scholarly journals An Integrated View on Neuronal Subsets in the Peripheral Nervous System and Their Role in Immunoregulation

2021 ◽  
Vol 12 ◽  
Author(s):  
Manuel O. Jakob ◽  
Michael Kofoed-Branzk ◽  
Divija Deshpande ◽  
Shaira Murugan ◽  
Christoph S. N. Klose

The peripheral nervous system consists of sensory circuits that respond to external and internal stimuli and effector circuits that adapt physiologic functions to environmental challenges. Identifying neurotransmitters and neuropeptides and the corresponding receptors on immune cells implies an essential role for the nervous system in regulating immune reactions. Vice versa, neurons express functional cytokine receptors to respond to inflammatory signals directly. Recent advances in single-cell and single-nuclei sequencing have provided an unprecedented depth in neuronal analysis and allowed to refine the classification of distinct neuronal subsets of the peripheral nervous system. Delineating the sensory and immunoregulatory capacity of different neuronal subsets could inform a better understanding of the response happening in tissues that coordinate physiologic functions, tissue homeostasis and immunity. Here, we summarize current subsets of peripheral neurons and discuss neuronal regulation of immune responses, focusing on neuro-immune interactions in the gastrointestinal tract. The nervous system as a central coordinator of immune reactions and tissue homeostasis may predispose for novel promising therapeutic approaches for a large variety of diseases including but not limited to chronic inflammation.

Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 599-608 ◽  
Author(s):  
M.R. Hirsch ◽  
M.C. Tiveron ◽  
F. Guillemot ◽  
J.F. Brunet ◽  
C. Goridis

Mash1, a mammalian homologue of the Drosophila proneural genes of the achaete-scute complex, is transiently expressed throughout the developing peripheral autonomic nervous system and in subsets of cells in the neural tube. In the mouse, targeted mutation of Mash1 has revealed a role in the development of parts of the autonomic nervous system and of olfactory neurons, but no discernible phenotype in the brain has been reported. Here, we show that the adrenergic and noradrenergic centres of the brain are missing in Mash1 mutant embryos, whereas most other brainstem nuclei are preserved. Indeed, the present data together with the previous results show that, except in cranial sensory ganglia, Mash1 function is essential for the development of all central and peripheral neurons that express noradrenergic traits transiently or permanently. In particular, we show that, in the absence of MASH1, these neurons fail to initiate expression of the noradrenaline biosynthetic enzyme dopamine beta-hydroxylase. We had previously shown that all these neurons normally express the homeodomain transcription factor Phox2a, a positive regulator of the dopamine beta-hydroxylase gene and that a subset of them depend on it for their survival. We now report that expression of Phox2a is abolished or massively altered in the Mash1−/− mutants, both in the noradrenergic centres of the brain and in peripheral autonomic ganglia. These results suggest that MASH1 controls noradrenergic differentiation at least in part by controlling expression of Phox2a and point to fundamental homologies in the genetic circuits that determine the noradrenergic phenotype in the central and peripheral nervous system.


Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 887
Author(s):  
Josephine Trichka ◽  
Wen-Quan Zou

The process of neuroinflammation contributes to the pathogenic mechanism of many neurodegenerative diseases. The deleterious attributes of neuroinflammation involve aberrant and uncontrolled activation of glia, which can result in damage to proximal brain parenchyma. Failure to distinguish self from non-self, as well as leukocyte reaction to aggregation and accumulation of proteins in the CNS, are the primary mechanisms by which neuroinflammation is initiated. While processes local to the CNS may instigate neurodegenerative disease, the existence or dysregulation of systemic homeostasis can also serve to improve or worsen CNS pathologies, respectively. One fundamental component of systemic homeostasis is the gut microbiota, which communicates with the CNS via microbial metabolite production, the peripheral nervous system, and regulation of tryptophan metabolism. Over the past 10–15 years, research focused on the microbiota–gut–brain axis has culminated in the discovery that dysbiosis, or an imbalance between commensal and pathogenic gut bacteria, can promote CNS pathologies. Conversely, a properly regulated and well-balanced microbiome supports CNS homeostasis and reduces the incidence and extent of pathogenic neuroinflammation. This review will discuss the role of the gut microbiota in exacerbating or alleviating neuroinflammation in neurodegenerative diseases, and potential microbiota-based therapeutic approaches to reduce pathology in diseased states.


PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e30373 ◽  
Author(s):  
Azadeh Kushki ◽  
Alexander J. Andrews ◽  
Sarah D. Power ◽  
Gillian King ◽  
Tom Chau

1995 ◽  
Vol XXVII (3-4) ◽  
pp. 45-50
Author(s):  
V. P. Veselovsky ◽  
А. P. Ladygin ◽  
О. S. Kochergina

At present, when classifying vertebrogenic diseases of the nervous system (VZNS), methodological recommendations "Clinical classification of diseases of the peripheral nervous system", approved by M3 of the USSR (1987), are used as the basis. The applied classification does not fully reflect modern concepts of patho- and sanogenesis and complicates the use of many methods (manual therapy and reflexotherapy) necessary for the treatment and rehabilitation of patients with VNS.


Author(s):  
N.K. Svyrydova ◽  
H.N. Chuprina ◽  
T.P. Parnykoza ◽  
V.H. Sereda ◽  
A.S. Kustkova

While neurological manifestations of osteochondrosis account for 60 to 70% of all diseases of the peripheral nervous system, vertebral radiculopathy make up 8 to 10% of other osteochondrosis complications. This often result in temporary and even permanent disability. There are three basic types of pain syndromes: somatogenic (nociceptive pain); neurogenic (neuropathic pain); psychogenic (psychogenic pain). The article provides clinical classification of vertebrogenic diseases of the peripheral nervous system and factors of vertebrogenic pain caused by degenerative changes of the spine. We have presented a quantitative and qualitative assessment of pain, special neurological and general neuroorthopedical methods of examination of patients with vertebral pain. Analyzed the clinical characteristics of muscle-tonic and dystrophic lesions of muscles and given differential diagnosis. For acute pain, treatment algorithms are suggested for vertebrogenic disease and radiculopathy, indicated possible side effects and complications.


2021 ◽  
Vol 347 ◽  
pp. 108967 ◽  
Author(s):  
Benjamin W. Metcalfe ◽  
Alan J. Hunter ◽  
Jonathan E. Graham-Harper-Cater ◽  
John T. Taylor

2021 ◽  
Author(s):  
Aurelia Mapps ◽  
Michael Thomsen ◽  
Erica Boehm ◽  
Haiqing Zhao ◽  
Samer Hattar ◽  
...  

Satellite glia are the major glial type found in ganglia of the peripheral nervous system and wrap around cell bodies of sympathetic and sensory neurons that are very diverse. Other than their close physical association with peripheral neurons, little is known about this glial population. Here, we performed single cell RNA sequencing analysis and identified five different populations of satellite glia from sympathetic and sensory ganglia. We identified three shared populations of satellite glia enriched in immune-response genes, immediate-early genes and ion channels/ECM-interactors, respectively. Sensory- and sympathetic-specific satellite glia are differentially enriched for modulators of lipid synthesis and metabolism. Sensory glia are also specifically enriched for genes involved in glutamate turnover. Further, satellite glia and Schwann cells can be distinguished by unique transcriptional signatures. This study reveals remarkable heterogeneity of satellite glia in the peripheral nervous system.


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