A role for interleukin 17A in <scp>IBD</scp>‐related neuroplasticity

Cervi, Andrea; Moynes, Derek M.; Chisholm, Susan; Nasser, Yasmin; Vanner, Stephen; Lomax, Alan E.

doi:10.1111/nmo.13112

Cited by 5 publications

(3 citation statements)

References 65 publications

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“…The loss of sympathetic fibers in the gut, as shown in the DSS colitis model, and also in specimens from patients with CD, is associated with increased expression of sympathetic repellents like semaphorin 3C and might result in reduced local inflammation control [28]. Sympathetic Nervous System and Chronic Inflammation However, using a DSS regimen in mice and TNBS regimen in rats, which leads to less severe colitis, even shows an increased growth of sympathetic axons, which may be mediated by the proinflammatory cytokine IL-17A [70,71]. Integrating both results, it seems that the balance between repellents like semaphorin 3C and sympathetic growth-promoting factors like IL-17A or nerve growth factor determines local sympathetic nerve density, leading to severely inflamed tissue without sympathetic neuronal control and areas of milder inflammation where central sympathetic control mechanisms might still be intact.…”

Section: And Below)mentioning

confidence: 99%

Chronic Effects of the Sympathetic Nervous System in Inflammatory Models

Pongratz¹,

Straub²

2023

Neuroimmunomodulation

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The immune system is embedded in a network of regulatory systems to keep homeostasis in case of an immunologic challenge. Neuroendocrine immunologic research has revealed several aspects of these interactions over the past decades, e.g., between the autonomic nervous system and the immune system. This review will focus on evidence revealing the role of the sympathetic nervous system (SNS) in chronic inflammation, like colitis, multiple sclerosis, systemic sclerosis, lupus erythematodes, and arthritis with a focus on animal models supported by human data. A theory of the contribution of the SNS in chronic inflammation will be presented that spans these disease entities. One major finding is the biphasic nature of the sympathetic contribution to inflammation, with proinflammatory effects until the point of disease outbreak and mainly anti-inflammatory influence thereafter. Since sympathetic nerve fibers are lost from sites of inflammation during inflammation, local cells and immune cells achieve the capability to endogenously produce catecholamines to fine-tune the inflammatory response independent of brain control. On a systemic level, it has been shown across models that the SNS is activated in inflammation as opposed to the parasympathetic nervous system. Permanent overactivity of the SNS contributes to many of the known disease sequelae. One goal of neuroendocrine immune research is defining new therapeutic targets. In this respect, it will be discussed that at least in arthritis, it might be beneficial to support β-adrenergic and inhibit α-adrenergic activity besides restoring autonomic balance. Overall, in the clinical setting, we now need controlled interventional studies to successfully translate the theoretical knowledge into benefits for patients.

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Section: And Below)mentioning

confidence: 99%

Chronic Effects of the Sympathetic Nervous System in Inflammatory Models

Pongratz¹,

Straub²

2023

Neuroimmunomodulation

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“…While it is unknown what factors control these processes, cytokines such as IL-17A could have a significant role. IL-17A induces the outgrowth of sympathetic neurons in the colon (48) and cultures from the SMG (54), although this has not been shown in secondary lymphoid organs, including the spleen. This role is also complicated by the ability of neurons to direct formation of lymphoid tissues during development and infection.…”

Section: A Innervation Of the Spleenmentioning

confidence: 99%

“…Prior three-dimensional imaging studies of mouse ileum revealed TH ϩ axons in the submucosa, with some, albeit sparse innervation in the macrophage rich mucosa (87). This sparse innervation in the naive mice does not seem to be static, with DSS-induced inflammation increasing the density of sympathetic axons in the colonic lamina propria (48). As an additional complication, tissue resident macrophages are phenotypically distinct from inflammatory monocyte-derived macrophages that have been recruited to a site of inflammation.…”

Section: A Neural Modulation Of Intestinal Immune Functionmentioning

confidence: 99%

Neuroimmune Communication in Health and Disease

Reardon

Murray

Lomax

2018

Physiological Reviews

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The immune and nervous systems are tightly integrated, with each system capable of influencing the other to respond to infectious or inflammatory perturbations of homeostasis. Recent studies demonstrating the ability of neural stimulation to significantly reduce the severity of immunopathology and consequently reduce mortality have led to a resurgence in the field of neuroimmunology. Highlighting the tight integration of the nervous and immune systems, afferent neurons can be activated by a diverse range of substances from bacterial-derived products to cytokines released by host cells. While activation of vagal afferents by these substances dominates the literature, additional sensory neurons are responsive as well. It is becoming increasingly clear that although the cholinergic anti-inflammatory pathway has become the predominant model, a multitude of functional circuits exist through which neuronal messengers can influence immunological outcomes. These include pathways whereby efferent signaling occurs independent of the vagus nerve through sympathetic neurons. To receive input from the nervous system, immune cells including B and T cells, macrophages, and professional antigen presenting cells express specific neurotransmitter receptors that affect immune cell function. Specialized immune cell populations not only express neurotransmitter receptors, but express the enzymatic machinery required to produce neurotransmitters, such as acetylcholine, allowing them to act as signaling intermediaries. Although elegant experiments have begun to decipher some of these interactions, integration of these molecules, cells, and anatomy into defined neuroimmune circuits in health and disease is in its infancy. This review describes these circuits and highlights continued challenges and opportunities for the field.

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