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Article: PGI2 as a regulator of CD4+ subset differentiation and function.

Boswell, Madison G / Zhou, Weisong / Newcomb, Dawn C / Peebles, R Stokes

2011 Volume 96, Issue 1-4, Page(s) 21–26

Abstract: Prostaglandin (PG)I(2) has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI(2) modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell ... ...

Abstract	Prostaglandin (PG)I(2) has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI(2) modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell responses. In vitro and in vivo studies support that PGI(2) generally has an inhibitory effect on Th1 and Th2 activation, differentiation, and cytokine production. In contrast, PGI(2) seems to enhance Th17-favoring polarization conditions, resulting in Th17 cytokine production. Therefore, PGI(2) may either promote or inhibit individual CD4+ cell subsets and impact adaptive immune responses.
MeSH term(s)	Adaptive Immunity/drug effects ; Animals ; Cell Differentiation/drug effects ; Cell Differentiation/immunology ; Cells, Cultured ; Cytokines/biosynthesis ; Epoprostenol/analogs & derivatives ; Epoprostenol/immunology ; Epoprostenol/metabolism ; Epoprostenol/pharmacology ; Humans ; Iloprost/pharmacology ; Immunity, Innate/drug effects ; Lymphocyte Activation/drug effects ; Mice ; Mice, Knockout ; Prostaglandins, Synthetic/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/immunology ; Th1 Cells/cytology ; Th1 Cells/drug effects ; Th1 Cells/immunology ; Th17 Cells/cytology ; Th17 Cells/drug effects ; Th17 Cells/immunology ; Th2 Cells/cytology ; Th2 Cells/drug effects ; Th2 Cells/immunology ; Vasodilator Agents/pharmacology
Chemical Substances	Cytokines ; Prostaglandins, Synthetic ; Vasodilator Agents ; Epoprostenol (DCR9Z582X0) ; Iloprost (JED5K35YGL) ; cicaprost (NE94J8CAMD)
Language	English
Publishing date	2011-08-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1426962-4
ISSN	2212-196X ; 1098-8823 ; 0090-6980
ISSN (online)	2212-196X
ISSN	1098-8823 ; 0090-6980
DOI	10.1016/j.prostaglandins.2011.08.003
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Article: PGI2 as a regulator of CD4+ subset differentiation and function

Boswell, Madison G / Zhou, Weisong / Newcomb, Dawn C / Peebles, R. Stokes, Jr

PROSTAGLANDINS & OTHER LIPID MEDIATORS. 2011 Nov., v. 96, no. 1-4

2011

Abstract: Prostaglandin (PG)I2 has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI2 modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell responses. ...

Abstract	Prostaglandin (PG)I2 has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI2 modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell responses. In vitro and in vivo studies support that PGI2 generally has an inhibitory effect on Th1 and Th2 activation, differentiation, and cytokine production. In contrast, PGI2 seems to enhance Th17-favoring polarization conditions, resulting in Th17 cytokine production. Therefore, PGI2 may either promote or inhibit individual CD4+ cell subsets and impact adaptive immune responses.
Keywords	CD4-positive T-lymphocytes ; adaptive immunity ; cytokines ; in vivo studies ; iodine ; prostaglandins
Language	English
Dates of publication	2011-11
Size	p. 21-26.
Publishing place	Elsevier Inc.
Document type	Article
ISSN	1098-8823
DOI	10.1016/j.prostaglandins.2011.08.003
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Deficiency of gp91phox inhibits allergic airway inflammation.

Sevin, Carla M / Newcomb, Dawn C / Toki, Shinji / Han, Wei / Sherrill, Taylor P / Boswell, Madison G / Zhu, Zhou / Collins, Robert D / Boyd, Kelli L / Goleniewska, Kasia / Huckabee, Matthew M / Blackwell, Timothy S / Peebles, R Stokes

American journal of respiratory cell and molecular biology

2013 Volume 49, Issue 3, Page(s) 396–402

Abstract: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a multienzyme complex, is the major source for production of reactive oxygen species (ROS). ROS are increased in allergic diseases, such as asthma, but the role of ROS in disease pathogenesis ... ...

