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Article: Mucosal Tuft Cell Density Is Increased in Diarrhea-Predominant Irritable Bowel Syndrome Colonic Biopsies.

Aigbologa, Jessica / Connolly, Maeve / Buckley, Julliette M / O'Malley, Dervla

2020 Volume 11, Page(s) 436

Abstract: Tuft cells are rare chemosensory sentinels found in the gut epithelium. When triggered by helminth infection, tuft cells secrete interleukin-25 (IL-25) basolaterally and subsequently evoke an immune response. Irritable bowel syndrome (IBS) is a common ... ...

Abstract	Tuft cells are rare chemosensory sentinels found in the gut epithelium. When triggered by helminth infection, tuft cells secrete interleukin-25 (IL-25) basolaterally and subsequently evoke an immune response. Irritable bowel syndrome (IBS) is a common and heterogeneous disorder characterized by bowel dysfunction and visceral pain sensitivity. Dysfunctional gut-brain communication and immune activation contribute to the pathophysiology of this disorder. The study aims were to investigate changes in tuft cell density in non-post-infectious IBS patients. Immunofluorescent labeling of DCLK1-positive tuft cells was carried out in mucosal biopsies from the distal colons of diarrhea and constipation-predominant IBS patients and healthy controls. Tuft cell numbers were also assessed in animal models. Concentrations of interleukin-25 (IL-25) secreted from colonic biopsies and in plasma samples were analyzed using an immunoassay. The density of tuft cells was increased in diarrhea-but not constipation-predominant IBS patient colonic biopsies. Biopsy secretions and plasma concentrations of IL-25 were elevated in diarrhea-but not constipation-predominant IBS participants. Tuft cell hyperplasia was detected in a rat model of IBS but not in mice exposed to chronic stress. Tuft cell hyperplasia is an innate immune response to helminth exposure. However, the patients with diarrhea-predominant IBS have not reported any incidents of enteric infection. Moreover, rats exhibiting IBS-like symptoms displayed increased tuft cell density but were not exposed to helminths. Our findings suggest that factors other than helminth exposure or chronic stress lead to tuft cell hyperplasia in IBS colonic biopsies.
Language	English
Publishing date	2020-05-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564218-2
ISSN	1664-0640
ISSN	1664-0640
DOI	10.3389/fpsyt.2020.00436
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Article ; Online: Aromatase inhibition to decrease background parenchymal enhancement: premedication before magnetic resonance imaging?

Buckley, Julliette M / Hughes, Kevin S

Menopause (New York, N.Y.)

2012 Volume 19, Issue 4, Page(s) 385–386

MeSH term(s)	Aromatase Inhibitors ; Breast/pathology ; Female ; Humans ; Image Enhancement/methods ; Magnetic Resonance Imaging/methods ; Postmenopause
Chemical Substances	Aromatase Inhibitors
Language	English
Publishing date	2012-04
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	1205262-0
ISSN	1530-0374 ; 1072-3714
ISSN (online)	1530-0374
ISSN	1072-3714
DOI	10.1097/gme.0b013e31824af478
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Article ; Online: GHSR-1 agonist sensitizes rat colonic intrinsic and extrinsic neurons to exendin-4: A role in the manifestation of postprandial gastrointestinal symptoms in irritable bowel syndrome?

Buckley, Maria M / O'Brien, Rebecca / Buckley, Julliette M / O'Malley, Dervla

Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society

2019 Volume 31, Issue 10, Page(s) e13684

Abstract: Background: Patients with irritable bowel syndrome (IBS) may experience postprandial symptom exacerbation. Nutrients stimulate intestinal release of glucagon-like peptide 1 (GLP-1), an incretin hormone with known gastrointestinal effects. However, prior ...

