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Article ; Online: A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.

Matsuda, Rina / Sorobetea, Daniel / Zhang, Jenna / Peterson, Stefan T / Grayczyk, James P / Yost, Winslow / Apenes, Nicolai / Kovalik, Maria E / Herrmann, Beatrice / O'Neill, Rosemary J / Bohrer, Andrea C / Lanza, Matthew / Assenmacher, Charles-Antoine / Mayer-Barber, Katrin D / Shin, Sunny / Brodsky, Igor E

The Journal of experimental medicine

2024 Volume 221, Issue 3

Abstract: Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the ... ...

Abstract	Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the intestinal mucosa and induces the recruitment of neutrophils and inflammatory monocytes into organized immune structures termed pyogranulomas (PG) that control Yersinia infection. Inflammatory monocytes are essential for the control and clearance of Yersinia within intestinal PG, but how monocytes mediate Yersinia restriction is poorly understood. Here, we demonstrate that TNF signaling in monocytes is required for bacterial containment following enteric Yersinia infection. We further show that monocyte-intrinsic TNFR1 signaling drives the production of monocyte-derived interleukin-1 (IL-1), which signals through IL-1 receptors on non-hematopoietic cells to enable PG-mediated control of intestinal Yersinia infection. Altogether, our work reveals a monocyte-intrinsic TNF-IL-1 collaborative inflammatory circuit that restricts intestinal Yersinia infection.
MeSH term(s)	Humans ; Interleukin-1 ; Yersinia ; Yersinia Infections ; Yersinia pseudotuberculosis ; Tumor Necrosis Factor-alpha ; Monocytes
Chemical Substances	Interleukin-1 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20230679
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Article ; Online: Co-infection of mice with SARS-CoV-2 and

Baker, Paul J / Amaral, Eduardo P / Castro, Ehydel / Bohrer, Andrea C / Torres-Juárez, Flor / Jordan, Cassandra M / Nelson, Christine E / Barber, Daniel L / Johnson, Reed F / Hilligan, Kerry L / Mayer-Barber, Katrin D

Frontiers in immunology

2023 Volume 14, Page(s) 1240419

Abstract: Viral co-infections have been implicated in worsening tuberculosis (TB) and during the COVID-19 pandemic, the global rate of TB-related deaths has increased for the first time in over a decade. We and others have previously shown that a resolved prior or ...

Abstract	Viral co-infections have been implicated in worsening tuberculosis (TB) and during the COVID-19 pandemic, the global rate of TB-related deaths has increased for the first time in over a decade. We and others have previously shown that a resolved prior or concurrent influenza A virus infection in
MeSH term(s)	Mice ; Animals ; Humans ; Mycobacterium tuberculosis ; SARS-CoV-2 ; Coinfection ; Pandemics ; COVID-19 ; Mice, Transgenic ; Interferon Type I ; Mice, Inbred C57BL
Chemical Substances	K-18 conjugate ; Interferon Type I
Language	English
Publishing date	2023-09-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1240419
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Article: The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication.

Baker, Paul J / Bohrer, Andrea C / Castro, Ehydel / Amaral, Eduardo P / Snow-Smith, Maryonne / Torres-Juárez, Flor / Gould, Sydnee T / Queiroz, Artur T L / Fukutani, Eduardo R / Jordan, Cassandra M / Khillan, Jaspal S / Cho, Kyoungin / Barber, Daniel L / Andrade, Bruno B / Johnson, Reed F / Hilligan, Kerry L / Mayer-Barber, Katrin D

bioRxiv : the preprint server for biology

2024

Abstract: SARS-CoV-2 infection leads to vastly divergent clinical outcomes ranging from asymptomatic infection to fatal disease. Co-morbidities, sex, age, host genetics and vaccine status are known to affect disease severity. Yet, how the inflammatory milieu of ... ...

Abstract	SARS-CoV-2 infection leads to vastly divergent clinical outcomes ranging from asymptomatic infection to fatal disease. Co-morbidities, sex, age, host genetics and vaccine status are known to affect disease severity. Yet, how the inflammatory milieu of the lung at the time of SARS-CoV-2 exposure impacts the control of viral replication remains poorly understood. We demonstrate here that immune events in the mouse lung closely preceding SARS-CoV-2 infection significantly impact viral control and we identify key innate immune pathways required to limit viral replication. A diverse set of pulmonary inflammatory stimuli, including resolved antecedent respiratory infections with
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.27.586885
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Article ; Online: Endogenous and Therapeutic 25-Hydroxycholesterols May Worsen Early SARS-CoV-2 Pathogenesis in Mice.

