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Article ; Online: Mechanism of TLR4-Mediated Anti-Inflammatory Response Induced by Exopolysaccharide from the Probiotic Bacillus subtilis.

Zamora-Pineda, Jesus / Kalinina, Olga / Sperling, Anne I / Knight, Katherine L

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 211, Issue 8, Page(s) 1232–1239

Abstract: Intestinal inflammatory diseases affect millions of people worldwide, and one class of drugs showing promise toward treatment of several inflammatory diseases is probiotics. Numerous studies have been performed using probiotics to prevent and treat ... ...

Abstract	Intestinal inflammatory diseases affect millions of people worldwide, and one class of drugs showing promise toward treatment of several inflammatory diseases is probiotics. Numerous studies have been performed using probiotics to prevent and treat intestinal inflammatory diseases. Most of these studies used intact bacteria, and neither the active molecule nor the molecular mechanisms by which they affect immune responses are known. We have shown that the probiotic Bacillus subtilis is anti-inflammatory and can protect mice from acute colitis induced by the enteric pathogen Citrobacter rodentium. We identified and purified the active molecule, exopolysaccharide (EPS), and showed that it protects mice from C. rodentium-induced colitis by inducing anti-inflammatory M2 macrophages or inhibitory dendritic cells (DCs), both of which inhibit excessive T cell responses. We showed previously that EPS affects macrophages and DCs in a TLR4-dependent manner, and in the current study we asked how EPS induces these anti-inflammatory cells and how they function to inhibit T cells. By investigating the signaling downstream of TLR4 that leads to acquisition of inhibitory properties of macrophages and DCs, we found that EPS induces expression of the inhibitory molecule IDO in bone marrow-derived DCs, and that inhibition of T cell proliferation by IDO-expressing bone marrow-derived DCs utilizes the kynurenine/aryl hydrocarbon receptor circuit. Furthermore, unlike LPS, EPS does not induce inflammatory cytokines upon injection in vivo, directly demonstrating different outcomes induced by two different TLR4 agonists.
MeSH term(s)	Humans ; Mice ; Animals ; Toll-Like Receptor 4/metabolism ; Bacillus subtilis ; Colitis ; Anti-Inflammatory Agents/pharmacology ; Probiotics ; Dendritic Cells
Chemical Substances	Toll-Like Receptor 4 ; Anti-Inflammatory Agents ; TLR4 protein, human
Language	English
Publishing date	2023-09-06
Publishing country	United States
Document type	Journal Article ; 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.2200855
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Article ; Online: Local, Quantitative Morphometry of Fibroproliferative Lung Injury Using Laminin.

Cox, Brendan P / Hannan, Riley T / Batrash, Noora / Raichura, Pearl / Sperling, Anne I / Shim, Yun Michael / Sturek, Jeffrey M

American journal of respiratory cell and molecular biology

2024

Abstract: Investigations into the mechanisms of injury and repair in fibroproliferative disease require consideration of the spatial heterogeneity inherent in the disease. Most scoring of fibrotic remodeling in preclinical animal models rely on the modified ... ...

Abstract	Investigations into the mechanisms of injury and repair in fibroproliferative disease require consideration of the spatial heterogeneity inherent in the disease. Most scoring of fibrotic remodeling in preclinical animal models rely on the modified Ashcroft score, which is a semi-quantitative scoring rubric of macroscopic resolution. The obvious limitations inherent in manual pathohistological grading have generated an unmet need for unbiased, repeatable scoring of fibroproliferative burden in tissue. Using computer vision approaches on immunofluorescent imaging of the extracellular matrix (ECM) component laminin, we generate a robust and repeatable quantitative remodeling scorer (QRS). In the bleomycin lung injury model, QRS shows agreement with modified Ashcroft scoring with a significant Spearman coefficient r=0.768. This antibody-based approach is easily integrated into larger multiplex immunofluorescent experiments, which we demonstrate by testing the spatial apposition of tertiary lymphoid structures (TLS) to fibroproliferative tissue. The tool reported in this manuscript is available as a standalone application which is usable without programming knowledge.
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2023-0294MA
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Article ; Online: Distinct dendritic cell subsets actively induce Th2 polarization.

Tjota, Melissa Y / Sperling, Anne I

Current opinion in immunology

2014 Volume 31, Page(s) 44–50

Abstract: The mechanisms by which dendritic cells induce Th2 polarization (DC(Th2) cells) have been controversial. Many have argued that DC(Th2) cells are not a distinct functional DC subset, but rather, DC-induced polarization of Th2 cells is a default pathway ... ...

