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PubMed1990

Effect of unilateral vagotomy on capsaicin-induced neurogenic inflammation in the trachea of rats.

This study reports the effect of unilateral vagotomy on neurogenic inflammation in the trachea. Neurogenic inflammation was produced in the trachea of vagotomized rats by a venous injection of capsaicin, the pungent ingredient of red pepper. Monastral blue was used as tracer dye to label the affected blood vessels. Vagus nerves and tracheal tissues were processed for light and electron microscopy. The damaged right vagus nerve was found to have degenerated. However, unilateral vagotomy did not completely block neurogenic inflammation in the trachea ipsilaterally and contralaterally, as shown in the whole mount preparations. Microscopic observations of tracheal tissue sections showed that neurogenic inflammation did not evenly occur on both sides of the trachea. The possible reason for this is discussed.

Animals↗
PubMed1990

[Neuropeptides and inflammation: presumed mechanisms in neurogenic inflammation].

Neuropeptides, among which substance P, VIP (Vasoactive intestinal peptide), somatostatin, neurotensin, dynorphin and enkephalins, are able to modulate inflammatory processes. Increasing interest is now devoted to these peptides in different inflammatory diseases, concerning skin, lung and joins. The effect of substance P can be dependent on its C-terminal moiety implicating by this way an interaction with specific neurokinin receptors or can be dependent on its N-terminal moiety which does not involve a specific membrane receptor. Such diversity of the action mechanisms of peptides should influence the evolution of the anti-inflammatory therapeutic.

Arthritis↗
PubMed1988

Respiratory tract infections increase susceptibility to neurogenic inflammation in the rat trachea.

This study reveals that respiratory tract infections make the tracheal mucosa of rats more susceptible to neurogenic inflammation, which is a type of inflammation mediated by neuropeptides released from sensory nerves. Neurogenic inflammation was produced in the tracheas of 2 groups of Long-Evans rats by electrical stimulation of the vagus nerve (5 V, 1 ms, 20 Hz for 5 min) or by an injection of capsaicin (15 to 200 micrograms/kg i.v.) or substance P (0.05 to 5.0 micrograms/kg i.v.). Rats of one group were pathogen-free; the others had serologic evidence of naturally occurring airway infections caused by Sendai virus, coronavirus, and Mycoplasma pulmonis. The stimuli produced neurogenic inflammation in both groups of rats, but the magnitude of this inflammation was much greater in the infected rats. The susceptibility of the infected rats to neurogenic inflammation was manifested by a 2.0 to 3.1 times larger increase in vascular permeability to Monastral blue, 5 times larger increase in number of neutrophils adhering to the endothelium of venules, and conspicuous morphologic changes in the tracheal epithelium. When pathogen-free rats acquired respiratory tract infections, they too became susceptible to neurogenic inflammation. Other experiments showed that infection by Sendai virus was essential for the change, although infection by M. pulmonis or coronavirus may also be necessary. The susceptibility to neurogenic inflammation outlasted the transient pathologic changes caused in the airway mucosa by the viral infections and may have been permanent.

Animals↗
PubMedDate not supplied

Clinical and experimental aspects of cutaneous neurogenic inflammation.

The aim of this paper is to present the state of knowledge on cutaneous neurogenic inflammation. Peripheral effector functions served by afferent sensory neurons underlie the so-called neurogenic inflammation. The mechanism of cutaneous neurogenic inflammation is connected with the release of neuropeptides from the sensory endings. They also exert a number of functions within the immune system. The activity of neuropeptides in the inflammation of the skin can be observed in the form of erythema, edema, hyperthermia and pruritus. Beside these peptides and their receptors, inflammatory skin response, is regulated by tryptase and proteinase-activated receptor 2 (PAR-2). Capsaicin decreases effects of inflammation-induced sensory neuropeptides, which was used in the treatment of diseases caused by inflammation. The activity of transient receptor potential vanilloid receptor 1 (TRP-V1) is associated with the neurogenic inflammation. In inflammatory processes, the neuro-immuno-cutaneous system undergoes activation, which is responsible for triggering and maintaining the inflammatory conditions, both in the healthy skin as well as in the pathological conditions, like psoriasis. Skin exposure to UV radiation influences the neuro-immuno-cutaneous system and causes the release of neuropeptides, thereby eliciting inflammatory response in photodermatosis. In conclusion, understanding the mechanisms and the factors controlling neurotransmitters and their receptors will lead to the identification of novel therapeutic targets for the treatment of cutaneous diseases e.g. pruritus, psoriasis, alopecia areata.