Fessler, Michael B / Madenspacher, Jennifer H / Baker, Paul J / Hilligan, Kerry L / Bohrer, Andrea C / Castro, Ehydel / Meacham, Julie / Chen, Shih-Heng / Johnson, Reed F / McDonald, Jeffrey G / Martin, Negin P / Tucker, Charles J / Mahapatra, Debabrata / Cesta, Mark / Mayer-Barber, Katrin D

American journal of respiratory cell and molecular biology

2023 Volume 69, Issue 6, Page(s) 638–648

Abstract: Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of cholesterol-25-hydroxylase (CH25H) on cholesterol, has recently been shown to be broadly antiviral, suggesting ... ...

Abstract	Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of cholesterol-25-hydroxylase (CH25H) on cholesterol, has recently been shown to be broadly antiviral, suggesting therapeutic potential against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, 25HC can also amplify inflammation and be converted by CYP7B1 (cytochrome P450 family 7 subfamily B member 1) to 7α,25-dihydroxycholesterol, a lipid with chemoattractant activity, via the G protein-coupled receptor EBI2 (Epstein-Barr virus-induced gene 2)/GPR183 (G protein-coupled receptor 183). Here, using
MeSH term(s)	Humans ; Animals ; Mice ; SARS-CoV-2 ; Epstein-Barr Virus Infections ; COVID-19 ; Herpesvirus 4, Human ; Hydroxycholesterols/pharmacology ; Cholesterol ; Receptors, G-Protein-Coupled ; Antiviral Agents/pharmacology ; Cytokines ; Weight Loss
Chemical Substances	25-hydroxycholesterol (767JTD2N31) ; NIBR189 ; Hydroxycholesterols ; Cholesterol (97C5T2UQ7J) ; Receptors, G-Protein-Coupled ; Antiviral Agents ; Cytokines ; Gpr183 protein, mouse
Language	English
Publishing date	2023-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2023-0007OC
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Article: A TNF-IL-1 circuit controls

Matsuda, Rina / Sorobetea, Daniel / Zhang, Jenna / Peterson, Stefan T / Grayczyk, James P / Herrmann, Beatrice / Yost, Winslow / O'Neill, Rosemary / Bohrer, Andrea C / Lanza, Matthew / Assenmacher, Charles-Antoine / Mayer-Barber, Katrin D / Shin, Sunny / Brodsky, Igor E

bioRxiv : the preprint server for biology

2023

Abstract: Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. ...

Abstract	Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens.
Language	English
Publishing date	2023-04-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.21.537749
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Article ; Online: Cutting Edge: IL-1R1 Mediates Host Resistance to

Bohrer, Andrea C / Tocheny, Claire / Assmann, Maike / Ganusov, Vitaly V / Mayer-Barber, Katrin D

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 201, Issue 6, Page(s) 1645–1650

Abstract: IL-1R1 deficiency in mice causes severe susceptibility ... ...

Abstract	IL-1R1 deficiency in mice causes severe susceptibility to
MeSH term(s)	Animals ; Immunity, Innate ; Lung/immunology ; Lung/pathology ; Macrophages/immunology ; Macrophages/pathology ; Mice ; Mice, Knockout ; Mycobacterium tuberculosis/immunology ; Receptors, Interleukin-1 Type I/genetics ; Receptors, Interleukin-1 Type I/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Tuberculosis, Pulmonary/genetics ; Tuberculosis, Pulmonary/immunology ; Tuberculosis, Pulmonary/pathology
Chemical Substances	IL1R1 protein, mouse ; Receptors, Interleukin-1 Type I
Language	English
Publishing date	2018-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
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.1800438
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Article ; Online: The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

Baker, Paul J / Bohrer, Andrea C / Castro, Ehydel / Amaral, Eduardo P / Snow-Smith, Maryonne / Torres-Juarez, Flor / Gould, Sydnee T / Queiroz, Artur TL / Fukutani, Eduardo R / Jordan, Cassandra M / Khillan, Jaspal S / Cho, Kyoungin / Barber, Daniel L / Andrade, Bruno B / Johnson, Reed F / Hilligan, Kerry L / Mayer-Barber, Katrin D

