Publications
111 results found
Wakabayashi K, Wilson M, Tatham K, et al., 2013, High-stretch, but not atelectasis, causes systemic cytokine release by lung-marginated monocytes, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Patel BV, Wilson MR, O'Dea KP, et al., 2013, TNF-Induced Death Signaling Triggers Alveolar Epithelial Dysfunction in Acute Lung Injury, J Immunol, Vol: 190, Pages: 4274-4282
Edey LF, O'Dea KP, Herbert BR, et al., 2013, The LPS Preterm Labour Model in Mice: An Inverse Relationship between Leukocyte Recruitment to the Myometrium and Delivery Time., 60th Annual Scientific Meeting of the Society-for-Gynecologic-Investigation (SGI), Publisher: SAGE PUBLICATIONS INC, Pages: 93A-94A, ISSN: 1933-7191
Edey LF, O'Dea KP, Herbert BR, et al., 2013, The Ability of Progesterone To Regulate the Inflammatory Monocyte Subset during Pregnancy, 60th Annual Scientific Meeting of the Society-for-Gynecologic-Investigation (SGI), Publisher: SAGE PUBLICATIONS INC, Pages: 121A-122A, ISSN: 1933-7191
Wakabayashi K, Wilson MR, Patel BV, et al., 2013, Inhibition Of TNF Receptor p55 By A Domain Antibody Attenuates Acid-Induced Lung Injury In Mice, American Thoracic Society
RationaleTumor necrosis factor (TNF) is strongly implicated in the evolution of acute lung injury (ALI), but its potential as a therapeutic target has been hampered by its complex biology. TNF signals through two cell surface receptors, p55 and p75, which play differential roles in ALI, with p55 promoting injury while p75 opposes this. We have recently shown that selective p55 blockade using novel domain antibody technology attenuates ventilator-induced lung injury (VILI) in mice. To further translate these findings to the bedside, we explored the potential for selective blockade of p55 in a clinically relevant mouse model of acid-induced ALI.MethodsMale C57BL6 mice were pretreated with intranasal administration of either specific domain antibody to p55 (dAb) or non-specific control domain antibody (‘dummy’). Four hours later, the mice were either instrumented for analysis without further instillation (i.e. baseline) or intratracheally challenged with hydrochloric acid (0.1M, 75μl) via an oro-tracheal tube to induce ALI. All acid-challenged animals were instrumented for analysis at 24 hours after acid instillation. Analysis consisted of mice being anesthetized, tracheostomized, and mechanically ventilated in order to evaluate PaO2/FiO2 ratio and respiratory mechanics. The left lung was taken for determining wet/dry ratio and a lunglavage sample was taken from the right lung to measure protein levels and neutrophil counts.ResultsHydrochloric acid instillation in the dummy group resulted in severe ALI, represented by hypoxemia, elastance increase, pulmonary edema and inflammation (Table 1). These mice were also visually very sick, showing considerably reduced locomotion and responsiveness. In contrast, pretreatment with p55 dAb dramatically improved the clinical symptoms, along with significant attenuation in all the physiological markers of lung injury. However, the dAb treatment did not significantly attenuate lung neutrophil recruitment represented b
Tatham KC, Xiao W, O'Dea KP, et al., 2013, Neutrophil-Dependent Shedding Of Heparan Sulfate From The Pulmonary Endothelium In An In Vitro Model Of Simulated Ischemia, American Journal of Respiratory and Critical Care Medicine, Vol: 187
Blackbeard J, Wallace VC, O'Dea KP, et al., 2012, The correlation between pain-related behaviour and spinal microgliosis in four distinct models of peripheral neuropathy, Eur.J Pain, Vol: 16, Pages: 1357-1367
