On Toll-like receptors and the innate immune response in sepsis caused by Burkholderia pseudomallei (melioidosis)

Thesis

Title page

Contents

List of contributors

Common abbreviations

Chapter 1: Setting the scene : introduction and outline of the thesis

Chapter 2: Melioidosis : insights into the pathogenicity of Burkholderia pseudomallei

Chapter 3: Inflammation patterns induced by different Burkholderia species in mice

Chapter 4: High throughput mRNA profiling characterizes the expression of inflammatory molecules in sepsis caused by Burkholderia pseudomallei (melioidosis)

Chapter 5: Gene-expression profiles in murine melioidosis

Chapter 6: Endogenous interleukin-18 improves the early antimicrobial host response in severe melioidosis

Chapter 7: The role of Toll-like receptors in sepsis

Chapter 8: Toll-like receptor 2 impairs host defense in gram-negative sepsis caused by Burkholderia pseudomallei (melioidosis).

Chapter 9: MyD88 dependent signaling contributes to protective host defense against Burkholderia pseudomallei

Chapter 10: CD14 impairs host defense against gram-negative sepsis caused by Burkholderia pseudomallei in mice

Chapter 11: Immunosuppression associated with IRAK-M upregulation predicts mortality in gram-negative sepsis (melioidosis)

Chapter 12: Expression profile and function of triggering receptor expressed on myeloid cells (TREM)-1 in melioidosis

Chapter 13: Expression and function of macrophage migration inhibitory factor (MIF) in melioidosis

Chapter 14: Coagulation in sepsis

Chapter 15: Activation of coagulation with concurrent impairment of anti-coagulant mechanisms correlates with a poor outcome in severe melioidosis

Chapter 16: Urokinase receptor is necessary for bacterial defense against pneumonia-derived septic melioidosis by facilitating phagocytosis

Chapter 17: Summary, general discussion and conclusion

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