Abstract	Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a multienzyme complex, is the major source for production of reactive oxygen species (ROS). ROS are increased in allergic diseases, such as asthma, but the role of ROS in disease pathogenesis remains uncertain. We hypothesized that mice unable to generate ROS via the NADPH oxidase pathway would have decreased allergic airway inflammation. To test this hypothesis, we studied gp91phox(-/-) mice in a model of allergic airway inflammation after sensitization and challenge with ovalbumin. Serum, bronchoalveolar lavage fluid, and lungs were then examined for evidence of allergic inflammation. We found that mice lacking a functional NADPH oxidase complex had significantly decreased ROS production and allergic airway inflammation, compared with wild-type (WT) control animals. To determine the mechanism by which allergic inflammation was inhibited by gp91phox deficiency, we cultured bone marrow-derived dendritic cells from WT and gp91phox(-/-) mice and activated them with LPS. IL-12 expression was significantly increased in the gp91phox(-/-) bone marrow-derived dendritic cells, suggesting that the cytokine profile produced in the absence of gp91phox enhanced the conditions leading to T helper (Th) type 1 differentiation, while inhibiting Th2 polarization. Splenocytes from sensitized gp91phox(-/-) animals produced significantly less IL-13 in response to ovalbumin challenge in vitro compared with splenocytes from sensitized WT mice, suggesting that NADPH oxidase promotes allergic sensitization. In contrast, inflammatory cytokines produced by T cells cultured from WT and gp91phox(-/-) mice under Th0, Th1, Th2, and Th17 conditions were not significantly different. This study demonstrates the importance of NADPH oxidase activity and ROS production in a murine model of asthma.
MeSH term(s)	Animals ; Asthma/chemically induced ; Asthma/genetics ; Asthma/immunology ; Asthma/pathology ; Bronchoalveolar Lavage Fluid/chemistry ; Cells, Cultured ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Female ; Gene Deletion ; Interleukin-12/biosynthesis ; Interleukin-12/immunology ; Interleukin-13/biosynthesis ; Interleukin-13/immunology ; Lipopolysaccharides/pharmacology ; Lung/immunology ; Lung/metabolism ; Lung/pathology ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/immunology ; Mice ; Mice, Knockout ; NADPH Oxidase 2 ; NADPH Oxidases/deficiency ; NADPH Oxidases/genetics ; NADPH Oxidases/immunology ; Ovalbumin/immunology ; Ovalbumin/pharmacology ; Reactive Oxygen Species/immunology ; Reactive Oxygen Species/metabolism ; Th1 Cells/immunology ; Th1 Cells/pathology ; Th1-Th2 Balance ; Th17 Cells/immunology ; Th17 Cells/pathology ; Th2 Cells/immunology ; Th2 Cells/pathology
Chemical Substances	Interleukin-13 ; Lipopolysaccharides ; Membrane Glycoproteins ; Reactive Oxygen Species ; Interleukin-12 (187348-17-0) ; Ovalbumin (9006-59-1) ; Cybb protein, mouse (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2013-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2012-0442OC
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Article ; Online: IL-17A induces signal transducers and activators of transcription-6-independent airway mucous cell metaplasia.

Newcomb, Dawn C / Boswell, Madison G / Sherrill, Taylor P / Polosukhin, Vasiliy V / Boyd, Kelli L / Goleniewska, Kasia / Brody, Steven L / Kolls, Jay K / Adler, Kenneth B / Peebles, R Stokes

American journal of respiratory cell and molecular biology

2013 Volume 48, Issue 6, Page(s) 711–716

Abstract: Mucous cell metaplasia is a hallmark of asthma, and may be mediated by signal transducers and activators of transcription (STAT)-6 signaling. IL-17A is increased in the bronchoalveolar lavage fluid of patients with severe asthma, and IL-17A also ... ...