BACKGROUND: Peripheral nerve injury is associated with a spinal microglial response that has been correlated with the development of behaviours reflective of neuropathic pain. METHODS: To examine whether this phenomenon is generalizable to neuropathic pain of non-traumatic aetiology, this study investigated the association between spinal microgliosis and behavioural measures of neuropathic hypersensitivity and pain-related anxiety behaviour in four distinct rat models of peripheral neuropathic pain. These were traumatic neuropathy [L5 spinal nerve transection (SNT)], HIV-related neuropathies (either treatment with the antiretroviral drug Zalcitabine (ddC) or combination of perineural exposure to the HIV-gp120 protein and ddC treatment) and varicella zoster virus (VZV) infection. RESULTS AND CONCLUSION: Persistent mechanical hypersensitivity developed in all 'neuropathic' rats. However, spinal microgliosis, as measured by increased CD11b/c immunohistochemical staining and increased numbers of cells expressing CD11b measured by flow cytometry, was evident in the SNT and to a lesser extent in the HIV neuropathy models but not the VZV model. These results suggest that behavioural hypersensitivity and thigmotaxis can only be linked to a microglial response in certain models of neuropathy
Petrie J, Wilson MR, Patel BV, et al., 2012, Obesity induced by high fat feeding attenuates ventilator-induced lung injury in mice., European Respiratory Society Annual Congress
BackgroundRetrospective analysis of Intensive Care data suggests that obesity may confer a survival advantage in Acute Lung Injury (ALI). Development of ventilator-induced lung injury (VILI) is a major determinant of ALI mortality. We have therefore investigated the impact of high fat diet-induced obesity on VILI in mice.MethodsMale C57BL/6 mice were fed high fat diet for a minimum of 13 weeks, resulting in a mean body weight 30% greater than lean age-matched controls. Animals were anaesthetised and ventilated with high-stretch, standardised as plateau pressure (Pplat) 35-37cmH2O. Tidal volumes were similar between groups (mean ∽1080μl). Mice were ventilated for 180mins or until Pplat increased by 20%. Lung tissue was harvested for wet:dry ratio or processed to a single cell suspension for leukocyte quantification by flow cytometry.ResultsHigh stretch ventilation induced increases in Pplat and lung wet:dry ratio, and a decrease in paO2 in lean mice, which were all significantly attenuated in obese animals. Leukocyte recruitment (cells/g dry lung mass) also tended to be reduced. High fat feeding attenuates pulmonary oedema and lung dysfunction associated with VILI in mice. Numerous metabolic and immunological differences exist between lean and obese subjects. Exploring the mechanisms behind this obesity-mediated protection from VILI may lead to identification of novel pathways and therapeutic targets.Funded by: BJA/Royal College of Anaesthetists.
O'Dea KP, Dokpesi JO, Tatham KC, et al., 2011, Regulation of monocyte subset proinflammatory responses within the lung microvasculature by the p38 MAPK/MK2 pathway, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 301, Pages: L812-L821, ISSN: 1040-0605
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- Citations: 29
Scott AJ, O'Dea KP, O'Callaghan D, et al., 2011, Reactive Oxygen Species and p38 Mitogen-activated Protein Kinase Mediate Tumor Necrosis Factor α-Converting Enzyme (TACE/ADAM-17) Activation in Primary Human Monocytes, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 286, Pages: 35466-35476
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- Citations: 78
O'Callaghan DJ, O'Dea KP, Gordon AC, et al., 2011, MONOCYTE TACE ACTIVITY MAY RESPOND TO ENVIRONMENTAL STIMULI, INTENSIVE CARE MEDICINE, Vol: 37, Pages: S258-S258, ISSN: 0342-4642
O'Callaghan DJ, O'Dea KP, Gordon AC, et al., 2011, MONOCYTE TACE ACTIVITY PROFILES ARE ALTERED BY INFLAMMATORY STIMULI, INTENSIVE CARE MEDICINE, Vol: 37, Pages: S258-S258, ISSN: 0342-4642
Dorr AD, Wilson MR, Wakabayashi K, et al., 2011, Sources of alveolar soluble TNF receptors during acute lung injury of different etiologies, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 111, Pages: 177-184, ISSN: 8750-7587
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- Citations: 14
Bertok S, Wilson MR, Dorr AD, et al., 2011, Characterization of TNF receptor subtype expression and signaling on pulmonary endothelial cells in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 300, Pages: L781-L789, ISSN: 1040-0605
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- Citations: 22