Abstract	The mechanisms by which dendritic cells induce Th2 polarization (DC(Th2) cells) have been controversial. Many have argued that DC(Th2) cells are not a distinct functional DC subset, but rather, DC-induced polarization of Th2 cells is a default pathway that occurs in the absence of inflammatory signals leading to DC-induced polarization of Th1/Th17 cells. However, recent studies demonstrate that distinct subsets of tissue DCs actively polarize Th2 cells after stimulation with type-2 inducing stimuli. DC(Th2) cells development is marked by the upregulation of specific transcription factors, cell surface molecules, and cytokines. These findings counter previous hypotheses that Th2 skewing by DCs is a passive response and support a model in which DCs are actively programmed to induce Th2 differentiation.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Cytokines/genetics ; Cytokines/immunology ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Humans ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Th1 Cells/immunology ; Th1 Cells/pathology ; Th17 Cells/immunology ; Th17 Cells/pathology ; Th2 Cells/immunology ; Th2 Cells/pathology ; Transcription Factors/genetics ; Transcription Factors/immunology ; Up-Regulation/immunology
Chemical Substances	Cytokines ; Transcription Factors
Language	English
Publishing date	2014-10-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2014.09.006
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Zs.A 2773: 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: Editorial overview: Allergy and hypersensitivity.

Sperling, Anne I / Ansel, K Mark

Current opinion in immunology

2014 Volume 31, Page(s) ix–xi

MeSH term(s)	Adaptive Immunity ; Animals ; Humans ; Hypersensitivity/genetics ; Hypersensitivity/immunology ; Hypersensitivity/pathology ; Immunity, Innate
Language	English
Publishing date	2014-12
Publishing country	England
Document type	Editorial ; Introductory Journal Article
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2014.10.011
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Zs.A 2773: 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: Central lung gene expression associates with myofibroblast features in idiopathic pulmonary fibrosis.

Huang, Yong / Guzy, Rob / Ma, Shwu-Fan / Bonham, Catherine A / Jou, Jonathan / Schulte, Jefree J / Kim, John S / Barros, Andrew J / Espindola, Milena S / Husain, Aliya N / Hogaboam, Cory M / Sperling, Anne I / Noth, Imre

BMJ open respiratory research

2023 Volume 10, Issue 1

Abstract: Rationale: Contribution of central lung tissues to pathogenesis of idiopathic pulmonary fibrosis (IPF) remains unknown.: Objective: To ascertain the relationship between cell types of IPF-central and IPF-peripheral lung explants using RNA sequencing ( ...

Abstract	Rationale: Contribution of central lung tissues to pathogenesis of idiopathic pulmonary fibrosis (IPF) remains unknown. Objective: To ascertain the relationship between cell types of IPF-central and IPF-peripheral lung explants using RNA sequencing (RNA-seq) transcriptome. Methods: Biopsies of paired IPF-central and IPF-peripheral along with non-IPF lungs were selected by reviewing H&E data. Criteria for differentially expressed genes (DEG) were set at false discovery rate <5% and fold change >2. Computational cell composition deconvolution was performed. Signature scores were computed for each cell type. Findings: Comparison of central IPF versus non-IPF identified 1723 DEG (1522 upregulated and 201 downregulated). Sixty-two per cent (938/1522) of the mutually upregulated genes in central IPF genes were also upregulated in peripheral IPF versus non-IPF. Moreover, 85 IPF central-associated genes (CAG) were upregulated in central IPF versus both peripheral IPF and central non-IPF. IPF single-cell RNA-seq analysis revealed the highest CAG signature score in myofibroblasts and significantly correlated with a previously published activated fibroblasts signature (r=0.88, p=1.6×10 Interpretation: Gene expression in central IPF lung regions demonstrates active myofibroblast features that contributes to disease progression. Further elucidation of pathological transcriptomic state of cells in the central regions of the IPF lung that are relatively spared from morphological rearrangements may provide insights into molecular changes in the IPF progression.
MeSH term(s)	Humans ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/pathology ; Lung/pathology ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression
Language	English
Publishing date	2023-01-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2736454-9
ISSN	2052-4439 ; 2052-4439
ISSN (online)	2052-4439
ISSN	2052-4439
DOI	10.1136/bmjresp-2022-001391
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Article ; Online: Lung cDC1 and cDC2 dendritic cells priming naive CD8

Si, Youhui / Wang, Yihan / Tian, Qiaomu / Wang, Qiang / Pollard, Jared M / Srivastava, Pramod K / Esser-Kahn, Aaron P / Collier, Joel H / Sperling, Anne I / Chong, Anita S

Cell reports

2023 Volume 42, Issue 10, Page(s) 113299

Abstract: The current paradigm indicates that naive T cells are primed in secondary lymphoid organs. Here, we present evidence that intranasal administration of peptide antigens appended to nanofibers primes naive ... ...