Abstract	Mucous cell metaplasia is a hallmark of asthma, and may be mediated by signal transducers and activators of transcription (STAT)-6 signaling. IL-17A is increased in the bronchoalveolar lavage fluid of patients with severe asthma, and IL-17A also increases mucus production in airway epithelial cells. Asthma therapeutics are being developed that inhibit STAT6 signaling, but the role of IL-17A in inducing mucus production in the absence of STAT6 remains unknown. We hypothesized that IL-17A induces mucous cell metaplasia independent of STAT6, and we tested this hypothesis in two murine models in which increased IL-17A protein expression is evident. In the first model, ovalbumin (OVA)-specific D011.10 Th17 cells were adoptively transferred into wild-type (WT) or STAT6 knockout (KO) mice, and the mice were challenged with OVA or PBS. WT-OVA and STAT6 KO-OVA mice demonstrated increased airway IL-17A and IL-13 protein expression and mucous cell metaplasia, compared with WT-PBS or STAT6 KO-PBS mice. In the second model, WT, STAT1 KO, STAT1/STAT6 double KO (DKO), or STAT1/STAT6/IL-17 receptor A (RA) triple KO (TKO) mice were challenged with respiratory syncytial virus (RSV) or mock viral preparation, and the mucous cells were assessed. STAT1 KO-RSV mice demonstrated increased airway mucous cell metaplasia compared with WT-RSV mice. STAT1 KO-RSV and STAT1/STAT6 DKO-RSV mice also demonstrated increased mucous cell metaplasia, compared with STAT1/STAT6/IL17RA TKO-RSV mice. We also treated primary murine tracheal epithelial cells (mTECs) from WT and STAT6 KO mice. STAT6 KO mTECs showed increased periodic acid-Schiff staining with IL-17A but not with IL-13. Thus, asthma therapies targeting STAT6 may increase IL-17A protein expression, without preventing IL-17A-induced mucus production.
MeSH term(s)	Adoptive Transfer ; Animals ; Bronchoalveolar Lavage Fluid/immunology ; Female ; Interleukin-13/metabolism ; Interleukin-17/genetics ; Interleukin-17/metabolism ; Lung/immunology ; Lung/pathology ; Metaplasia/immunology ; Metaplasia/pathology ; Metaplasia/virology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mucus/metabolism ; Neutrophils/metabolism ; Ovalbumin/administration & dosage ; Ovalbumin/immunology ; Peptide Fragments/administration & dosage ; Peptide Fragments/immunology ; Receptors, Interleukin-17/genetics ; Receptors, Interleukin-17/immunology ; Receptors, Interleukin-17/metabolism ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Virus Infections/pathology ; Respiratory Syncytial Viruses/immunology ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; STAT6 Transcription Factor/genetics ; STAT6 Transcription Factor/metabolism ; Th17 Cells/immunology ; Transcriptional Activation
Chemical Substances	Il17a protein, mouse ; Il17ra protein, mouse ; Interleukin-13 ; Interleukin-17 ; OVA 323-339 ; Peptide Fragments ; Receptors, Interleukin-17 ; STAT1 Transcription Factor ; STAT6 Transcription Factor ; Stat1 protein, mouse ; Stat6 protein, mouse ; Ovalbumin (9006-59-1)
Language	English
Publishing date	2013-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2013-0017OC
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Article ; Online: IL-17A inhibits airway reactivity induced by respiratory syncytial virus infection during allergic airway inflammation.