Wakabayashi K, Wilson MR, O'Dea KP, et al., 2011, Atelectasis Induces Chemokine Upregulation And Lung Injury In The Isolated Perfused Mouse Lung, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Wakabayashi K, Wilson MR, O'Dea KP, et al., 2010, COMPARISON OF HIGH-STRETCH VERSUS ATELECTASIS IN THE PATHOPHYSIOLOGY OF VENTILATOR-INDUCED LUNG INJURY USING THE MOUSE ISOLATED PERFUSED LUNG, British-Thoracic-Society-Winter-Meeting 2010, Publisher: B M J PUBLISHING GROUP, Pages: A49-A50, ISSN: 0040-6376
Waite AC, O'Dea KP, Wilson MR, et al., 2010, FLOW CYTOMETRIC DETECTION OF INTRACELLULAR ACTIVATION MARKERS OF PULMONARY CELLS DURING ACUTE LUNG INJURY, Publisher: B M J PUBLISHING GROUP, Pages: A182-A183, ISSN: 0040-6376
Wilson MR, O'Dea KP, Dorr AD, et al., 2010, Efficacy and safety of inhaled carbon monoxide during pulmonary inflammation in mice, PLOS One, Vol: 5, ISSN: 1932-6203
Handy JM, Scott AJ, Cross AM, et al., 2010, HLA-DR expression and differential trafficking of monocyte subsets following low to intermediate risk surgery, ANAESTHESIA, Vol: 65, Pages: 27-35, ISSN: 0003-2409
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- Citations: 16
Scott AJ, O'Dea KP, Handy JM, et al., 2009, ROS-DEPENDENT ACTIVATION OF P38 MAPK IS REQUIRED FOR LPS-INDUCED UPREGULATION OF TNFα-CONVERTING ENZYME (TACE/ADAM-17) ACTIVITY ON PRIMARY HUMAN MONOCYTES, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A47-A48, ISSN: 0040-6376
Dokpesi JO, O'Dea KP, Takata M, 2009, DIFFERENTIAL ACTIVATION OF THE P38 MAP KINASE PATHWAY IN MOUSE MONOCYTE SUBSETS DURING CO-CULTURE WITH PULMONARY ENDOTHELIAL CELLS, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A49-A49, ISSN: 0040-6376
Wakabayashi K, Wilson MR, O'Dea KP, et al., 2009, ROLE OF INTRAVASCULAR LEUCOCYTES IN VENTILATOR-INDUCED LUNG INJURY IN THE ISOLATED PERFUSED MOUSE LUNG, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A48-A49, ISSN: 0040-6376
Dorr AD, Wilson MR, O'Dea KP, et al., 2009, SOURCES OF INCREASED PLASMA SOLUBLE TNF RECEPTORS DURING INJURIOUS MECHANICAL VENTILATION IN MICE, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A46-A47, ISSN: 0040-6376
Handy JM, Scott AJ, Cross AM, et al., 2009, LOW AND INTERMEDIATE RISK SURGERY INDUCES ACUTE DEPRESSION OF MONOCYTE HLA-DR EXPRESSION AND DYNAMIC TRAFFICKING OF MONOCYTE SUBSETS, 22nd Annual Congress of the European-Society-of-Intensive-Care-Medicine, Publisher: SPRINGER, Pages: 274-274, ISSN: 0342-4642
Wilson MR, O'Dea KP, Zhang D, et al., 2009, Role of Lung-marginated Monocytes in an <i>In Vivo</i> Mouse Model of Ventilator-induced Lung Injury, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, Pages: 914-922, ISSN: 1073-449X
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- Citations: 64
O'Dea KP, Wilson MR, Dokpesi JO, et al., 2009, Mobilization and Margination of Bone Marrow Gr-1<SUP>high</SUP> Monocytes during Subclinical Endotoxemia Predisposes the Lungs toward Acute Injury, JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 1155-1166, ISSN: 0022-1767
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- Citations: 58
Alvarez-Iglesias M, Wayne G, O'Dea KP, et al., 2009, Continuous real-time measurement of tumor necrosis factor-α converting enzyme activity on live cells (vol 85, pg 1440, 2005), LABORATORY INVESTIGATION, Vol: 89, Pages: 106-106, ISSN: 0023-6837
Bertok S, Wilson MR, Dokpesi J, et al., 2009, Tumour Necrosis Factor-α (TNF) Receptor p75 Plays a Substantial Role in TNF-Mediated Upregulation of Leukocyte Adhesion Molecules in Mouse Lung Microvasculature, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Dorr AD, Wilson MR, Wakabayashi K, et al., 2009, Injurious Ventilation and Intratracheal Lipopolysaccharide Increase Soluble TNF Receptors in the Alveoli Via Distinct Mechanisms, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Bertok S, Wilson MR, Dokpesi J, et al., 2008, ROLE OF TUMOUR NECROSIS FACTOR a RECEPTOR SUBTYPES IN TUMOUR NECROSIS FACTOR-INDUCED MOUSE LUNG MICROVASCULAR ENDOTHELIAL CELL ACTIVATION, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A141-A141, ISSN: 0040-6376
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