Abstract
Microglia have selectively evolved as a morphologically and chemically distinct class of immuno-competent CNS resident cells with potent bidirectional signaling capabilities linked to induction of a macrophage-like phenotype following metabolic, microbiological, or viral insults. It has been empirically determined that a conserved set of shared chemical messengers connects a communication network mediating reciprocal exchange of regulatory information between immune, central nervous, and neuroendocrine systems. From an evolutionary perspective, the pluripotent neuro-protective capabilities of invertebrate microglia have been extended and amplified in classes of mammalian microglia. The state-dependent plasticity of microglia has provoked considerable empirical investigation into their functional/regulatory roles in mediating innate immune surveillance and neural protection within the CNS. Upon pathophysiological dysregulation, aberrant microglial activities may provide significant contributory factors in the etiology and persistence of major neurological, degenerative, and psychiatric disorders. Within this context, invertebrate microglia appear to represent highly appropriate model systems to investigate underlying cellular and molecular mechanisms involved in higher order neuroimmune regulation of multiple CNS activities by mammalian microglia
Highlights
Selective evolutionary pressure has provided the CNS with a morphologically and chemically distinct class of immuno-competent “vigilante” cell, microglia, with potent bidirectional signaling capabilities linked to induction of a macrophage-like phenotype [1,2,3]
The listed functional similarities include taken from these reports includes: 1) expression of immunocyte-responsive cytokinelike molecules closely resembling those found in higher animals; 2) cross activation of human immunocytes by invertebrate cytokine-like molecules; 3) initiation of a cytokine-like cascade mechanism induced by lipopolysaccharide (LPS) administration; 4) functional involvement of opioid peptide and opioid receptor mechanisms in cytokine production and release related to manifestation of neural trauma; 5) similarities in the metabolic enzyme pathways responsible for the degradation of peptidergic signal molecules; 6) utilization of nitric oxide (NO) as a major regulatory molecule in immunological and neurological tissues [44,68,69,70] 7) regulated biosynthesis and utilization of endogenous morphine and its stereo-selective mu receptor subtypes as regulatory factors in neural, immune and neuroimmune signaling [45,71,72,73]
Retroactively-directed, blueprint for elucidation of neural-immune bidirectional communication mechanisms of higher animals may be gleaned from examination of neural and immune processes of invertebrate microglia
Summary
Selective evolutionary pressure has provided the CNS with a morphologically and chemically distinct class of immuno-competent “vigilante” cell, microglia, with potent bidirectional signaling capabilities linked to induction of a macrophage-like phenotype [1,2,3]. Mature unstimulated microglia maintain a branched or ramified morphology that is transformed into an activated macrophage-like amoeboid state following microbiological or pathophysiological insults [11,12,13]. As discussed in depth below, the intrinsic, state-dependent, plasticity of microglia has provoked considerable empirical investigation into their functional/regulatory roles in mediating innate immune surveillance and neural protection within the CNS. When dysregulated, it appears that aberrant microglial activities represent significant contributory factors in the etiology and persistence of major neurological, degenerative, and psychiatric disorders [11,12,14,15]
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