Neuroimmune Interaction in Inflammatory Diseases

Otmishi, Peyman; Gordon, J.L; El-Oshar, Seraj; Li, Huafeng; Guardiola, Juan; Saad, Mohamed; Proctor, Mary; Yu, Jerry

doi:10.4137/ccrpm.s547

Cited by 30 publications

(27 citation statements)

References 95 publications

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“…Additionally, immune mediators directly influence neurons through their specific receptors, thus expressing effects from peripheral nerve modulation to complex cognitive alterations. These chemicals can also induce vagal or circumventricular organ-mediated reflexes, thus modulating autonomous nervous system [9].…”

Section: Neuro-immune Molecular Overlapmentioning

confidence: 99%

Nociception and role of immune system in pain

2014

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Both pain and inflammation are protective responses. However, these self-limiting conditions (with well-established negative feedback loops) become pathological if left uncontrolled. Both pain and inflammation can interact with each other in a multi-dimensional manner. These interactions are known to create an array of 'difficult to manage' pathologies. This review explains in detail the role of immune system and the related cells in peripheral sensitization and neurogenic inflammation. Various neuro-immune interactions are analyzed at peripheral, sensory and central nervous system levels. Innate immunity plays a critical role in central sensitization and in establishing acute pain as chronic condition. Moreover, inflammatory mediators also exhibit psychological effects, thus contributing towards the emotional elements associated with pain. However, there is also a considerable anti-inflammatory and analgesic role of immune system. This review also attempts to enlist various novel pharmacological approaches that exhibit their actions through modification of neuro-immune interface.

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Section: Neuro-immune Molecular Overlapmentioning

confidence: 99%

Nociception and role of immune system in pain

2014

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“…Since TDI is both a potent immune sensitiser and sensory irritant, this chemical agent provides a unique opportunity to investigate the interaction between immunological and neurological processes. It has indeed been proposed that asthma is an immune-neuronal disorder [25], like other inflammatory conditions [26]. However, the link between activation of neuronal receptors and immune responses is not well established in asthma.…”

Section: Introductionmentioning

confidence: 99%

Neuro-immune interactions in chemical-induced airway hyperreactivity

et al. 2016

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Asthma may be induced by chemical sensitisers, via mechanisms that are still poorly understood. This type of asthma is characterised by airway hyperreactivity (AHR) and little airway inflammation. Since potent chemical sensitisers, such as toluene-2,4-diisocyanate (TDI), are also sensory irritants, it is suggested that chemical-induced asthma relies on neuro-immune mechanisms.We investigated the involvement of transient receptor potential channels (TRP) A1 and V1, major chemosensors in the airways, and mast cells, known for their ability to communicate with sensory nerves, in chemical-induced AHR.In vitro intracellular calcium imaging and patch-clamp recordings in TRPA1- and TRPV1-expressing Chinese hamster ovarian cells showed that TDI activates murine TRPA1, but not TRPV1. Using an in vivo model, in which an airway challenge with TDI induces AHR in TDI-sensitised C57Bl/6 mice, we demonstrated that AHR does not develop, despite successful sensitisation, in Trpa1 and Trpv1 knockout mice, and wild-type mice pretreated with a TRPA1 blocker or a substance P receptor antagonist. TDI-induced AHR was also abolished in mast cell deficient Kit(Wsh) (/Wsh) mice, and in wild-type mice pretreated with the mast cell stabiliser ketotifen, without changes in immunological parameters.These data demonstrate that TRPA1, TRPV1 and mast cells play an indispensable role in the development of TDI-elicited AHR.

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“…1). However, when chronic stress goes on, the body is in a state of continuous physiological provocation that can lead to health problems (Pasquali et al, 2006;Otmishi et al, 2008). As a result, a high amount of cortisol leads to severe fatigue, difficulty concentrating, irritability that leads to anxiety and depression (Schneiderman et al, 2005;Ebrecht et al, 2004).…”

Section: The Stress Response System: Hypothalamus Pituitary Adrenal Axismentioning

confidence: 99%

Psychophysiology of Chronic Stress: An Example of Mind-body Interaction

Cacha

Poznański

Ariff³

et al. 2019

NeuroQuantology

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We present an example of mind-body interaction through the psychophysiology of chronic stress. We show the dynamic pattern of effects on the mind and body associated with chronic stress response and recognize how the mind coordinates the body systems to sustain internal equilibrium for optimal function. In fact many other bodily illnesses are caused by an interaction of mental and physical subtleties. It is important to note that these psychophysiological disorders bring actual physical damage. This review provides a clear direction in understanding how the mind controls the stress response, facilitates positive change, and improves the ability to cope with stress that can be the key to successful healing for overall physical and mental health.

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Neuroimmune Interaction in Inflammatory Diseases

Cited by 30 publications

References 95 publications

Nociception and role of immune system in pain

Nociception and role of immune system in pain

Neuro-immune interactions in chemical-induced airway hyperreactivity

Psychophysiology of Chronic Stress: An Example of Mind-body Interaction

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