Humans↗
PubMed2005

CGRP and migraine: neurogenic inflammation revisited.

For more than a century neurogenic inflammation has been proposed to have a role in various human diseases. The present review will cover the conceptual steps of the itinerary that has led to the conclusion that neurogenic inflammation is important in migraine. Of particular relevance for the object of this article is the observation that tachykin-independent neurogenic inflammatory responses are evident in rodents, but much less pronounced or absent in other mammal species, including man, whereas neurogenic vasodilatation, most likely mediated by CGRP, occurs in most mammalian species and also in man. Recent evidence that a CGRP receptor antagonist was effective in the treatment of migraine attack supports the hypothesis that neurogenic vasodilatation is a major underlying mechanism of migraine.

Animals↗
PubMed1992

Neurogenic inflammation and asthma.

The release of neurotransmitters may exacerbate the inflammatory response. Such neurogenic inflammation has been documented in a number of inflammatory diseases. Neurogenic inflammation due to release of neuropeptides from sensory nerves has been demonstrated in airways of several species, particularly rodents, and may contribute to the inflammatory response in asthmatic airways. Tachykinins (substance P and neurokinin A) released from airway sensory nerves may cause bronchoconstriction, vasodilatation, plasma exudation, and mucus secretion, whereas another sensory neuropeptide, calcitonin generelated peptide, may contribute to hyperemia of inflammation. Airway epithelial damage in asthma exposes sensory nerves which may become sensitized by inflammatory products (including prostaglandins and cytokines) so that neuropeptides are released via a local reflex trigger such as bradykinin, resulting in exaggerated inflammation. The effects of tachykinins may be amplified further by loss of the major degrading enzyme, neutral endopeptidase, from epithelial cells. Direct evidence for neurogenic inflammation in asthma is still awaited, however. Several strategies for reducing neurogenic inflammation are possible, particularly inhibition of neuropeptide release from sensory nerves by stimulating prejunctional receptors such as mu-opioid receptors.

Animals↗
PubMed1990

Modulation of neurogenic inflammation: novel approaches to inflammatory disease.

Neurogenic inflammation, which involves the release of neuropeptides from capsaicin-sensitive sensory nerves, may contribute to inflammatory diseases of the airways, joints, bladder, skin, eye and gut. Peter Barnes and colleagues review some of the therapeutic strategies that can be used to inhibit this neurogenic inflammation, with particular reference to the respiratory tract.

Animals↗
PubMed1996

Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation.

We investigated the role of neurogenic inflammation and the subsequent mechanisms in cigarette smoke-induced airway hyperresponsiveness in guinea pigs. Exposure to cigarette smoke was carried out at tidal volume for 3 min. Airway responsiveness to histamine was determined before and after smoke exposure followed by bronchoalveolar lavage (BAL). Plasma extravasation was evaluated by measuring the extravasation of Evans blue dye in the airway. Cigarette smoke produced significant airway hyperresponsiveness and plasma extravasation, with an influx of neutrophils in BAL fluid. FK-224 (10 mg/kg i.v.), a tachykinin antagonist at NK1 and NK2 receptors, significantly inhibited these changes. The thromboxane (Tx) B2 concentration was increased in BAL fluid after smoke exposure and was significantly inhibited by FK-224. OKY-046 (10 mg/kg i.v.), a Tx synthase inhibitor, significantly inhibited airway hyperresponsiveness but had no effect on neutrophil influx or plasma extravasation. The results suggest that neurogenic inflammation and the subsequent generation of Tx in the airway are important in the development of the airway hyperresponsiveness induced by cigarette smoke.

Animals↗
PubMed1992

Neurogenic inflammation and the oral mucosa.

Since the rôle of neurogenic inflammation in various pathological conditions is well-established, we presume that it also has great importance in the development of several inflammatory processes in the oral mucosa. In the course of experimentally-induced neurogenic inflammation of the oral mucosa in rats, vasodilation and plasma extravasation occur in the area supplied by unmyelinated capsaicin-sensitive fibres. Upon activating these fibres in the oral mucosa, mediators such as histamine, substance P (SP) and calcitonin gene related peptide (CGRP) are released from the peripheral terminals of afferent nerves causing characteristic symptoms of neurogenic inflammation. By histochemical techniques, SP- and CGRP-immunoreactive fibres have occurred in the area of the rat oral mucosa stimulated mostly in the free and attached gingiva around the molar teeth in the lower jaw. Capsaicin pretreatment performed neonatally or at adult age causes a loss of SP-immunoreactive fibres and prevents the vasodilatory responses, as well as the increase in vascular permeability elicited by the antidromic stimulation of the inferior alveolar nerve. As the transection of inferior alveolar nerve decreased the extravasation of Evans blue on the ipsilateral side and did not affect the capsaicin-induced enhancement in blood flow, we suggest that the two symptoms of the inflammation, i.e., the increased vascular permeability and decreased vascular resistance, should be produced by different mechanisms. The results of all the morphological and functional studies seem to confirm the possibility that there is an important neurogenic component of the inflammatory alterations caused by different mechanical and chemical stimuli in the oral mucosa.