Newcomb, Dawn Catherine / Boswell, Madison G / Reiss, Sara / Zhou, Weisong / Goleniewska, Kasia / Toki, Shinji / Harintho, Melissa T / Lukacs, Nicholas W / Kolls, Jay K / Peebles, R Stokes

Thorax

2013 Volume 68, Issue 8, Page(s) 717–723

Abstract: Background: Viral infections are the most frequent cause of asthma exacerbations and are linked to increased airway reactivity (AR) and inflammation. Mice infected with respiratory syncytial virus (RSV) during ovalbumin (OVA)-induced allergic airway ... ...

Abstract	Background: Viral infections are the most frequent cause of asthma exacerbations and are linked to increased airway reactivity (AR) and inflammation. Mice infected with respiratory syncytial virus (RSV) during ovalbumin (OVA)-induced allergic airway inflammation (OVA/RSV) had increased AR compared with OVA or RSV mice alone. Furthermore, interleukin 17A (IL-17A) was only increased in OVA/RSV mice. Objective: To determine whether IL-17A increases AR and inflammation in the OVA/RSV model. Methods: Wild-type (WT) BALB/c and IL-17A knockout (KO) mice underwent mock, RSV, OVA or OVA/RSV protocols. Lungs, bronchoalveolar lavage (BAL) fluid and/or mediastinal lymph nodes (MLNs) were harvested after infection. Cytokine expression was determined by ELISA in the lungs or BAL fluid. MLNs were restimulated with either OVA (323-229) peptide or RSV M2 (127-135) peptide and IL-17A protein expression was analysed. AR was determined by methacholine challenge. Results: RSV increased IL-17A protein expression by OVA-specific T cells 6 days after infection. OVA/RSV mice had decreased interferon-β protein expression compared with RSV mice. OVA/RSV mice had increased IL-23p19 mRNA expression in lung homogenates compared with mock, OVA or RSV mice. Unexpectedly, IL-17A KO OVA/RSV mice had increased AR compared with WT OVA/RSV mice. Furthermore, IL-17A KO OVA/RSV mice had increased eosinophils, lymphocytes and IL-13 protein expression in BAL fluid compared with WT OVA/RSV mice. Conclusions: IL-17A negatively regulated AR and airway inflammation in OVA/RSV mice. This finding is important because IL-17A has been identified as a potential therapeutic target in asthma, and inhibiting IL-17A in the setting of virally-induced asthma exacerbations may have adverse consequences.
MeSH term(s)	Animals ; Asthma/genetics ; Asthma/metabolism ; Asthma/pathology ; Bronchoalveolar Lavage Fluid/chemistry ; Cytokines/biosynthesis ; Cytokines/genetics ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Female ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Interleukin-17/biosynthesis ; Interleukin-17/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Respiratory Syncytial Virus Infections/genetics ; Respiratory Syncytial Virus Infections/metabolism ; Respiratory Syncytial Virus Infections/virology
Chemical Substances	Cytokines ; Interleukin-17 ; RNA, Messenger
Language	English
Publishing date	2013-02-19
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	204353-1
ISSN	1468-3296 ; 0040-6376
ISSN (online)	1468-3296
ISSN	0040-6376
DOI	10.1136/thoraxjnl-2012-202404
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Article ; Online: Estrogen and progesterone decrease let-7f microRNA expression and increase IL-23/IL-23 receptor signaling and IL-17A production in patients with severe asthma.

Newcomb, Dawn C / Cephus, Jacqueline Yvonne / Boswell, Madison G / Fahrenholz, John M / Langley, Emily W / Feldman, Amy S / Zhou, Weisong / Dulek, Daniel E / Goleniewska, Kasia / Woodward, Kimberly B / Sevin, Carla M / Hamilton, Robert G / Kolls, Jay K / Peebles, R Stokes

The Journal of allergy and clinical immunology

2015 Volume 136, Issue 4, Page(s) 1025–34.e11

Abstract: Background: Women have an increased prevalence of severe asthma compared with men. IL-17A is associated with severe asthma and requires IL-23 receptor (IL-23R) signaling, which is negatively regulated by let-7f microRNA.: Objective: We sought to ... ...

