Caister Academic Press

Bacterial Evasion of the Host Immune System

"The figures are expertly drawn" (SIMB News)
Publisher: Caister Academic Press
Edited by: Pedro Escoll
Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris Cedex 15, France
Pages: vi + 224
Publication date: August 2017
ISBN: 978-1-910190-69-2
Price: GB £159 or US $319Buy book or Buy online
Publication date: August 2017
ISBN: 978-1-910190-70-8
Price: US $319Buy ebook

Infectious diseases continue to be a major threat to human health with predictions that these will account for one of five deaths globally over the coming decades. The worrying rise in antibiotic resistance in bacterial pathogens only serves to exacerbate this situation. Many pathogenic bacteria have evolved an array of sophisticated mechanisms to evade the host's immune response: some even exploit host functions to avoid detection by immune cells. Understanding the mechanisms of this subversion is critical for the understanding of bacterial pathogenesis and could be used for the development of novel antibacterial strategies.

In this volume expert authors critically review the most important current research in this exciting field. Topics include: the seven most important bacterial secretion systems; within-host envelope remodelling; subversion of macrophages; pathogen manipulation of host autophagy; mechanisms involved in sensing and restriction of bacterial replication; mechanisms of evasion by Salmonella; evasion strategies of mycobacteria; and role of Cyclic di-GMP in virulence and evasion of plant immune systems.

This text is essential reading for everyone involved in bacterial pathogenesis research and an invaluable reference work for those working in fields as diverse as medicine, biotechnology, agriculture, food and industry. A recommended acquisition for all microbiology laboratories.


"The figures are expertly drawn ... the tables are well organized ... the material and the depth of coverage make this book appropriate for use by researchers, faculty, and graduate students" from SIMB News