Capsaicin↗
PubMed1999

Mast cell tryptase in dermal neurogenic inflammation.

BACKGROUND: Mast cell activation has been assumed to play a role in dermal neurogenic inflammation: C fibre-derived neuropeptides activating mast cells and releasing histamine, which in turn would activate C fibres. OBJECTIVE: To test this hypothesis mast cell tryptase (MCT) was measured inside the axon reflex flare area. Axon reflexes were elicited by histamine or compound 48/80, a polyanionic mast cell-degranulating substance. The time course of plasma extravasation and release of histamine and MCT from dermal mast cells in neurogenic inflammation was measured in vivo by intradermal microdialysis in humans. METHODS: Single hollow plasmapheresis fibres (pore cutoff size: 3000 kDa) were inserted intracutaneously at the volar forearm and perfused with Ringer's solution (4 microL/min) with one microdialysis fibre located at the planned stimulation site and a second inside the axon reflex area. Neurogenic inflammation was induced by intraprobe delivery of either histamine or the mast cell-degranulating agent compound 48/80. Mediator release was measured at the stimulation sites and inside the arising axon reflex flare area. RESULTS: Mast cell degranulation induced marked plasma protein extravasation (PPE 0.25 +/- 0.04-1.31 +/- 0.6 mg/mL; pre- and post-stimulation, mean +/- sem, n = 7) and release of histamine (2.0 +/- 0.9-38.7 +/- 1.4 ng/mL) and MCT (9.84 +/- 2.4-92.2 +/- 21.6 ng/mL). Interestingly, in addition to increasing PPE (0.33 +/- 0. 11-1.85 +/- 0.9 mg/mL), histamine also induced a slight but significant increase in MCT (11.3 +/- 3.0-12.4 +/- 2.3 ng/mL). No evidence for mast cell activation was observed inside the axon reflex areas, where PPE (0.34 +/- 0.03-0.25 +/- 0.02 mg/mL), histamine (1.64 +/- 0.5-1.46 +/- 0.4 ng/mL) and MCT concentration (11.6 +/- 3.1-7.6 +/- 1.7 ng/mL) gradually decreased. CONCLUSION: It is concluded that dermal neurogenic inflammation does not degranulate mast cells.

Adult↗
PubMed1993

Small reduction of capsaicin-induced neurogenic inflammation in human forearm skin by the glucocorticoid prednicarbate.

Capsaicin applied to human skin provokes a response known as neurogenic inflammation. Neuropeptides (substance P, CGRP), released from afferent C-fiber terminals and histamine, secondarily released from mast cells, are supposed to participate in this reaction. We investigated the contribution of arachidonic acid and metabolic products to neurogenic inflammation, using a potent topically applied glucocorticoid and the corresponding vehicle. Arachidonic acid is liberated from membrane phospholipids by phospholipase A2, an enzyme that can be blocked by glucocorticoids. In 12 healthy volunteers, neurogenic inflammation was induced by capsaicin 1% on both upper forearms after 16 h of topical pretreatment with either prednicarbate or vehicle. Neurogenic inflammation was assessed by laser Doppler flowmetry and by planimetry of flare sizes. Prednicarbate significantly reduced the laser Doppler flow values inside the flare responses, as well as the flare sizes themselves. These results show that to some extent glucocorticoids reduce capsaicin-induced neurogenic inflammation.

Administration, Topical↗
PubMed2003

Neurogenic inflammation in mice deficient in heparin-synthesizing enzyme.

