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archives@tulane.edu / Ethanol consumption is known to increase the prevalence and severity of respiratory infection and impaired immunity. The relationships between ethanol exposure, vitamin D levels, the anti-microbial protein cathelicidin/LL-37, other chemokines and cytokines, and their roles in pulmonary infections are explored in this report. Information from experimental model systems that included pulmonary cell culture, mice, and primates were compared to data from humans with alcohol use disorder (AUD) and normal controls. Cathelicidin/LL-37 levels were reduced by ethanol exposure of Nuli-1 airway epithelial cells, which is consistent with the model of enhanced airway sensitivity to infection. The vitamin D receptor positively regulates cathelicidin/LL-37 levels. A reduction in the circulating vitamin D in the Rhesus monkey model following ethanol exposure that may impact cathelicidin/LL-37 expression. Serum samples from ethanol exposed mice, Rhesus monkeys and humans with AUD showed variable expression patterns with respect to cytokines and chemokine, some of which may relate to changes in immunity and infection sensitivity. Protein microarrays revealed altered inflammatory biomarkers in the ethanol-exposed population with AUD. Principle component analysis-derived clustering methodology signaled the presence of systemic inflammation in AUD subjects. The combination of immunological impairment and persistent inflammatory biomarkers are consistent with the known predisposition of individuals with AUD to the development of respiratory infections and acute respiratory distress syndrome. / 1 / Phanuwat Sriyotha