Table of contents
1. Secretion Systems Used by Bacteria to Subvert Host Functions
Chiara Rapisarda and Rémi Fronzes
Pages: 1-42.
In this review we examine the use of secretion systems by bacteria to subvert host functions. Bacteria have evolved multiple systems to interact with and overcome their eukaryotic host and other prokaryotes. Secretion systems are required for the release of several effectors through the bacterial membrane(s) into the extracellular space or directly into the cytoplasm of the host. We review the secretion systems of Gram-positive and Gram-negative bacteria and describe briefly the structural composition of the seven secretion systems that have been associated with increased virulence through subversion of host functions. Some of the effects of such systems on eukaryotic host processes have been studied extensively. We also describe the best-characterized effectors of each secretion system to give an overview of the molecular mechanisms employed by bacteria to hide from the immune system and convert eukaryotic cells into optimal ecological niches for their replication.
2. Within-Host Envelope Remodelling and its Impact in Bacterial Pathogen Recognition
M. Graciela Pucciarelli and Francisco García-del Portillo
Pages: 43-60.
Following colonization of host tissues, bacterial pathogens encounter new niches in which they must gain access to nutrients and cope with stresses and defence signals generated by the host. For some pathogens, the adaptation to a new 'within-host' lifestyle involves modifications of envelope components that bear molecular patterns normally recognized by the host innate immune system. These new modified patterns limit host recognition, therefore promoting immune evasion and pathogenicity. In this review, we describe how envelope components like the peptidoglycan or lipopolysaccharide can be altered within the host to impair responses triggered by pattern recognition receptors (PRR). We also discuss the few cases reported to date of chemical modifications that occur in the envelope of some intracellular bacterial pathogens when they reside inside eukaryotic cells. These envelope alterations may have evolved due to the sentinel role performed by PRRs over pathogen-specific molecular patterns. The available data indicate that only selected pathogens seem to evade recognition due to 'within-host' envelope changes, with most of them displaying such patterns also in non host environments. Given the importance of these alterations, future studies should focus in the responsible pathogen regulators, most yet unknown, that could be targeted to prevent immune evasion.
3. Subversion of Macrophage Functions by Bacterial Protein Toxins and Effectors
Muyang Wan, Yan Zhou and Yongqun Zhu
Pages: 61-80.
Macrophages represent one of the first lines of host immune defenses against the invasion of pathogenic bacteria. Many receptors, immune signaling pathways and cellular processes in macrophages, including Toll-like receptors, Nod-like receptors, phagocytosis, autophagy and programmed cell death, are involved in combating the infection of bacterial pathogens. For efficient colonization in the host, bacterial pathogens have evolved diverse mechanisms to interfere with macrophage functions to evade host defenses. The major weapons utilized by bacterial pathogens are protein toxins and effectors secreted via specific bacterial secretion systems, including type I-VII secretion apparatuses. In recent years, great advances have been achieved in understanding how bacterial toxins and effectors subvert immune signaling and cellular processes of macrophages. In this review, we focus on the toxins and effectors that modulate the phagocytosis, intracellular immune signaling pathways, autophagy and programmed cell death processes of macrophages from the bacterium Legionella pneumophila, Shigella flexneri, Listeria monocytogenes, Salmonella spp., Yersinia spp., enteropathogenic E. coli and Mycobacterium tuberculosis.
4. Manipulation of Autophagy by Bacterial Pathogens Impacts Host Immunity
Tobias C. Kunz, Flávia Viana, Carmen Buchrieser and Pedro Escoll
Pages: 81-98.
Autophagy is a highly conserved catabolic process, degrading unnecessary or damaged components in the eukaryotic cell to maintain cellular homeostasis, but it is also an intrinsic cellular defence mechanism to remove invading pathogens. A crosstalk between autophagy and innate or adaptive immune responses has been recently reported, whereby autophagy influences both, innate and adaptive immunity like the production and secretion of pro-inflammatory cytokines or MHC class II antigen presentation to T cells. Pathogenic bacteria have evolved diverse strategies to manipulate autophagy, mechanisms that also impact host immune responses at different levels. Here we discuss the influence of autophagy on self-autonomous, innate and adaptive immunity and then focus on how bacterial mechanisms that shape autophagy may impact the host immune system.
5. Inflammasome-dependent Mechanisms Involved in Sensing and Restriction of Bacterial Replication
Warrison A. Andrade and Dario S. Zamboni
Pages: 99-132.
Inflammasomes are multiprotein platforms assembled in the cytosol in response to pathogens and cell stress. Inflammasomes are recognized by their important role on defenses against bacterial infections and have been also implicated in a range of human inflammatory disorders. Intracellular sensors such as NLRP1, NLRP3, NLRC4, AIM2 and Pyrin induce assembly of inflammasomes, while caspase-11 induces the non-canonical pathway for activation of the NLRP3 inflammasome. The formation of the inflammasome leads to caspase-1 activation that triggers pyroptosis and activation of interleukin-1β (IL-1β) and IL-18. Pyroptotic cell death and cytokines production are involved in restriction of bacterial replication by limiting the replication niche of intracellular bacteria and by inducing inflammatory responses. In this review we focus on the mechanisms mediated by inflammasome activation that leads to inflammatory responses and restriction of bacterial infection.
6. Molecular Mechanisms Used by Salmonella to Evade the Immune System   Free download
Joaquín Bernal-Bayard and Francisco Ramos-Morales
Pages: 133-168.
Human and animal pathogens are able to circumvent, at least temporarily, the sophisticated immune defenses of their hosts. Several serovars of the Gram-negative bacterium Salmonella enterica have been used as models for the study of pathogen-host interactions. In this review we discuss the strategies used by Salmonella to evade or manipulate three levels of host immune defenses: physical barriers, innate immunity and adaptive immunity. During its passage through the digestive system, Salmonella has to face the acidic pH of the stomach, bile and antimicrobial peptides in the intestine, as well as the competition with resident microbiota. After host cell invasion, Salmonella manipulates inflammatory pathways and the autophagy process. Finally, Salmonella evades the adaptive immune system by interacting with dendritic cells, and T and B lymphocytes. Mechanisms allowing the establishment of persistent infections are also discussed.
7. Immune-evasion Strategies of Mycobacteria and Their Implications for the Protective Immune Response
Alexandra G. Fraga, Ana Margarida Barbosa, Catarina M. Ferreira, João Fevereiro, Jorge Pedrosa and Egídio Torrado
Pages: 169-198.
Mycobacteria are intracellular pathogens that have macrophages as their main host cells. However, macrophages are also the primary line of defense against invading microorganisms. To survive in the intracellular compartment, virulent mycobacteria have developed several strategies to modulate the activation and the effector functions of macrophages. Despite this, antigen-specific T cells develop during infection. While T cell responses are critical for protection they can also contribute to the success of mycobacteria as human pathogens, as immunopathology associated with these responses facilitates transmission. Here, we provide a brief overview of different immune-evasion strategies of mycobacteria and their impact on the protective immune response. This understanding will further our knowledge in host-pathogen interactions and may provide critical insights for the development of novel host-specific therapies.
8. Role of Cyclic di-GMP in the Bacterial Virulence and Evasion of the Plant Immunity
Marta Martinez-Gil and Cayo Ramos
Pages: 199-222.
Plant pathogenic bacteria are responsible for the loss of hundreds of millions of dollars each year, impacting a wide range of economically relevant agricultural crops. The plant immune system detects conserved bacterial molecules and deploys an arsenal of effective defense measures at different levels; however, during compatible interactions, some pathogenic bacteria suppress and manipulate the host immunity and colonize and infect the plant host. Different bacteria employ similar strategies to circumvent plant innate immunity, while other tactics are specific to certain bacterial species. Recent studies have highlighted the secondary messenger c-di-GMP as a key molecule in the transmission of environmental cues in an intracellular regulatory network that controls virulence traits in many plant pathogenic bacteria. In this review, we focus on the recent knowledge of the molecular basis of c-di-GMP signaling mechanisms that promote or prevent the evasion of bacterial phytopathogens from the plant immune system. This review will highlight the considerable diversity of mechanisms evolved in plant-associated bacteria to elude plant immunity.

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(EAN: 9781910190692 9781910190708 Subjects: [bacteriology] [medical microbiology] [microbiology] )