Abstract	The current paradigm indicates that naive T cells are primed in secondary lymphoid organs. Here, we present evidence that intranasal administration of peptide antigens appended to nanofibers primes naive CD8
MeSH term(s)	Mice ; Animals ; CD8-Positive T-Lymphocytes ; Dendritic Cells ; Lung ; Cross-Priming ; Lymph Nodes
Language	English
Publishing date	2023-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113299
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Article ; Online: Exopolysaccharide-Treated Dendritic Cells Effectively Ameliorate Acute Graft-versus-Host Disease.

Kalinina, Olga / Minter, Lisa M / Sperling, Anne I / Hollinger, Maile K / Le, Phong / Osborne, Barbara A / Zhang, Shubin / Stiff, Patrick / Knight, Katherine L

Transplantation and cellular therapy

2023 Volume 30, Issue 1, Page(s) 79.e1–79.e10

Abstract: Graft-versus-host disease (GVHD) is a primary and often lethal complication of allogenic hematopoietic stem cell transplantation (HSCT). Prophylactic regimens for GVHD are given as standard pretransplantation therapy; however, up to 50% of these patients ...

Abstract	Graft-versus-host disease (GVHD) is a primary and often lethal complication of allogenic hematopoietic stem cell transplantation (HSCT). Prophylactic regimens for GVHD are given as standard pretransplantation therapy; however, up to 50% of these patients develop acute GVHD (aGVHD) and require additional immunosuppressive intervention. Using a mouse GVHD model, we previously showed that injecting mice with exopolysaccharide (EPS) from Bacillus subtilis prior to GVHD induction significantly increased 80-day survival after transplantation of complete allogeneic major histocompatibility complex-mismatched cells. To ask whether EPS might also inhibit GVHD in humans, we used humanized NSG-HLA-A2 mice and induced GVHD by i.v. injection of A2
MeSH term(s)	Animals ; Humans ; Transplantation, Homologous/adverse effects ; HLA-A2 Antigen ; Leukocytes, Mononuclear ; Graft vs Host Disease/prevention & control ; Disease Models, Animal ; Dendritic Cells
Chemical Substances	HLA-A2 Antigen
Language	English
Publishing date	2023-11-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	3062231-1
ISSN	2666-6367
ISSN (online)	2666-6367
DOI	10.1016/j.jtct.2023.10.023
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Zs.A 5082: Show issues

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Article ; Online: Effects of an FcγRIIA polymorphism on leukocyte gene expression and cytokine responses to anti-CD3 and anti-CD28 antibodies.

Stein, Michelle M / Hrusch, Cara L / Sperling, Anne I / Ober, Carole

Genes and immunity

2018 Volume 20, Issue 6, Page(s) 462–472

Abstract: The low affinity Fcγ receptor, FcγRIIA, harbors a common missense mutation, rs1801274 (G>A, Arg131His) that modifies binding affinity to human IgG2 and mouse IgG1 antibodies and is associated with increased risk of autoimmune disease. Despite the ... ...

Abstract	The low affinity Fcγ receptor, FcγRIIA, harbors a common missense mutation, rs1801274 (G>A, Arg131His) that modifies binding affinity to human IgG2 and mouse IgG1 antibodies and is associated with increased risk of autoimmune disease. Despite the important role of the Arg131His variant, little is understood about heterozygous genotype effects on global gene expression and cytokine production during an FcγR-dependent response. To address this gap in knowledge, we treated human whole-blood samples from 130 individuals with mouse IgG1 anti-CD3 and anti-CD28 antibodies and characterized the genome-wide gene expression profiles and cytokine production among individuals stratified by rs1801274 genotype. Our analysis revealed that the levels of four cytokines (IFNγ, IL-12, IL-2, TNFα) and global gene expression patterns differed between all three genotype classes. Surprisingly, the heterozygotes showed suboptimal T cell activation compared to cells from individuals homozygous for the higher-affinity FcγRIIA allele (GG; Arg/Arg). The results of this study demonstrate that IgG response varies among all rs1801274 genotype classes and results in profound differences in both cytokine responses and gene expression patterns in blood leukocytes. Because even heterozygotes showed dampened global responses, our data may provide insight into the heterogeneity of outcomes in cytokine release assays and immunotherapy efficacy.
MeSH term(s)	Adolescent ; Adult ; Aged ; Alleles ; Antibodies/pharmacology ; CD28 Antigens/antagonists & inhibitors ; CD28 Antigens/immunology ; CD3 Complex/antagonists & inhibitors ; CD3 Complex/immunology ; Child ; Genotype ; Heterozygote ; Homozygote ; Humans ; Interferon-gamma/blood ; Interferon-gamma/metabolism ; Interleukin-12/blood ; Interleukin-12/metabolism ; Interleukin-2/blood ; Interleukin-2/metabolism ; Leukocytes/immunology ; Leukocytes/metabolism ; Middle Aged ; Polymorphism, Genetic ; Receptors, IgG/genetics ; T-Lymphocytes/metabolism ; Transcriptome/immunology ; Tumor Necrosis Factor-alpha/blood ; Tumor Necrosis Factor-alpha/metabolism ; Young Adult
Chemical Substances	Antibodies ; CD28 Antigens ; CD3 Complex ; Fc gamma receptor IIA ; Interleukin-2 ; Receptors, IgG ; Tumor Necrosis Factor-alpha ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2018-07-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2060566-3
ISSN	1476-5470 ; 1466-4879
ISSN (online)	1476-5470
ISSN	1466-4879
DOI	10.1038/s41435-018-0038-8
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Zs.A 5592: Show issues