Abstract	Background: Women have an increased prevalence of severe asthma compared with men. IL-17A is associated with severe asthma and requires IL-23 receptor (IL-23R) signaling, which is negatively regulated by let-7f microRNA. Objective: We sought to Determine the mechanism by which 17β-estradiol (E2) and progesterone (P4) increase IL-17A production. Methods: IL-17A production was determined by using flow cytometry in TH17 cells from women (n = 14) and men (n = 15) with severe asthma. Cytokine levels were measured by using ELISA, and IL-23R and let-7f expression was measured by using quantitative PCR in TH17-differentiated cells from healthy women (n = 13) and men (n = 14). In sham-operated or ovariectomized female mice, 17β-E2, P4, 17β-E2+P4, or vehicle pellets were administered for 3 weeks before ex vivo TH17 cell differentiation. Airway neutrophil infiltration and CXCL1 (KC) expression were also determined in ovalbumin (OVA)-challenged wild-type female recipient mice with an adoptive transfer of OVA-specific TH17 cells from female and male mice. Results: In patients with severe asthma and healthy control subjects, IL-17A production was increased in TH17 cells from women compared with men. IL-23R expression was increased and let-7f expression was decreased in TH17-differentiated cells from women compared with men. In ovariectomized mice IL-17A and IL-23R expression was increased and Let-7f expression was decreased in TH17 cells from mice administered 17β-E2+P4 compared with those administered vehicle. Furthermore, transfer of female OVA-specific TH17 cells increased acute neutrophil infiltration in the lungs of OVA-challenged recipient mice compared with transfer of male OVA-specific TH17 cells. Conclusions: 17β-E2+P4 increased IL-17A production from TH17 cells, providing a potential mechanism for the increased prevalence of severe asthma in women compared with men.
MeSH term(s)	Adolescent ; Adult ; Animals ; Asthma/immunology ; Asthma/pathology ; Estrogens/immunology ; Female ; Gene Expression Regulation/immunology ; Humans ; Interleukin-17/immunology ; Interleukin-23/immunology ; Male ; Mice ; MicroRNAs/immunology ; Middle Aged ; Progesterone/immunology ; Receptors, Interleukin/immunology ; Signal Transduction/immunology ; Th17 Cells/immunology ; Th17 Cells/pathology
Chemical Substances	Estrogens ; IL17A protein, human ; IL23R protein, human ; Il17a protein, mouse ; Interleukin-17 ; Interleukin-23 ; MicroRNAs ; Receptors, Interleukin ; interleukin-23 receptor, mouse ; mirnlet7 microRNA, human ; mirnlet7 microRNA, mouse ; Progesterone (4G7DS2Q64Y)
Language	English
Publishing date	2015-10
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2015.05.046
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Article ; Online: Cyclooxygenase inhibition abrogates aeroallergen-induced immune tolerance by suppressing prostaglandin I2 receptor signaling.

Zhou, Weisong / Goleniewska, Kasia / Zhang, Jian / Dulek, Daniel E / Toki, Shinji / Lotz, Matthew T / Newcomb, Dawn C / Boswell, Madison G / Polosukhin, Vasiliy V / Milne, Ginger L / Wu, Pingsheng / Moore, Martin L / FitzGerald, Garret A / Peebles, R Stokes

The Journal of allergy and clinical immunology

2014 Volume 134, Issue 3, Page(s) 698–705.e5

Abstract: Background: The prevalence of allergic diseases has doubled in developed countries in the past several decades. Cyclooxygenase (COX)-inhibiting drugs augmented allergic diseases in mice by increasing allergic sensitization and memory immune responses. ... ...

