The nervous system of airways and its remodeling in inflammatory lung diseases

Audrit, Katrin Julia; Delventhal, Lucas; Aydin, Öznur; Nassenstein, Christina

doi:10.1007/s00441-016-2559-7

Cited by 60 publications

(65 citation statements)

References 199 publications

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“…6a). The nodose/jugular ganglion and thoracic dorsal root ganglia (DRG) both contain sensory afferent neurons innervating the lung 28,30 , and neurons in the DRG, although not in the nodose/jugular ganglion, express Nmu (Extended Data Fig. 6b).…”

Section: Ilc2-specific Expression Of Nmur1mentioning

confidence: 99%

The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Wallrapp

Riesenfeld

Burkett

et al. 2017

Nature

526

480

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Type 2 innate lymphoid cells (ILC2s) both contribute to mucosal homeostasis and initiate pathologic inflammation in allergic asthma. However, the signals that direct ILC2s to promote homeostasis versus inflammation are unclear. To identify such molecular cues, we profiled mouse lung-resident ILCs using single-cell RNA sequencing at steady state and after in vivo stimulation with the alarmin cytokines IL-25 and IL-33. ILC2s were transcriptionally heterogeneous after activation, with subpopulations distinguished by expression of proliferative, homeostatic and effector genes. The neuropeptide receptor Nmur1 was preferentially expressed by ILC2s at steady state and after IL-25 stimulation. Neuromedin U (NMU), the ligand of NMUR1, activated ILC2s in vitro, and in vivo co-administration of NMU with IL-25 strongly amplified allergic inflammation. Loss of NMU–NMUR1 signalling reduced ILC2 frequency and effector function, and altered transcriptional programs following allergen challenge in vivo. Thus, NMUR1 signalling promotes inflammatory ILC2 responses, highlighting the importance of neuro-immune crosstalk in allergic inflammation at mucosal surfaces.

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Section: Ilc2-specific Expression Of Nmur1mentioning

confidence: 99%

The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Wallrapp

Riesenfeld

Burkett

et al. 2017

Nature

526

480

View full text Add to dashboard Cite

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“…The main function of pulmonary cholinergic neurons is the induction of smooth muscle contraction and consequent bronchoconstriction (117). Noncholinergic postganglionic neurons originate in the myenteric plexus of the esophagus and in the outer striated longitudinal muscle layers (118). Acetylcholine signals through muscarinic receptors and nAChRs in immune cells.…”

Section: Neuronal Inputs In the Lungmentioning

confidence: 99%

“…Activation of sensory lung neurons leads to neuropeptide production that activates central reflexes such as cough. Central reflexes are immune dependent, since inflammation can modulate the activation of sensory neurons (118). Nociceptors can also be activated by proinflammatory cytokines and communicate these signals to the brain (143).…”

Section: Immune-derived Signals and Nervous System Functionmentioning

confidence: 99%

Neuro–Immune Cell Units: A New Paradigm in Physiology

Godinho-Silva

Cardoso²,

Veiga-Fernandes³

2019

Annu. Rev. Immunol.

174

150

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The interplay between the immune and nervous systems has been acknowledged in the past, but only more recent studies have started to unravel the cellular and molecular players of such interactions. Mounting evidence indicates that environmental signals are sensed by discrete neuro–immune cell units (NICUs), which represent defined anatomical locations in which immune and neuronal cells colocalize and functionally interact to steer tissue physiology and protection. These units have now been described in multiple tissues throughout the body, including lymphoid organs, adipose tissue, and mucosal barriers. As such, NICUs are emerging as important orchestrators of multiple physiological processes, including hematopoiesis, organogenesis, inflammation, tissue repair, and thermogenesis. In this review we focus on the impact of NICUs in tissue physiology and how this fast-evolving field is driving a paradigm shift in our understanding of immunoregulation and organismal physiology.

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“…Allergic lung diseases are accompanied by bronchial hyperreactivity, cough, spasm and inflammation. [77][78][79] These features can be explained by an impaired airway innervation and/or dysregulated immune responses, 80 putting forward a pivotal role of neuro-immune interactions in lung homeostasis and defence. While multiple studies described spatial interaction between airway nerves and infiltrating immune cells, few reports adequately defined the nerve fibres and/or the immune cell populations that may underlie neuro-immune interactions.…”

Section: Pulmonary Neuro-immune Interactionsmentioning

confidence: 99%

Neuro-immune regulation of mucosal physiology

2019

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Mucosal barriers constitute major body surfaces that are in constant contact with the external environment. Mucosal sites are densely populated by a myriad of distinct neurons and immune cell types that sense, integrate and respond to multiple environmental cues. In the recent past, neuro-immune interactions have been reported to play central roles in mucosal health and disease, including chronic inflammatory conditions, allergy and infectious diseases. Discrete neuro-immune cell units act as building blocks of this bidirectional multi-tissue cross-talk, ensuring mucosal tissue health and integrity. Herein, we will focus on reciprocal neuro-immune interactions in the airways and intestine. Such neuro-immune cross-talk maximizes sensing and integration of environmental aggressions, which can be considered an important paradigm shift in our current views of mucosal physiology and immune regulation.

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The nervous system of airways and its remodeling in inflammatory lung diseases

Cited by 60 publications

References 199 publications

The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Neuro–Immune Cell Units: A New Paradigm in Physiology

Neuro-immune regulation of mucosal physiology

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