Abstract	Background: Patients with irritable bowel syndrome (IBS) may experience postprandial symptom exacerbation. Nutrients stimulate intestinal release of glucagon-like peptide 1 (GLP-1), an incretin hormone with known gastrointestinal effects. However, prior to the postprandial rise in GLP-1, levels of the hunger hormone, ghrelin, peak. The aims of this study were to determine if ghrelin sensitizes colonic intrinsic and extrinsic neurons to the stimulatory actions of a GLP-1 receptor agonist, and if this differs in a rat model of IBS. Methods: Calcium imaging of enteric neurons was compared between Sprague Dawley and Wistar Kyoto rats. Colonic contractile activity and vagal nerve recordings were also compared between strains. Key results: Circulating GLP-1 concentrations differ between IBS subtypes. Mechanistically, we have provided evidence that calcium responses evoked by exendin-4, a GLP-1 receptor agonist, are potentiated by a ghrelin receptor (GHSR-1) agonist, in both submucosal and myenteric neurons. Although basal patterns of colonic contractility varied between Sprague Dawley and Wister Kyoto rats, the capacity of exendin-4 to alter smooth muscle function was modified by a GHSR-1 agonist in both strains. Gut-brain signaling via GLP-1-mediated activation of vagal afferents was also potentiated by the GHSR-1 agonist. Conclusions & inferences: These findings support a temporal interaction between ghrelin and GLP-1, where the preprandial peak in ghrelin may temporarily sensitize colonic intrinsic and extrinsic neurons to the neurostimulatory actions of GLP-1. While the sensitizing effects of the GHSR-1 agonist were identified in both rat strains, in the rat model of IBS, underlying contractile activity was aberrant.
MeSH term(s)	Animals ; Colon/drug effects ; Colon/innervation ; Colon/metabolism ; Constipation/metabolism ; Constipation/physiopathology ; Diarrhea/metabolism ; Diarrhea/physiopathology ; Electrophysiological Phenomena ; Enteric Nervous System/cytology ; Enteric Nervous System/drug effects ; Exenatide/pharmacology ; Ghrelin/metabolism ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/agonists ; Humans ; Incretins/pharmacology ; Irritable Bowel Syndrome/metabolism ; Irritable Bowel Syndrome/physiopathology ; Muscle Contraction/drug effects ; Muscle, Smooth/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Rats ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Receptors, Ghrelin/agonists ; Vagus Nerve/drug effects ; Vagus Nerve/metabolism
Chemical Substances	Ghrelin ; Glucagon-Like Peptide-1 Receptor ; Incretins ; Receptors, Ghrelin ; Glucagon-Like Peptide 1 (89750-14-1) ; Exenatide (9P1872D4OL)
Language	English
Publishing date	2019-07-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1186328-6
ISSN	1365-2982 ; 1350-1925
ISSN (online)	1365-2982
ISSN	1350-1925
DOI	10.1111/nmo.13684
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Article: Glucagon-Like Peptide-1 Secreting L-Cells Coupled to Sensory Nerves Translate Microbial Signals to the Host Rat Nervous System.

Buckley, Maria M / O'Brien, Rebecca / Brosnan, Eilish / Ross, R Paul / Stanton, Catherine / Buckley, Julliette M / O'Malley, Dervla

Frontiers in cellular neuroscience

2020 Volume 14, Page(s) 95

Abstract: An intact gut epithelium preserves the immunological exclusion of "non-self" entities in the external environment of the gut lumen. Nonetheless, information flows continuously across this interface, with the host immune, endocrine, and neural systems all ...

Abstract	An intact gut epithelium preserves the immunological exclusion of "non-self" entities in the external environment of the gut lumen. Nonetheless, information flows continuously across this interface, with the host immune, endocrine, and neural systems all involved in monitoring the luminal environment of the gut. Both pathogenic and commensal gastrointestinal (GI) bacteria can modulate centrally-regulated behaviors and brain neurochemistry and, although the vagus nerve has been implicated in the microbiota-gut-brain signaling axis, the cellular and molecular machinery that facilitates this communication is unclear. Studies were carried out in healthy Sprague-Dawley rats to understand cross-barrier communication in the absence of disease. A novel colonic-nerve electrophysiological technique was used to examine gut-to-brain vagal signaling by bacterial products. Calcium imaging and immunofluorescent labeling were used to explore the activation of colonic submucosal neurons by bacterial products. The findings demonstrate that the neuromodulatory molecule, glucagon-like peptide-1 (GLP-1), secreted by colonic enteroendocrine L-cells in response to the bacterial metabolite, indole, stimulated colonic vagal afferent activity. At a local level indole modified the sensitivity of submucosal neurons to GLP-1. These findings elucidate a cellular mechanism by which sensory L-cells act as cross-barrier signal transducers between microbial products in the gut lumen and the host peripheral nervous system.
Language	English
Publishing date	2020-04-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2020.00095
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Article ; Online: Imaging of the complications of acute pancreatitis.