Mast cell activation, or neurogenic inflammation, is known to induce lowering of interstitial fluid pressure (P(if)) and plasma protein extravasation (PPE) in several tissues from both rats and mice. To examine a possible role of connective tissue mast cells (CTMCs) in these inflammatory responses, we used mice with dysfunctional CTMCs due to lack of the N-deacetylase/N-sulfotransferase-2 enzyme (NDST-2(-/-)). P(if) and PPE were measured after challenge with compound 48/80 (C48/80), and P(if) alone was measured after treatment either with capsaicin, substance P (SP), or calcitonin gene-related peptide (CGRP). Measurements of P(if) in anesthetized (fentanyl/fluanison and midazolam, 1:1) mice were performed in paw skin with glass capillaries connected to a servo-controlled counterpressure system. PPE was measured with microdialysis by using hollow plasmapheresis fibers (cutoff at 3,000 kDa) placed subcutaneously on the back. Intravenous administration of C48/80 lowered P(if) significantly (P < 0.05) in NDST-2(-/-) mice (-1.67 +/- 0.42 mmHg) compared with vehicle (-0.57 +/- 0.17 mmHg) but the lowering was significantly (P < 0.05) less compared with that of the NDST-2(+/+) mice (-2.31 +/- 0.47 mmHg). PPE was increased 300% after treatment with C48/80 in NDST-2(+/+) mice, whereas there was no increase in PPE in NDST-2(-/-) mice. Capsaicin, SP, and CGRP lowered P(if) significantly (P < 0.05) compared with vehicle and to the same extent in both NDST-2(+/+) and NDST-2(-/-) mice. We can conclude that although NDST-2(-/-) mice demonstrate an altered response in P(if) after mast cell activation, there was no similar alteration after neurogenic inflammation. Therefore, we suggest that neurogenic inflammation in mouse skin is not exclusively dependent on intact CTMCs.

Acute Disease↗
PubMed1990

Relationships between permeable vessels, nerves, and mast cells in rat cutaneous neurogenic inflammation.

Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed "neurogenic inflammation". Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 microns of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.

Animals↗
PubMed2002

Cellular mechanisms of neurogenic inflammation.

Since the initial observations that stimulation of sensory neurons produces vasodilation, plasma extravasation, and hypersensitivity, much progress has been made in understanding the etiology of neurogenic inflammation. Studies have focused largely on the role of the neuropeptides, substance P and calcitonin gene-related peptide, which are released in the periphery by activation of small diameter sensory neurons. Recent work, however, has begun to emphasize the cellular mechanisms involved in regulating the release of proinflammatory substances from sensory neurons. In this perspective, discussion centers on a number of inflammatory mediators that activate various signal transduction pathways to augment excitability of and transmitter release from sensory neurons. Emphasis is placed on those pathways where multiple lines of evidence support their importance in initiating neurogenic inflammation. Recent studies, however, support the notion that there are novel compounds released during injury that can stimulate or sensitize sensory neurons. Furthermore, only now are intracellular signaling pathways that have been identified in other cell systems being studied in sensory neurons to establish their role in neurogenic inflammation. The challenge remains to ascertain the critical transduction pathways that regulate transmitter release from sensory neurons since this phenomenon triggers neurogenic inflammation. In addition, the cellular mechanisms involved in alterations in neuronal excitability during injury and the cellular pathways that maintain the inflammatory response over time need to be determined. With these advances, we will be able to develop therapeutic interventions to minimize deleterious consequences of neurogenic inflammation.

Animals↗
PubMed2002

[Neurogenic inflammation. I. Basic mechanisms, physiology and pharmacology].

Activation of sensory unmyelinated neurons by noxious stimuli evokes the release of neuropeptides, such as substance P and calcitonin gene-related peptide (CGRP) from peripheral nerve endings. These neuropeptides and subsequently released mediators cause a local oedema, hyperaemia and an erythema which extends beyond the site of stimulation (so-called flare response). Since these inflammatory signs depend on the function and integrity of peripheral sensory nervous systems, the response has been termed neurogenic inflammation. Due to the fact that nearly all tissues in mammals including humans are innervated by afferent sensory neurons, this neurogenic inflammation can occur ubiquitously throughout the body. Albeit first evidence showing that sensory neurons contribute to the inflammatory signs, described as antidromic vasodilatation, axon reflex, triple response, neurogenic inflammation, elicited at the level of tissue that they innervate was first obtained more than one hundred years ago, it was in the last two decades that inflammation caused by the release of neuropeptides from afferent nerve endings was recognised as a physiologically and pathologically relevant process. A large number of exogenous and endogenous substances and autacoids may stimulate or sensitise sensory nerve endings, thus simultaneously producing pain and nociceptive responses, as well as neurogenic inflammation. On the basis of recent research a variety of pharmacological substances and antagonists of putative mediators have been identified to modulate or suppress neurogenic inflammation, thus providing a rationale for therapeutical strategies for various diseases in which neurogenic inflammation is suggested to be involved. Among them, capsaicin and other newly developed agonists and antagonists at the vanilloid receptor have attracted particular attention, since they were found to be capable of desensitizing nociceptive nerve structures and thus of preventing development of neurogenic inflammation or even of abolishing an ongoing inflammatory process.