bioRxiv

Abstract	SARS-CoV-2 infection leads to vastly divergent clinical outcomes ranging from asymptomatic infection to fatal disease. Co-morbidities, sex, age, host genetics and vaccine status are known to affect disease severity. Yet, how the inflammatory milieu of the lung at the time of SARS-CoV-2 exposure impacts the control of viral replication remains poorly understood. We demonstrate here that immune events in the mouse lung closely preceding SARS-CoV-2 infection significantly impact viral control and we identify key innate immune pathways required to limit viral replication. A diverse set of pulmonary inflammatory stimuli, including resolved antecedent respiratory infections with S. aureus or influenza, ongoing pulmonary M. tuberculosis infection, ovalbumin/alum-induced asthma or airway administration of defined TLR ligands and recombinant cytokines, all establish an antiviral state in the lung that restricts SARS-CoV-2 replication upon infection. In addition to antiviral type I interferons, the broadly inducible inflammatory cytokines TNFα and IL-1 precondition the lung for enhanced viral control. Collectively, our work shows that SARS-CoV-2 may benefit from an immunologically quiescent lung microenvironment and suggests that heterogeneity in pulmonary inflammation that precedes or accompanies SARS-CoV-2 exposure may be a significant factor contributing to the population-wide variability in COVID-19 disease outcomes.
Keywords	covid19
Language	English
Publishing date	2024-03-27
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.03.27.586885
Database	COVID19

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Article ; Online: Rapid GPR183-mediated recruitment of eosinophils to the lung after Mycobacterium tuberculosis infection.

Bohrer, Andrea C / Castro, Ehydel / Tocheny, Claire E / Assmann, Maike / Schwarz, Benjamin / Bohrnsen, Eric / Makiya, Michelle A / Legrand, Fanny / Hilligan, Kerry L / Baker, Paul J / Torres-Juarez, Flor / Hu, Zhidong / Ma, Hui / Wang, Lin / Niu, Liangfei / Wen, Zilu / Lee, Sang H / Kamenyeva, Olena / Kauffman, Keith D /

Donato, Michele / Sher, Alan / Barber, Daniel L / Via, Laura E / Scriba, Thomas J / Khatri, Purvesh / Song, Yanzheng / Wong, Ka-Wing / Bosio, Catharine M / Klion, Amy D / Mayer-Barber, Katrin D

Cell reports

2022 Volume 40, Issue 4, Page(s) 111144

Abstract: Influx of eosinophils into the lungs is typically associated with type II responses during allergy and fungal and parasitic infections. However, we previously reported that eosinophils accumulate in lung lesions during type I inflammatory responses to ... ...

Abstract	Influx of eosinophils into the lungs is typically associated with type II responses during allergy and fungal and parasitic infections. However, we previously reported that eosinophils accumulate in lung lesions during type I inflammatory responses to Mycobacterium tuberculosis (Mtb) in humans, macaques, and mice, in which they support host resistance. Here we show eosinophils migrate into the lungs of macaques and mice as early as one week after Mtb exposure. In mice this influx is CCR3 independent and instead requires cell-intrinsic expression of the oxysterol receptor GPR183, which is highly expressed on human and macaque eosinophils. Murine eosinophils interact directly with bacilli-laden alveolar macrophages, which upregulate the oxysterol-synthesizing enzyme Ch25h, and eosinophil recruitment is impaired in Ch25h-deficient mice. Our findings show that eosinophils are among the earliest cells from circulation to sense and respond to Mtb infection of alveolar macrophages and reveal a role for GPR183 in the migration of eosinophils into lung tissue.
MeSH term(s)	Animals ; Eosinophils/metabolism ; Humans ; Lung/pathology ; Macrophages, Alveolar ; Mice ; Mycobacterium tuberculosis/physiology ; Receptors, G-Protein-Coupled/metabolism ; Tuberculosis/pathology
Chemical Substances	GPR183 protein, human ; Gpr183 protein, mouse ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2022-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111144
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Article ; Online: CARD9

Drummond, Rebecca A / Swamydas, Muthulekha / Oikonomou, Vasileios / Zhai, Bing / Dambuza, Ivy M / Schaefer, Brian C / Bohrer, Andrea C / Mayer-Barber, Katrin D / Lira, Sergio A / Iwakura, Yoichiro / Filler, Scott G / Brown, Gordon D / Hube, Bernhard / Naglik, Julian R / Hohl, Tobias M / Lionakis, Michail S

Nature immunology

2019 Volume 20, Issue 5, Page(s) 559–570

Abstract: The C-type lectin receptor-Syk (spleen tyrosine kinase) adaptor CARD9 facilitates protective antifungal immunity within the central nervous system (CNS), as human deficiency in CARD9 causes susceptibility to fungus-specific, CNS-targeted infection. CARD9 ...