O'Connor, Owen J / Buckley, Julliette M / Maher, Michael M

AJR. American journal of roentgenology

2011 Volume 197, Issue 3, Page(s) W375–81

MeSH term(s)	Diagnostic Imaging ; Humans ; Pancreatitis/complications ; Pancreatitis/epidemiology ; Pancreatitis/physiopathology ; Severity of Illness Index
Language	English
Publishing date	2011-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	82076-3
ISSN	1546-3141 ; 0361-803X ; 0092-5381
ISSN (online)	1546-3141
ISSN	0361-803X ; 0092-5381
DOI	10.2214/AJR.10.4339
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Article ; Online: Doctor, would you drain this collection?

O'Connor, Owen J / Buckley, Julliette M / Arellano, Ronald S

Journal of vascular and interventional radiology : JVIR

2012 Volume 23, Issue 4, Page(s) 519

MeSH term(s)	Collagen/adverse effects ; Drainage ; Extravasation of Diagnostic and Therapeutic Materials/diagnostic imaging ; Extravasation of Diagnostic and Therapeutic Materials/etiology ; Extravasation of Diagnostic and Therapeutic Materials/surgery ; Humans ; Liver/diagnostic imaging ; Male ; Middle Aged ; Tomography, X-Ray Computed
Chemical Substances	Alloderm ; Collagen (9007-34-5)
Language	English
Publishing date	2012-04
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	1137756-2
ISSN	1535-7732 ; 1051-0443
ISSN (online)	1535-7732
ISSN	1051-0443
DOI	10.1016/j.jvir.2012.01.054
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Article ; Online: Reassessing risk models for atypical hyperplasia: age may not matter.

Mazzola, Emanuele / Coopey, Suzanne B / Griffin, Molly / Polubriaginof, Fernanda / Buckley, Julliette M / Parmigiani, Giovanni / Garber, Judy E / Smith, Barbara L / Gadd, Michele A / Specht, Michelle C / Guidi, Anthony / Hughes, Kevin S

Breast cancer research and treatment

2017 Volume 165, Issue 2, Page(s) 285–291

Abstract: Purpose: The aim of this study was to investigate the influence of age at diagnosis of atypical hyperplasia ("atypia", ductal [ADH], lobular [ALH], or severe ADH) on the risk of developing subsequent invasive breast cancer or ductal carcinoma in situ ( ... ...

Abstract	Purpose: The aim of this study was to investigate the influence of age at diagnosis of atypical hyperplasia ("atypia", ductal [ADH], lobular [ALH], or severe ADH) on the risk of developing subsequent invasive breast cancer or ductal carcinoma in situ (DCIS). Methods: Using standard survival analysis methods, we retrospectively analyzed 1353 women not treated with chemoprevention among a cohort of 2370 women diagnosed with atypical hyperplasia to determine the risk relationship between age at diagnosis and subsequent breast cancer. Results: For all atypia diagnoses combined, our cohort showed a 5-, 10-, and 15-year risk of invasive breast cancer or DCIS of 0.56, 1.25, and 1.30, respectively, with no significant difference in the (65,75] year age group. For women aged (35,75] years, we observed no significant difference in the 15-year risk of invasive breast cancer or DCIS after atypical hyperplasia, although the baseline risk for a 40-year-old woman is approximately 1/8 the risk of a 70-year-old woman. The risks associated with invasive breast cancer or DCIS for women in our cohort diagnosed with ADH, severe ADH, or ALH, regardless of age, were 7.6% (95% CI 5.9-9.3%) at 5 years, 25.1% (20.7-29.2%) at 10 years, and 40.1% (32.8-46.6%) at 15 years. Conclusion: In contrast to current risk prediction models (e.g., Gail, Tyrer-Cuzick) which assume that the risk of developing breast cancer increases in relation to age at diagnosis of atypia, we found the 15-year cancer risk in our cohort was not significantly different for women between the ages of 35 (excluded) and 75. This implies that the "hits" received by the breast tissue along the "high-risk pathway" to cancer might possibly supersede other factors such as age.
MeSH term(s)	Adult ; Age Factors ; Aged ; Aged, 80 and over ; Biomarkers ; Breast/pathology ; Breast Neoplasms/diagnosis ; Breast Neoplasms/epidemiology ; Female ; Humans ; Hyperplasia ; Kaplan-Meier Estimate ; Middle Aged ; Neoplasm Grading ; Precancerous Conditions/epidemiology ; Precancerous Conditions/pathology ; Prognosis ; Risk Assessment
Chemical Substances	Biomarkers
Language	English
Publishing date	2017-06-06
Publishing country	Netherlands
Document type	Journal Article ; Meta-Analysis ; Review
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-017-4320-7
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Article ; Online: ST2 negatively regulates TLR2 signaling, but is not required for bacterial lipoprotein-induced tolerance.

