Expert international authors critically review the most important current research in bacterial evasion of the host immune response. Topics range from an overview of the seven most important bacterial secretion systems to a thorough review of evsaion by mycobacteria. Essential reading for everyone involved in bacterial pathogenesis research.

The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.

Our survival as multicellular organisms requires the constant surveillance of our internal and external (mucosal) environments by the multifarious elements of the innate and acquired systems of immunity. The objective of this surveillance, expensive as it is to the organisms, is to recognise and kill invading microorganisms. Over the past fifty years the cells and mediators involved in our immune defences have been painstakingly identified. However, it is only relatively recently that the ability of microorganisms to evade immunity has been recognised and investigated. Bacterial Evasion of Host Immune Responses introduces the reader to the mechanisms used by bacteria to evade both humoral and cellular immune responses, using systems ranging in complexity from the simple quorum sensing molecules - acyl homoserine lactones - to the supramolecular syringe-like devices of type III secretion systems. This book will be of interest to researchers and graduate students in microbiology, immunology, pharmacology and molecular medicine.

Established almost 30 years ago, Methods in Microbiology is the most prestigious series devoted to techniques and methodology in the field. Now totally revamped, revitalized, with a new format and expanded scope, Methods in Microbiology will continue to provide you with tried and tested, cutting-edge protocols to directly benefit your research. - Focuses on the methods most useful for the microbiologist interested in the way in which bacteria cause disease - Includes section devoted to 'Approaches to characterising pathogenic mechanisms' by Stanley Falkow - Covers safety aspects, detection, identification and speciation - Includes techniques for the study of host interactions and reactions in animals and plants - Describes biochemical and molecular genetic approaches - Essential methods for gene expression and analysis - Covers strategies and problems for disease control

Humans coexist with millions of harmless microorganisms, but emerging diseases, resistance to antibiotics, and the threat of bioterrorism are forcing scientists to look for new ways to confront the microbes that do pose a danger. This report identifies innovative approaches to the development of antimicrobial drugs and vaccines based on a greater understanding of how the human immune system interacts with both good and bad microbes. The report concludes that the development of a single superdrug to fight all infectious agents is unrealistic.

Bacterial pathogenicity factors are functionally diverse. They may facilitate the adhesion and colonization of bacteria, influence the host immune response, assist spreading of the bacterium by e.g. evading recognition by immune cells, or allow bacteria to dwell within protected niches inside the eukaryotic cell. Exotoxins can be single polypeptides or heteromeric protein complexes that act on different parts of the cells. At the cell surface, they may insert into the membrane to cause damage; bind to receptors to initiate their uptake; or facilitate the interaction with other cell types. For example, bacterial superantigens specifically bind to major histocompatibility complex (MHC) II molecules on the surface of antigen presenting cells and the T cell receptor, while cytolysins cause pore formation. For intracellular activity, exotoxins need to be translocated across the eukaryotic membrane. Gram-negative bacteria can directly inject effector proteins in a receptor-independent manner by use of specialized needle apparatus such as bacterial type II, III, or type IV secretion systems. Other methods of translocation include the phagocytic uptake of bacteria followed by toxin secretion, or receptor-mediated endocytosis which allows the targeting of distinct cell types. Receptor-based uptake is initiated by the binding of heteromeric toxin complexes to the cell surface and completed by the translocation of the effector protein(s) across the endosomal membrane. In the cytosol, toxins interact with specific eukaryotic target proteins to cause post-translational modifications that often result in the manipulation of cellular signalling cascades and inflammatory responses. It has become evident that the actions of some bacterial toxins may exceed their originally assumed cytotoxic function. For example, pore-forming toxins do not only cause cytolysis, but may also induce autophagy, pyroptosis, or activation of the MAPK pathways, resulting in adjustment of the host immune response to infection and modification of inflammatory responses both locally and systemically. Other recently elucidated examples of the immunomodulatory function of cell death-inducing exotoxins include TcdB of Clostridium difficile which activates the inflammasome through modification of cellular Rho GTPases, or the Staphyloccocus d-toxin which activates mast cells. The goal of this research topic was to gather current knowledge on the interaction of bacterial exotoxins and effector proteins with the host immune system. The following 16 research and review articles in this special issue describe mechanisms of immune modification and evasion and provide an overview over the complexity of bacterial toxin interaction with different cells of the immune system.

During the past twenty years Listeria monocytogenes has emerged as one of the most intensely studied bacterial pathogens. New windows are constantly being opened into the complexity of host cell biology and the interplay of the signals connecting the various cells and organs involved in the host response. This volume includes research from studies at the molecular level on the pathogenesis of Listeria monocytogenes and the response of the host to its infections.

Leishmania parasites plague the mammalian host causing high morbidity and mortality. The parasites persist in the hostile milieu, crippling its defensive arsenal. In the face of mounting resistance to an antiquated drug arsenal, new approaches are urgently desired to keep the infection at bay. Furthermore, to strengthen the leishmaniasis elimination drive, particular emphasis has to be laid on identification of new targets and vaccination strategies. This book gives a brief glimpse of the epidemiology of leishmaniasis, immune evasion, vaccination, and therapeutic modalities that may work by untangling the immunological cross-wires of pathogenic cross-talk. The Conventional treatment and its drawbacks, the prospects of phytotherapy and nanomedicines, are also discussed. The identification of drug targets with the aim of designing inhibitors is also exemplified.

Microbial pathogenesis is the study of the mechanisms by which microbes (bacteria, viruses, protozoa, and multicellular parasites) cause infectious disease and make their hosts (humans) ill. Bacterial infections we thought were easily treatable are again a huge cause for concern with the well-publicized rise of antibiotic resistance. There are very few effective antiviral drugs and we live with the threat of epidemics such as bird flu and the outbreaks of viruses such the recent (and ongoing) Ebola crisis. Parasitic diseases such as malaria continue to pose a heavy burden in the developing world and with climate change could spread into the developed world. There is therefore an urgent need to understand microbial mechanisms, with research programmes and university courses dedicated to the subject.