Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; CARD Signaling Adaptor Proteins ; Calcium-Binding Proteins ; DNA-Binding Proteins ; IL1B protein, human ; Inflammasomes ; Interleukin-1beta ; MEFV protein, human ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLR Proteins ; NLRC4 protein, human ; NLRP1 protein, human ; NLRP3 protein, human ; Pyrin ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2017-09-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2000024-8
ISSN	1467-3045 ; 1467-3037
ISSN (online)	1467-3045
ISSN	1467-3037
DOI	10.21775/cimb.025.099
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Article ; Online: The IRAK1/IRF5 axis initiates IL-12 response by dendritic cells and control of Toxoplasma gondii infection.

Pereira, Milton / Ramalho, Theresa / Andrade, Warrison A / Durso, Danielle F / Souza, Maria C / Fitzgerald, Katherine A / Golenbock, Douglas T / Silverman, Neal / Gazzinelli, Ricardo T

Cell reports

2024 Volume 43, Issue 2, Page(s) 113795

Abstract: Activation of endosomal Toll-like receptor (TLR) 7, TLR9, and TLR11/12 is a key event in the resistance against the parasite Toxoplasma gondii. Endosomal TLR engagement leads to expression of interleukin (IL)-12 via the myddosome, a protein complex ... ...

Abstract	Activation of endosomal Toll-like receptor (TLR) 7, TLR9, and TLR11/12 is a key event in the resistance against the parasite Toxoplasma gondii. Endosomal TLR engagement leads to expression of interleukin (IL)-12 via the myddosome, a protein complex containing MyD88 and IL-1 receptor-associated kinase (IRAK) 4 in addition to IRAK1 or IRAK2. In murine macrophages, IRAK2 is essential for IL-12 production via endosomal TLRs but, surprisingly, Irak2
MeSH term(s)	Animals ; Mice ; Dendritic Cells ; Interferon Regulatory Factors/genetics ; Interleukin-1 Receptor-Associated Kinases ; Interleukin-12 ; Toxoplasmosis
Chemical Substances	Interferon Regulatory Factors ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Interleukin-12 (187348-17-0) ; Irf5 protein, mouse ; Irak1 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2024-02-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2024.113795
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Article ; Online: Cyclic GMP-AMP Synthase Is the Cytosolic Sensor of

Gallego-Marin, Carolina / Schrum, Jacob E / Andrade, Warrison A / Shaffer, Scott A / Giraldo, Lina F / Lasso, Alvaro M / Kurt-Jones, Evelyn A / Fitzgerald, Katherine A / Golenbock, Douglas T

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 200, Issue 2, Page(s) 768–774

Abstract: Innate immune receptors have a key role in the sensing of malaria and initiating immune responses. As a consequence of infection, systemic inflammation emerges and is directly related to signs and symptoms during acute disease. We have previously ... ...

Abstract	Innate immune receptors have a key role in the sensing of malaria and initiating immune responses. As a consequence of infection, systemic inflammation emerges and is directly related to signs and symptoms during acute disease. We have previously reported that plasmodial DNA is the primary driver of systemic inflammation in malaria, both within the phagolysosome and in the cytosol of effector cells. In this article, we demonstrate that
MeSH term(s)	Adolescent ; Adult ; Cells, Cultured ; DNA, Protozoan/metabolism ; Erythrocytes/metabolism ; Erythrocytes/parasitology ; Female ; Humans ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/metabolism ; Malaria, Falciparum/metabolism ; Malaria, Falciparum/parasitology ; Male ; Membrane Proteins/metabolism ; Middle Aged ; Nucleotides, Cyclic/metabolism ; Nucleotidyltransferases/metabolism ; Phosphorylation ; Plasmodium falciparum/genetics ; Signal Transduction ; Young Adult
Chemical Substances	DNA, Protozoan ; IRF3 protein, human ; Interferon Regulatory Factor-3 ; Interferon Type I ; Membrane Proteins ; Nucleotides, Cyclic ; STING1 protein, human ; cyclic guanosine monophosphate-adenosine monophosphate ; Nucleotidyltransferases (EC 2.7.7.-) ; cGAS protein, human (EC 2.7.7.-)
Language	English
Publishing date	2017-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.1701048
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Article ; Online: Chronic

Souza, Maria C / Fonseca, Denise M / Kanashiro, Alexandre / Benevides, Luciana / Medina, Tiago S / Dias, Murilo S / Andrade, Warrison A / Bonfá, Giuliano / Silva, Marcondes A B / Gozzi, Aline / Borges, Marcos C / Gazzinelli, Ricardo T / Alves-Filho, José C / Cunha, Fernando Q / Silva, João S

Frontiers in cellular and infection microbiology

2017 Volume 7, Page(s) 116

Abstract: Sepsis is a severe syndrome that arises when the host response to an insult is exacerbated, leading to organ failure and frequently to death. How a chronic infection that causes a prolonged Th1 expansion affects the course of sepsis is unknown. In this ... ...

Abstract	Sepsis is a severe syndrome that arises when the host response to an insult is exacerbated, leading to organ failure and frequently to death. How a chronic infection that causes a prolonged Th1 expansion affects the course of sepsis is unknown. In this study, we showed that mice chronically infected with
MeSH term(s)	Animals ; Coinfection/pathology ; Disease Models, Animal ; Interferon-gamma/secretion ; Mice ; Nitric Oxide/metabolism ; Sepsis/complications ; Sepsis/pathology ; Th1 Cells/immunology ; Th2 Cells/immunology ; Toxoplasmosis/complications
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2017.00116
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