Abstract	Background: The prevalence of allergic diseases has doubled in developed countries in the past several decades. Cyclooxygenase (COX)-inhibiting drugs augmented allergic diseases in mice by increasing allergic sensitization and memory immune responses. However, whether COX inhibition can promote allergic airway diseases by inhibiting immune tolerance is not known. Objective: To determine the role of the COX pathway and prostaglandin I2 (PGI2) signaling through the PGI2 receptor (IP) in aeroallergen-induced immune tolerance. Methods: Wild-type (WT) BALB/c mice and IP knockout mice were aerosolized with ovalbumin (OVA) to induce immune tolerance prior to immune sensitization with an intraperitoneal injection of OVA/alum. The COX inhibitor indomethacin or vehicle was administered in drinking water to inhibit enzyme activity during the sensitization phase. Two weeks after sensitization, the mice were challenged with OVA aerosols. Mouse bronchoalveolar lavage fluid was harvested for cell counts and TH2 cytokine measurements. Results: WT mice treated with indomethacin had greater numbers of total cells, eosinophils, and lymphocytes, and increased IL-5 and IL-13 protein expression in BAL fluid compared to vehicle-treated mice. Similarly, IP knockout mice had augmented inflammation and TH2 cytokine responses compared to WT mice. In contrast, the PGI2 analog cicaprost attenuated the anti-tolerance effect of COX inhibition. Conclusion: COX inhibition abrogated immune tolerance by suppressing PGI2 IP signaling, suggesting that PGI2 signaling promotes immune tolerance and that clinical use of COX-inhibiting drugs may increase the risk of developing allergic diseases.
MeSH term(s)	Air Pollution/adverse effects ; Allergens/adverse effects ; Allergens/immunology ; Animals ; Enzyme Inhibitors/administration & dosage ; Epoprostenol/metabolism ; Humans ; Hypersensitivity/immunology ; Immune Tolerance ; Indomethacin/administration & dosage ; Indomethacin/pharmacology ; Mice ; Mice, 129 Strain ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Ovalbumin/immunology ; Prostaglandin-Endoperoxide Synthases/metabolism ; Receptors, Epoprostenol/genetics ; Receptors, Epoprostenol/metabolism ; Signal Transduction
Chemical Substances	Allergens ; Enzyme Inhibitors ; Receptors, Epoprostenol ; Ovalbumin (9006-59-1) ; Epoprostenol (DCR9Z582X0) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2014-07-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2014.06.004
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Article ; Online: Human TH17 cells express a functional IL-13 receptor and IL-13 attenuates IL-17A production.

Newcomb, Dawn C / Boswell, Madison G / Zhou, Weisong / Huckabee, Matthew M / Goleniewska, Kasia / Sevin, Carla M / Hershey, Gurjit K Khurana / Kolls, Jay K / Peebles, R Stokes

The Journal of allergy and clinical immunology

2011 Volume 127, Issue 4, Page(s) 1006–13.e1–4

Abstract: Background: IL-13 is a central mediator of airway responsiveness and mucus expression in patients with allergic airway inflammation, and IL-13 is currently a therapeutic target for asthma. However, little is known about how IL-13 regulates human CD4(+) ... ...