Liu, Jinghua / Buckley, Julliette M / Redmond, H Paul / Wang, Jiang Huai

Journal of immunology (Baltimore, Md. : 1950)

2010 Volume 184, Issue 10, Page(s) 5802–5808

Abstract: Activation of TLR signaling is critical for host innate immunity against bacterial infection. Previous studies reported that the ST2 receptor, a member of the Toll/IL-1 receptor superfamily, functions as a negative regulator of TLR4 signaling and ... ...

Abstract	Activation of TLR signaling is critical for host innate immunity against bacterial infection. Previous studies reported that the ST2 receptor, a member of the Toll/IL-1 receptor superfamily, functions as a negative regulator of TLR4 signaling and maintains LPS tolerance. However, it is undetermined whether ST2 negatively regulates TLR2 signaling and furthermore, whether a TLR2 agonist, bacterial lipoprotein (BLP)-induced tolerance is dependent on ST2. In this study, we show that BLP stimulation-induced production of proinflammatory cytokines and immunocomplex formation of TLR2-MyD88 and MyD88-IL-1R-associated kinase (IRAK) were significantly enhanced in ST2-deficient macrophages compared with those in wild-type controls. Furthermore, overexpression of ST2 dose-dependently attenuated BLP-induced NF-kappaB activation, suggesting a negative regulatory role of ST2 in TLR2 signaling. A moderate but significantly attenuated production of TNF-alpha and IL-6 on a second BLP stimulation was observed in BLP-pretreated, ST2-deficient macrophages, which is associated with substantially reduced IRAK-1 protein expression and downregulated TLR2-MyD88 and MyD88-IRAK immunocomplex formation. ST2-deficient mice, when pretreated with a nonlethal dose of BLP, benefitted from an improved survival against a subsequent lethal BLP challenge, indicating BLP tolerance develops in the absence of the ST2 receptor. Taken together, our results demonstrate that ST2 acts as a negative regulator of TLR2 signaling, but is not required for BLP-induced tolerance.
MeSH term(s)	Animals ; Bacterial Proteins/physiology ; Cells, Cultured ; Down-Regulation/genetics ; Down-Regulation/immunology ; Humans ; Immune Tolerance/genetics ; Interleukin-1 Receptor-Like 1 Protein ; Lipoproteins/physiology ; Macrophages, Peritoneal/immunology ; Macrophages, Peritoneal/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Receptors, Interleukin/deficiency ; Receptors, Interleukin/genetics ; Receptors, Interleukin/physiology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Toll-Like Receptor 2/agonists ; Toll-Like Receptor 2/antagonists & inhibitors ; Toll-Like Receptor 2/physiology
Chemical Substances	Bacterial Proteins ; Il1rl1 protein, mouse ; Interleukin-1 Receptor-Like 1 Protein ; Lipoproteins ; Receptors, Interleukin ; Tlr2 protein, mouse ; Toll-Like Receptor 2
Language	English
Publishing date	2010-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.0904127
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Article: Cellular reprogramming by gram-positive bacterial components: a review.

Buckley, Julliette M / Wang, Jiang Huai / Redmond, H Paul

Journal of leukocyte biology

2006 Volume 80, Issue 4, Page(s) 731–741

Abstract: LPS tolerance has been the focus of extensive scientific and clinical research over the last several decades in an attempt to elucidate the sequence of changes that occur at a molecular level in tolerized cells. Tolerance to components of gram-positive ... ...

