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      Do β -Defensins and Other Antimicrobial Peptides Play a Role in Neuroimmune Function and Neurodegeneration?

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          Abstract

          It is widely accepted that the brain responds to mechanical trauma and development of most neurodegenerative diseases with an inflammatory sequelae that was once thought exclusive to systemic immunity. Mostly cationic peptides, such as the β -defensins, originally assigned an antimicrobial function are now recognized as mediators of both innate and adaptive immunity. Herein supporting evidence is presented for the hypothesis that neuropathological changes associated with chronic disease conditions of the CNS involve abnormal expression and regulatory function of specific antimicrobial peptides. It is also proposed that these alterations exacerbate proinflammatory conditions within the brain that ultimately potentiate the neurodegenerative process.

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          Taking dendritic cells into medicine.

          Ralph M. Steinman, Jacques Banchereau (2007)
          Dendritic cells (DCs) orchestrate a repertoire of immune responses that bring about resistance to infection and silencing or tolerance to self. In the settings of infection and cancer, microbes and tumours can exploit DCs to evade immunity, but DCs also can generate resistance, a capacity that is readily enhanced with DC-targeted vaccines. During allergy, autoimmunity and transplant rejection, DCs instigate unwanted responses that cause disease, but, again, DCs can be harnessed to silence these conditions with novel therapies. Here we present some medical implications of DC biology that account for illness and provide opportunities for prevention and therapy.
          Article 0 comments Cited 547 times – based on 0 reviews     Review now
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            Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism.

            Michelle L. Block, Jau-Shyong Hong (2005)
            Inflammation, a common denominator among the diverse list of neurodegenerative diseases, has recently been implicated as a critical mechanism responsible for the progressive nature of neurodegeneration. Microglia are the resident innate immune cells in the central nervous system and produce a barrage of factors (IL-1, TNFalpha, NO, PGE2, superoxide) that are toxic to neurons. Evidence supports that the unregulated activation of microglia in response to environmental toxins, endogenous proteins, and neuronal death results in the production of toxic factors that propagate neuronal injury. In the following review, we discuss the common thread of microglial activation across numerous neurodegenerative diseases, define current perceptions of how microglia are damaging neurons, and explain how the microglial response to neuronal damage results in a self-propelling cycle of neuron death.
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              The role of inflammation in CNS injury and disease.

              Sian-Marie Lucas, Nancy J Rothwell, Rosemary Gibson (2006)
              For many years, the central nervous system (CNS) was considered to be 'immune privileged', neither susceptible to nor contributing to inflammation. It is now appreciated that the CNS does exhibit features of inflammation, and in response to injury, infection or disease, resident CNS cells generate inflammatory mediators, including proinflammatory cytokines, prostaglandins, free radicals and complement, which in turn induce chemokines and adhesion molecules, recruit immune cells, and activate glial cells. Much of the key evidence demonstrating that inflammation and inflammatory mediators contribute to acute, chronic and psychiatric CNS disorders is summarised in this review. However, inflammatory mediators may have dual roles, with detrimental acute effects but beneficial effects in long-term repair and recovery, leading to complications in their application as novel therapies. These may be avoided in acute diseases in which treatment administration might be relatively short-term. Targeting interleukin (IL)-1 is a promising novel therapy for stroke and traumatic brain injury, the naturally occurring antagonist (IL-1ra) being well tolerated by rheumatoid arthritis patients. Chronic disorders represent a greater therapeutic challenge, a problem highlighted in Alzheimer's disease (AD); significant data suggested that anti-inflammatory agents might reduce the probability of developing AD, or slow its progression, but prospective clinical trials of nonsteroidal anti-inflammatory drugs or cyclooxygenase inhibitors have been disappointing. The complex interplay between inflammatory mediators, ageing, genetic background, and environmental factors may ultimately regulate the outcome of acute CNS injury and progression of chronic neurodegeneration, and be critical for development of effective therapies for CNS diseases.
              Article 0 comments Cited 303 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): ScientificWorldJournal
                Journal ID (iso-abbrev): ScientificWorldJournal
                Journal ID (publisher-id): TSWJ
                Title: The Scientific World Journal
                Publisher: The Scientific World Journal
                ISSN (Electronic): 1537-744X
                Publication date Collection: 2012
                Publication date (Electronic): 19 April 2012
                Volume: 2012
                Electronic Location Identifier: 905785
                Affiliations
                1Department of Biological Sciences, Case Western Reserve University, Cleveland, OH 44106, USA
                2Department of Pathology, University of Maryland, Baltimore, MD 20742, USA
                3UTSA Neurosciences Institute and Department of Biology, University of Texas at San Antonio, San Antonio, TX 78249, USA
                4Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
                Author notes
                *Wesley M. Williams: wmw5@ 123456case.edu

                Academic Editor: R. E. Tanzi

                Article
                DOI: 10.1100/2012/905785
                PMC ID: 3346844
                PubMed ID: 22606066
                SO-VID: bbf7ffce-466f-4e0a-8ceb-5c40b3059854
                Copyright © Copyright © 2012 Wesley M. Williams et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 June 2011
                Date accepted : 26 October 2011
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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