Abstract	Background: IL-13 is a central mediator of airway responsiveness and mucus expression in patients with allergic airway inflammation, and IL-13 is currently a therapeutic target for asthma. However, little is known about how IL-13 regulates human CD4(+) T-cell lineages because IL-13 receptor (IL-13R) α1, a subunit of IL-13R, has not previously been reported to exist on human T cells. Objective: We sought to determine whether human CD4(+) T(H)17 cells express IL-13Rα1 and whether IL-13 regulates T(H)17 cytokine production. Methods: Naive human CD4(+) cells were isolated from whole blood, activated with anti-CD3 and anti-CD28, and polarized to T(H)1, T(H)2, T(H)17, or induced regulatory T cells in the presence of IL-13 (0-10 ng/mL). Cell supernatants, total RNA, or total protein was examined 4 days after T(H)17 polarization. Results: T(H)17 cells, but not T(H)0, T(H)1, T(H)2, or induced regulatory T cells, expressed IL-13Rα1. IL-13 attenuated IL-17A production, as well as expression of retinoic acid-related orphan receptor, runt-related transcription factor-1, and interferon regulatory factor 4 in T(H)17-polarized cells. IL-13 neither inhibited IFN-γ production from T(H)1 cells nor inhibited IL-4 production from T(H)2 cells. Furthermore, attenuation of IL-17A production only occurred when IL-13 was present within 24 hours of T-cell activation or at the time of restimulation. Conclusions: IL-13Rα1 is expressed on human CD4(+) T(H)17 cells, and IL-13 attenuates IL-17A production at polarization and restimulation. Although IL-13 is an attractive therapeutic target for decreasing symptoms associated with asthma, these results suggest that therapies inhibiting IL-13 production could have adverse side effects by increasing IL-17A production.
MeSH term(s)	Cell Separation ; Flow Cytometry ; Humans ; Immunoblotting ; Interleukin-13/immunology ; Interleukin-13/metabolism ; Interleukin-13 Receptor alpha1 Subunit/biosynthesis ; Interleukin-13 Receptor alpha1 Subunit/immunology ; Interleukin-17/biosynthesis ; Interleukin-17/immunology ; Lymphocyte Activation/immunology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Th17 Cells/immunology ; Th17 Cells/metabolism
Chemical Substances	IL13RA1 protein, human ; Interleukin-13 ; Interleukin-13 Receptor alpha1 Subunit ; Interleukin-17
Language	English
Publishing date	2011-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2010.11.043
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Article ; Online: IL-13 regulates Th17 secretion of IL-17A in an IL-10-dependent manner.

Newcomb, Dawn C / Boswell, Madison G / Huckabee, Matthew M / Goleniewska, Kasia / Dulek, Daniel E / Reiss, Sara / Lukacs, Nicholas W / Kolls, Jay K / Peebles, R Stokes

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 188, Issue 3, Page(s) 1027–1035

Abstract: IL-13 is a central mediator of airway hyperresponsiveness and mucus expression, both hallmarks of asthma. IL-13 is found in the sputum of patients with asthma; therefore, IL-13 is an attractive drug target for treating asthma. We have shown previously ... ...

Abstract	IL-13 is a central mediator of airway hyperresponsiveness and mucus expression, both hallmarks of asthma. IL-13 is found in the sputum of patients with asthma; therefore, IL-13 is an attractive drug target for treating asthma. We have shown previously that IL-13 inhibits Th17 cell production of IL-17A and IL-21 in vitro. Th17 cells are associated with autoimmune diseases, host immune responses, and severe asthma. In this study, we extend our in vitro findings and determine that IL-13 increases IL-10 production from Th17-polarized cells and that IL-13-induced IL-10 production negatively regulates the secretion of IL-17A and IL-21. To determine if IL-13 negatively regulates lung IL-17A expression via an IL-10-dependent mechanism in vivo, we used a model of respiratory syncytial virus (RSV) strain A2 infection in STAT1 knockout (KO) mice that increases lung IL-17A and IL-13 expression, cytokines not produced during RSV infection in wild-type mice. To test the hypothesis that IL-13 negatively regulates lung IL-17A expression, we created STAT1/IL-13 double KO (DKO) mice. We found that RSV-infected STAT1/IL-13 DKO mice had significantly greater lung IL-17A expression compared with that of STAT1 KO mice and that increased IL-17A expression was abrogated by anti-IL-10 Ab treatment. RSV-infected STAT1/IL-13 DKO mice also had increased neutrophil infiltration compared with that of RSV-infected STAT1 KO mice. Neutralizing IL-10 increased the infiltration of inflammatory cells into the lungs of STAT1 KO mice but not STAT1/IL-13 DKO mice. These findings are vital to understanding the potential side effects of therapeutics targeting IL-13. Inhibiting IL-13 may decrease IL-10 production and increase IL-17A production, thus potentiating IL-17A-associated diseases.
MeSH term(s)	Animals ; Cell Movement ; Interleukin-10/physiology ; Interleukin-13/physiology ; Interleukin-17/metabolism ; Lung/immunology ; Lung/metabolism ; Mice ; Mice, Knockout ; Neutrophil Infiltration/immunology ; Pneumonia/immunology ; Pneumonia/pathology ; Pneumonia/virology ; Respiratory Syncytial Virus Infections/immunology ; Th17 Cells/metabolism
Chemical Substances	IL10 protein, mouse ; Interleukin-13 ; Interleukin-17 ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2011-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
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.1102216
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Human TH17 cells express a functional IL-13 receptor and IL-13 attenuates IL-17A production