Abstract	LPS tolerance has been the focus of extensive scientific and clinical research over the last several decades in an attempt to elucidate the sequence of changes that occur at a molecular level in tolerized cells. Tolerance to components of gram-positive bacterial cell walls such as bacterial lipoprotein and lipoteichoic acid is a much lesser studied, although equally important, phenomenon. This review will focus on cellular reprogramming by gram-positive bacterial components and examines the alterations in cell surface receptor expression, changes in intracellular signaling, gene expression and cytokine production, and the phenomenon of cross-tolerance.
MeSH term(s)	Animals ; Cytokines/biosynthesis ; Cytokines/drug effects ; Gram-Positive Bacteria/immunology ; Humans ; Immune Tolerance/immunology ; Lipopolysaccharides/immunology ; Lipopolysaccharides/pharmacology ; Lipoproteins/pharmacology ; Receptors, Cell Surface/biosynthesis ; Receptors, Cell Surface/drug effects ; Receptors, Cell Surface/immunology ; Signal Transduction/drug effects ; Signal Transduction/immunology ; Teichoic Acids/pharmacology
Chemical Substances	Cytokines ; Lipopolysaccharides ; Lipoproteins ; Receptors, Cell Surface ; Teichoic Acids ; lipoteichoic acid (56411-57-5)
Language	English
Publishing date	2006-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0506312
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Article ; Online: Factors Associated with Recurrence Rates and Long-Term Survival in Women Diagnosed with Breast Cancer Ages 40 and Younger.

Plichta, Jennifer K / Rai, Upahvan / Tang, Rong / Coopey, Suzanne B / Buckley, Julliette M / Gadd, Michele A / Specht, Michelle C / Hughes, Kevin S / Taghian, Alphonse G / Smith, Barbara L

Annals of surgical oncology

2016 Volume 23, Issue 10, Page(s) 3212–3220

Abstract: Background: Young age at breast cancer diagnosis has been associated with increased risk of recurrence and mortality. We reevaluated this assumption in a large, modern cohort of women diagnosed with breast cancer at age ≤40 years.: Methods: We ... ...

Abstract	Background: Young age at breast cancer diagnosis has been associated with increased risk of recurrence and mortality. We reevaluated this assumption in a large, modern cohort of women diagnosed with breast cancer at age ≤40 years. Methods: We identified women with breast cancer at age ≤40 years at a single institution from 1996-2008. We assessed locoregional recurrence (LRR), distant recurrence, disease-free survival (DFS), and overall survival (OS), and correlated patient and tumor characteristics with outcomes. Results: We identified 584 women aged ≤40 years with breast cancer. Median age was 37 years, and median follow-up was 124 months; 61.5 % were stages 0-I and 38.5 % were stages II-III. Overall, 57.4 % had lumpectomies and 42.5 % mastectomies. DFS was 93 % at 5 years and 84.5 % at 10 years. OS was 93 % at 5 years and 86.5 % at 10 years. On multivariate analysis, worse DFS was associated with positive nodes (p = 0.002); worse OS was associated with larger tumor size (p = 0.042). When stratified by lumpectomy versus mastectomy, there were no significant differences in survival or recurrence. For lumpectomy patients, DFS was 96 % at 5 years and 88 % at 10 years; OS was 96 % at 5 years and 89 % at 10 years. For mastectomy patients, DFS was 89.5 % at 5 years and 79 % at 10 years; OS was 90 % at 5 years and 83 % at 10 years. Lumpectomy LRR rates were 1 % at 5 years and 4 % at 10 years. Mastectomy LRR rates were 3.5 % at 5 years and 8.7 % at 10 years. Conclusions: Outcomes for women with breast cancer at age ≤40 years have improved. Lumpectomy recurrence rates are low, suggesting that lumpectomy is oncologically safe for young breast cancer patients.
MeSH term(s)	Adult ; Age of Onset ; Breast Neoplasms/diagnosis ; Breast Neoplasms/pathology ; Breast Neoplasms/surgery ; Disease-Free Survival ; Female ; Follow-Up Studies ; Humans ; Lymphatic Metastasis ; Mastectomy, Segmental ; Neoplasm Recurrence, Local/epidemiology ; Neoplasm Staging ; Risk Factors ; Survival Rate ; Time Factors ; Tumor Burden ; Young Adult
Language	English
Publishing date	2016-07-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	1200469-8
ISSN	1534-4681 ; 1068-9265
ISSN (online)	1534-4681
ISSN	1068-9265
DOI	10.1245/s10434-016-5404-z
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