Animals↗
PubMed1991

Early loss of neurogenic inflammation in the human diabetic foot.

1. Neurogenic inflammation, mediated by nociceptor C fibres, is part of the acute neurovascular response to injury producing the axon reflex flare. Laser Doppler flowmetry was used to measure the flare response induced by the electrophoresis, at various current strengths, of a ring of acetylcholine solution into dorsal foot skin. 2. Nineteen control subjects and 52 long-duration insulin-dependent (Type 1) diabetic patients of similar age (20 without complications; 19 with laser-treated retinopathy; 13 with reduced vibration perception and retinopathy) were studied in order to investigate the possible attenuation of this defence mechanism in diabetes. 3. The maximal (1 mA) flare response [control median (interquartile range): 1.55 (1.16-2.06) arbitrary units] was reduced greatly in neuropathic patients [0.37 (0.24-0.66) arbitrary units; P less than or equal to 0.001 with respect to all other groups], especially those with a previous history of foot ulceration. The flare was also reduced in some patients with retinopathy alone [1.06 (0.56-1.27) arbitrary units; P less than 0.005 with respect to control subjects]. 4. No rightward shift of the curve of hyperaemic response plotted against current strength was found, suggesting that the abnormal response was due to axonal loss rather than to dysfunction. 5. Neurogenic inflammation, mediated by small pain fibres, was markedly impaired in a group of diabetic patients at risk of foot ulceration. Furthermore, impairment of this nociceptor C fibre response can develop before clinical large-fibre neuropathy and could itself predispose to foot complications.

Acetylcholine↗
PubMed1989

Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections.

Neuropeptides such as substance P are implicated in inflammation mediated by sensory nerves (neurogenic inflammation), but the roles in disease of these peptides and the peptidases that degrade them are not understood. It is well established that inflammation is a prominent feature of several airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis. These diseases are characterized by cough, airway edema, and abnormal secretory and bronchoconstrictor responses, all of which can be elicited by substance P. The effects of substance P and other peptides that may be involved in inflammation are decreased by endogenous neutral endopeptidase (NEP; also called enkephalinase, EC 3.4.24.11), which is a peptidase that degrades substance P and other peptides. In the present study, we report that rats with histories of infections caused by common respiratory tract pathogens (parainfluenza virus type 1, rat corona-virus, and Mycoplasma pulmonis) not only have greater susceptibility to neurogenic inflammatory responses than do pathogen-free rats but also have a lower activity of NEP in the trachea. This reduction in NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentrations of substance P to reach tachykinin receptors in the trachea. Thus decreased NEP activity may exacerbate some of the pathological responses in animals with respiratory tract infections.

Animals↗
PubMed1985

The contribution of neurogenic inflammation in experimental arthritis.

The release of the peptide neurotransmitter substance P from the peripheral terminals of nociceptive afferent neurons and the release of catecholamines from postganglionic sympathetic efferent neurons produce physiologic changes associated with acute inflammation. The contribution of these neurogenic mechanisms to inflammatory diseases has not been determined. Activation of central neural circuits elicits similar physiologic changes, and lesions of the peripheral and central nervous system are associated with alteration in activity of inflammatory diseases. We have evaluated the contribution of neurogenic inflammation to the severity of joint injury in experimentally induced arthritis in the rat. The finding of a greater density of substance P-containing nociceptive afferents in a joint that develops more severe arthritis (ankle) suggests a role of substance P in joint injury. Direct evidence that the proinflammatory factor released from these nociceptors is substance P is provided by the finding that the injection of substance P into a joint which normally develops less severe arthritis (knee) increases the severity of arthritis in that joint. A contribution of catecholamines to the severity of joint injury was suggested by the finding that both guanethidine-induced sympathectomy and reserpine-induced depletion of catecholamines attenuated the severity of joint injury. Finally, a contribution of central neural circuits to inflammatory processes was studied in a model in which activation of nociceptive afferents elicited swelling and tenderness at a remote site. This reflex neurogenic inflammation was inhibited by intracerebroventricular injections of morphine, which also attenuated the severity of arthritis. These studies provide evidence that elements of the peripheral afferent and sympathetic efferent neurons and of descending supraspinal, opioid-mediated, circuits in the central nervous system modulate the severity of joint injury in experimental arthritis in the rat.

Animals↗