Newcomb, Dawn C / Boswell, Madison G / Zhou, Weisong / Huckabee, Matthew M / Goleniewska, Kasia / Sevin, Carla M / Khurana Hershey, Gurjit K / Kolls, Jay K / Peebles, R. Stokes, Jr

The Journal of Allergy and Clinical Immunology. 2011 Apr., v. 127, no. 4

2011

Abstract: BACKGROUND: IL-13 is a central mediator of airway responsiveness and mucus expression in patients with allergic airway inflammation, and IL-13 is currently a therapeutic target for asthma. However, little is known about how IL-13 regulates human CD4+ T- ... ...

Abstract	BACKGROUND: IL-13 is a central mediator of airway responsiveness and mucus expression in patients with allergic airway inflammation, and IL-13 is currently a therapeutic target for asthma. However, little is known about how IL-13 regulates human CD4+ T-cell lineages because IL-13 receptor (IL-13R) α1, a subunit of IL-13R, has not previously been reported to exist on human T cells. OBJECTIVE: We sought to determine whether human CD4+ TH17 cells express IL-13Rα1 and whether IL-13 regulates TH17 cytokine production. METHODS: Naive human CD4+ cells were isolated from whole blood, activated with anti-CD3 and anti-CD28, and polarized to TH1, TH2, TH17, or induced regulatory T cells in the presence of IL-13 (0-10 ng/mL). Cell supernatants, total RNA, or total protein was examined 4 days after TH17 polarization. RESULTS: TH17 cells, but not TH0, TH1, TH2, or induced regulatory T cells, expressed IL-13Rα1. IL-13 attenuated IL-17A production, as well as expression of retinoic acid–related orphan receptor, runt-related transcription factor-1, and interferon regulatory factor 4 in TH17-polarized cells. IL-13 neither inhibited IFN-γ production from TH1 cells nor inhibited IL-4 production from TH2 cells. Furthermore, attenuation of IL-17A production only occurred when IL-13 was present within 24 hours of T-cell activation or at the time of restimulation. CONCLUSIONS: IL-13Rα1 is expressed on human CD4+ TH17 cells, and IL-13 attenuates IL-17A production at polarization and restimulation. Although IL-13 is an attractive therapeutic target for decreasing symptoms associated with asthma, these results suggest that therapies inhibiting IL-13 production could have adverse side effects by increasing IL-17A production.
Keywords	CD4-positive T-lymphocytes ; RNA ; adverse effects ; asthma ; humans ; inflammation ; interferon regulatory factor-4 ; interferon-gamma ; interleukin-13 ; interleukin-17 ; interleukin-4 ; mucus ; patients
Language	English
Dates of publication	2011-04
Size	p. 1006-1013.e4.
Publishing place	Mosby, Inc.
Document type	Article
ZDB-ID	121011-7
ISSN	1085-8725 ; 1097-6825 ; 0091-6749
ISSN (online)	1085-8725 ; 1097-6825
ISSN	0091-6749
DOI	10.1016/j.jaci.2010.11.043
Database	NAL-Catalogue (AGRICOLA)

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