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Wong, Tsz Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 140-159). / Abstracts in English and Chinese. / Acknowledgements --- p.I / Abbreviations --- p.III / Abstract --- p.V / 摘要 --- p.VIII / Publications --- p.XI / Table of Contents --- p.XII / Chapter Chapter 1: --- General Information / Chapter 1.1 --- Characteristics and Prevalence of SLE --- p.1 / Chapter 1.2 --- Diagnosis of SLE --- p.2 / Chapter 1.3 --- Assessment of Disease Activity --- p.4 / Chapter 1.4 --- Causes of SLE --- p.4 / Chapter 1.4.1 --- Genetic Factors --- p.4 / Chapter 1.4.2 --- Hormonal Factors --- p.6 / Chapter 1.4.3 --- Environment Factors --- p.7 / Chapter 1.5 --- Drug Treatments of SLE --- p.8 / Chapter 1.6 --- Immunological Dysregulation in SLE --- p.9 / Chapter 1.6.1 --- Types and Properties of Lymphocytes --- p.9 / Chapter 1.6.2 --- Cytokines and Chemokines --- p.14 / Chapter 1.6.3 --- Toll-like Receptors --- p.17 / Chapter 1.6.4 --- Intracellular Signal Transduction Pathways --- p.21 / Chapter 1.7 --- Objectives of Our study --- p.25 / Chapter Chapter 2: --- Material and Methods / Chapter 2.1 --- Materials --- p.27 / Chapter 2.1.1 --- SLE Patients and Control Subjects --- p.27 / Chapter 2.1.2 --- Reagents for cell culture --- p.28 / Chapter 2.1.3 --- Reagents for Flow Cytometry --- p.30 / Chapter 2.1.4 --- Reagents for Phosphorylation State Analysis --- p.33 / Chapter 2.1.5 --- Reagents for Total RNA Extraction --- p.35 / Chapter 2.1.6 --- Reagents for Polymerase Chain Reaction (PCR) --- p.36 / Chapter 2.1.7 --- Reagents for Gel Electrophoresis --- p.38 / Chapter 2.1.8 --- Reagents for Real-Time Polymerase Chain Reaction --- p.39 / Chapter 2.1.9 --- Other Reagents --- p.40 / Chapter 2.2 --- Methods --- p.41 / Chapter 2.2.1 --- Preparation of Plasma and Purification of Peripheral Blood Mononuclear Cells (PBMC) from EDTA-Blood --- p.41 / Chapter 2.2.2 --- Immunophenotyping of Cell Surface Molecules by Flow Cytometry --- p.42 / Chapter 2.2.3 --- Immunophenotyping of Intracellular Molecules by Flow Cytometry --- p.43 / Chapter 2.2.4 --- Phosphorylation State Analysis of Intracellular Signaling Molecules --- p.43 / Chapter 2.2.5 --- Cytometric Bead Array of Cytokines and Chemokines --- p.44 / Chapter 2.2.6 --- Total RNA Extraction from PBMC --- p.46 / Chapter 2.2.7 --- Reverse Transcription of the Extracted Total RNA --- p.46 / Chapter 2.2.8 --- Real-time Polymerase Chain Reaction --- p.46 / Chapter 2.2.9 --- Enzyme-Linked Immunosorbent Assay (ELISA) --- p.48 / Chapter 2.2.10 --- Enzyme-Linked Immunosorbent Spot (ELISPOT) --- p.48 / Chapter 2.2.11 --- Statistical Analysis --- p.49 / Chapter Chapter 3: --- B Cell Chemokine CXCL13 in SLE / Chapter 3.1 --- Introduction --- p.49 / Chapter 3.2 --- Methods --- p.52 / Chapter 3.3 --- Results --- p.52 / Chapter 3.3.1 --- Characteristics of SLE Patients and Control Subjects --- p.52 / Chapter 3.3.2 --- Expression of Plasma CXCL13 --- p.53 / Chapter 3.3.3 --- Gene Expression of TNF-α in PBMC --- p.53 / Chapter 3.3.4 --- Expression of sTNFRl in Plasma --- p.53 / Chapter 3.4 --- Discussion --- p.57 / Chapter Chapter 4: --- T lymphocyte Co-stimulatory Molecule CD26 in SLE / Chapter 4.1 --- Introduction --- p.61 / Chapter 4.2 --- Methods --- p.64 / Chapter 4.3 --- Results --- p.66 / Chapter 4.3.1 --- Characteristic of SLE Patients and Control Subjects --- p.66 / Chapter 4.3.2 --- Expression of Human CD26 in Plasma --- p.66 / Chapter 4.3.3 --- "Cell Surface Expression of CD26 on Monocytes, Th, Tc plus Ts, B and iNKT Lymphocytes" --- p.66 / Chapter 4.3.4 --- Circulating Number of iNKT Lymphocytes --- p.67 / Chapter 4.4 --- Discussion --- p.71 / Chapter Chapter 5: --- Thl7 Lymphocytes and Expression of IL-17 in SLE / Chapter 5.1 --- Introduction --- p.76 / Chapter 5.2 --- Methods --- p.78 / Chapter 5.3 --- Results --- p.79 / Chapter 5.3.1 --- Characteristics of SLE Patients and Control Subjects --- p.79 / Chapter 5.3.2 --- Ex vivo production of IL-17A from PBMC --- p.79 / Chapter 5.3.3 --- Circulating Number of Thl7 Lymphocytes --- p.79 / Chapter 5.4 --- Discussion --- p.82 / Chapter Chapter 6: --- Intracellular Mitogen Activated Protein Kinases in SLE / Chapter 6.1 --- Introduction --- p.87 / Chapter 6.2 --- Methods --- p.89 / Chapter 6.3 --- Results --- p.91 / Chapter 6.3.1 --- Characteristics of SLE Patients and Control Subjects --- p.91 / Chapter 6.3.2 --- Expression of Phospho-p38 MAPK in PBMC --- p.91 / Chapter 6.3.3 --- Expression of Phospho-ERK in PBMC --- p.92 / Chapter 6.3.4 --- Expression of Phospho-JNK in PBMC --- p.92 / Chapter 6.3.5 --- "Relative Percentage Increase of Phosphorylated p38 MAPK, ERK and JNK upon IL-18 Activation" --- p.93 / Chapter 6.4 --- Discussion --- p.104 / Chapter Chapter 7: --- Toll-like Receptors in SLE / Chapter 7.1 --- Introduction --- p.111 / Chapter 7.2 --- Methods --- p.113 / Chapter 7.3 --- Results --- p.115 / Chapter 7.3.1 --- Characteristics of SLE Patients and Control Subjects --- p.115 / Chapter 7.3.2 --- Expression of TLRl to TLR9 of PBMC --- p.115 / Chapter 7.3.3 --- Preliminary Results of Cytokine and Chemokine Expression Upon TLR Lignad Activation --- p.116 / Chapter 7.4 --- Discussion --- p.126 / Chapter Chapter 8: --- Conclusion and Future Perspectives --- p.133 / Appendix --- p.138 / References --- p.140

Thesis (M.D.)--University of Hong Kong, 1991.

Thesis (M.D.)--University of Hong Kong, 1991. / Also available in print.

Thesis (M. Res.)--University of Hong Kong, 2005.

No description available.

No description available.

No description available.