Abstract	The C-type lectin receptor-Syk (spleen tyrosine kinase) adaptor CARD9 facilitates protective antifungal immunity within the central nervous system (CNS), as human deficiency in CARD9 causes susceptibility to fungus-specific, CNS-targeted infection. CARD9 promotes the recruitment of neutrophils to the fungus-infected CNS, which mediates fungal clearance. In the present study we investigated host and pathogen factors that promote protective neutrophil recruitment during invasion of the CNS by Candida albicans. The cytokine IL-1β served an essential function in CNS antifungal immunity by driving production of the chemokine CXCL1, which recruited neutrophils expressing the chemokine receptor CXCR2. Neutrophil-recruiting production of IL-1β and CXCL1 was induced in microglia by the fungus-secreted toxin Candidalysin, in a manner dependent on the kinase p38 and the transcription factor c-Fos. Notably, microglia relied on CARD9 for production of IL-1β, via both transcriptional regulation of Il1b and inflammasome activation, and of CXCL1 in the fungus-infected CNS. Microglia-specific Card9 deletion impaired the production of IL-1β and CXCL1 and neutrophil recruitment, and increased fungal proliferation in the CNS. Thus, an intricate network of host-pathogen interactions promotes antifungal immunity in the CNS; this is impaired in human deficiency in CARD9, which leads to fungal disease of the CNS.
MeSH term(s)	Animals ; Brain/immunology ; Brain/metabolism ; Brain/microbiology ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/immunology ; CARD Signaling Adaptor Proteins/metabolism ; Candida albicans/immunology ; Candida albicans/physiology ; Candidiasis/genetics ; Candidiasis/immunology ; Candidiasis/microbiology ; Chemokine CXCL1/genetics ; Chemokine CXCL1/immunology ; Chemokine CXCL1/metabolism ; Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; Host-Pathogen Interactions/immunology ; Inflammasomes/genetics ; Inflammasomes/immunology ; Inflammasomes/metabolism ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; Interleukin-1beta/metabolism ; Mice, Knockout ; Mice, Transgenic ; Microglia/immunology ; Microglia/metabolism ; Microglia/microbiology ; Neutrophil Infiltration/genetics ; Neutrophil Infiltration/immunology ; Neutrophils/immunology ; Neutrophils/metabolism ; Neutrophils/microbiology
Chemical Substances	CARD Signaling Adaptor Proteins ; Card9 protein, mouse ; Chemokine CXCL1 ; Cxcl1 protein, mouse ; Cytokines ; Inflammasomes ; Interleukin-1beta
Language	English
Publishing date	2019-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-019-0377-2
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Eosinophils are part of the granulocyte response in tuberculosis and promote host resistance in mice.

Bohrer, Andrea C / Castro, Ehydel / Hu, Zhidong / Queiroz, Artur T L / Tocheny, Claire E / Assmann, Maike / Sakai, Shunsuke / Nelson, Christine / Baker, Paul J / Ma, Hui / Wang, Lin / Zilu, Wen / du Bruyn, Elsa / Riou, Catherine / Kauffman, Keith D / Moore, Ian N / Del Nonno, Franca / Petrone, Linda / Goletti, Delia /

Martineau, Adrian R / Lowe, David M / Cronan, Mark R / Wilkinson, Robert J / Barry, Clifton E / Via, Laura E / Barber, Daniel L / Klion, Amy D / Andrade, Bruno B / Song, Yanzheng / Wong, Ka-Wing / Mayer-Barber, Katrin D

The Journal of experimental medicine

2021 Volume 218, Issue 10

Abstract: Host resistance to Mycobacterium tuberculosis (Mtb) infection requires the activities of multiple leukocyte subsets, yet the roles of the different innate effector cells during tuberculosis are incompletely understood. Here we uncover an unexpected ... ...

Abstract	Host resistance to Mycobacterium tuberculosis (Mtb) infection requires the activities of multiple leukocyte subsets, yet the roles of the different innate effector cells during tuberculosis are incompletely understood. Here we uncover an unexpected association between eosinophils and Mtb infection. In humans, eosinophils are decreased in the blood but enriched in resected human tuberculosis lung lesions and autopsy granulomas. An influx of eosinophils is also evident in infected zebrafish, mice, and nonhuman primate granulomas, where they are functionally activated and degranulate. Importantly, using complementary genetic models of eosinophil deficiency, we demonstrate that in mice, eosinophils are required for optimal pulmonary bacterial control and host survival after Mtb infection. Collectively, our findings uncover an unexpected recruitment of eosinophils to the infected lung tissue and a protective role for these cells in the control of Mtb infection in mice.
MeSH term(s)	Adult ; Animals ; Eosinophils/physiology ; Female ; Granulocytes/microbiology ; Granulocytes/physiology ; Host-Pathogen Interactions/physiology ; Humans ; Latent Tuberculosis/microbiology ; Lung/microbiology ; Lung/pathology ; Macaca mulatta ; Male ; Mice, Mutant Strains ; Mycobacterium tuberculosis/pathogenicity ; Tuberculosis/drug therapy ; Tuberculosis/microbiology ; Tuberculosis/pathology ; Zebrafish/microbiology ; Mice
Language	English
Publishing date	2021-08-04
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20210469
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