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Article ; Online: IL-33-mediated Eosinophilia Protects against Acute Lung Injury.

Krishack, Paulette A / Hollinger, Maile K / Kuzel, Timothy G / Decker, Trevor S / Louviere, Tyler J / Hrusch, Cara L / Sperling, Anne I / Verhoef, Philip A

American journal of respiratory cell and molecular biology

2021 Volume 64, Issue 5, Page(s) 569–578

Abstract: Pneumonia-induced lung injury and acute respiratory distress syndrome can develop because of an inappropriate inflammatory response to acute infections, leading to a compromised alveolar barrier. Recent work suggests that hospitalized patients with ... ...

Abstract	Pneumonia-induced lung injury and acute respiratory distress syndrome can develop because of an inappropriate inflammatory response to acute infections, leading to a compromised alveolar barrier. Recent work suggests that hospitalized patients with allergies/asthma are less likely to die of pulmonary infections and that there is a correlation between survival from acute respiratory distress syndrome and higher eosinophil counts; thus, we hypothesized that eosinophils associated with a type 2 immune response may protect against pneumonia-induced acute lung injury. To test this hypothesis, mice were treated with the type 2-initiating cytokine IL-33 intratracheally 3 days before induction of pneumonia with airway administration of a lethal dose of
MeSH term(s)	Acute Lung Injury/etiology ; Acute Lung Injury/immunology ; Acute Lung Injury/microbiology ; Acute Lung Injury/prevention & control ; Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Bronchoalveolar Lavage Fluid/cytology ; Diphtheria Toxin/pharmacology ; Disease Models, Animal ; Eosinophils/drug effects ; Eosinophils/immunology ; Female ; Gene Expression ; Humans ; Interleukin-33/genetics ; Interleukin-33/immunology ; Interleukin-33/pharmacology ; Interleukin-5/deficiency ; Interleukin-5/genetics ; Interleukin-5/immunology ; Leukocyte Count ; Leukocyte Reduction Procedures ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils/drug effects ; Neutrophils/immunology ; Pneumonia, Staphylococcal/complications ; Pneumonia, Staphylococcal/immunology ; Pneumonia, Staphylococcal/microbiology ; Pneumonia, Staphylococcal/mortality ; Pulmonary Edema/complications ; Pulmonary Edema/immunology ; Pulmonary Edema/microbiology ; Pulmonary Edema/mortality ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/immunology ; Respiratory Distress Syndrome/microbiology ; Respiratory Distress Syndrome/prevention & control ; Staphylococcus aureus/immunology ; Staphylococcus aureus/pathogenicity ; Survival Analysis
Chemical Substances	Diphtheria Toxin ; Il33 protein, mouse ; Interleukin-33 ; Interleukin-5
Language	English
Publishing date	2021-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2020-0166OC
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Article ; Online: A

Kasal, Darshan N / Liang, Zhitao / Hollinger, Maile K / O'Leary, Crystal Y / Lisicka, Wioletta / Sperling, Anne I / Bendelac, Albert

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

2021 Volume 118, Issue 32

Abstract: The type 2 helper effector program is driven by the master transcription factor GATA3 and can be expressed by subsets of both innate lymphoid cells (ILCs) and adaptive ... ...

Abstract	The type 2 helper effector program is driven by the master transcription factor GATA3 and can be expressed by subsets of both innate lymphoid cells (ILCs) and adaptive CD4
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Enhancer Elements, Genetic ; Female ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/metabolism ; Homeostasis/genetics ; Immunity, Innate/genetics ; Inflammation/genetics ; Inflammation/physiopathology ; Lymphocytes/cytology ; Lymphocytes/physiology ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Strongyloidiasis/parasitology ; Strongyloidiasis/physiopathology ; Th2 Cells/pathology ; Th2 Cells/physiology ; Mice
Chemical Substances	GATA3 Transcription Factor ; Gata3 protein, mouse
Language	English
Publishing date	2021-08-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.2106311118
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