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Results for “Neurogenic Inflammation”

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At least 19 recordsLinked to original sources

PubMed1987

Nociceptor functions in intact skin and in neurogenic or non-neurogenic inflammation.

Acute neurogenic or non-neurogenic inflammation was elicited in skin patches innervated by the saphenous nerve of anaesthetized Sprague Dawley rats. Lambda carrageenan was used to induce non-neurogenic inflammation, mustard oil (allyl-iso-thio-cyanate) or antidromic nerve stimulation to induce neurogenic inflammation. Antidromic nerve stimulation yielded plasma extravasation but no significant sensitization of unmyelinated nociceptor units. In contrast, mustard oil and carrageenan yielded plasma extravasation and sensitization of nociceptors, though carrageenan sensitized only part of them. Sensitization resulted in ongoing spike discharges and in a shift of response curves to lower temperatures when controlled radiant heat stimuli were applied to the receptive fields. Responses to mechanical stimuli with v. FREY hairs were not significantly altered. Effects of neurogenic and non-neurogenic inflammation on unmyelinated nociceptor units are compared.

Animals↗

PubMed1993

[Neurogenic inflammation].

Airway neurogenic inflammation is caused by neuropeptides released from airway sensory nerves, and may be involved in the pathogenesis of asthma. Airway sensory nerves are stimulated by chemical mediators such as bradykinin and leukotrienes, hyperventilation and cigarette smoke. Presynaptic modulation of airway sensory nerves by opioids, histamine H3-agonists, NPY, and potassium channel openers is effective in the control of neurogenic inflammation. Tachykinin receptor antagonists also inhibit airway neurogenic inflammation. Recently, we have demonstrated that pretreatment with a tachykinin receptor antagonist can protect against bradykinin-induced airway narrowing in asthmatic patients. This evidence indicates that endogenously released tachykinins have a functional role in the airways of asthmatics.

Asthma↗

PubMed1989

Pharmacological modulation of neurogenic inflammation.

A neurogenic inflammation was induced by electrical stimulation of the exposed saphenous or sciatic nerve of male rats. The increase in paw weight of the stimulated leg was used as parameter for degree of inflammation. The content of substance P decreased significantly in the skin supplied by the antidromic stimulated nerves. Substances were tested whose effectivity in neurogenic inflammation is as yet unknown. Inhibition of the angiotensin converting enzyme by the inhibitor captopril did not yield an indirect reference for a causative role of substance P in neurogenic inflammation. The activity of catecholamines refers to the possible importance of blood vessel and/or cyclic nucleotide level alteration in this special type of inflammation.

Animals↗

PubMed1992

[Effect electroacupuncture on the neurogenic inflammation].

The neurogenic inflammation caused by antidromic stimulation of the saphenous nerve was taken as an index of peripheral release of substance P. Electroacupuncture could reduce the plasma extravasation from the neurogenic inflammation by 69.7%, but electroacupuncture per se did not cause obvious plasma extravasation. In rats pretreated with capsaicin the plasma extravasation could be markedly reduced, in consistent with the reduction of substance P-like immunoreactivity in dorsal horn. It is referred that electroacupuncture might block the conveying the signals induced by nerve stimulation along the C-fibers and the axo-axonal reflex, leading to the reduction of peripheral release of substance P. Besides the mediation by different central structures, acupuncture might have direct effects on regulating peripherally the release of some inflammatory and painful mediators.

Animals↗

PubMed1990

Neurogenic inflammation, vascular permeability, and mast cells. II. Additional evidence indicating that mast cells are not involved in neurogenic inflammation.

Activation of cutaneous sensory nerves induces vasodilatation and vascular permeability, i.e., neurogenic inflammation. We examined the histology and possible mast cell involvement in cutaneous neurogenic inflammation induced by electrical nerve stimulation (ENS). Three lines of evidence indicated that mast cells were not involved in rodent cutaneous neurogenic inflammation induced by electrical stimulation of the saphenous nerve. 1) Most mast cells (86.5% of all mast cells in the dorsal skin of the paw) were found in the deep dermis, whereas vessels developing increased vascular permeability after nerve stimulation (visualized with the supravital dye Monastral blue B, a macro-molecular tracer) were localized predominantly in the superficial dermis. By contrast, i.v. substance P, which also causes increased cutaneous vascular permeability, predominantly caused deeper vessels to leak. As analyzed by electron microscopy, the vessels that developed permeability in response to nerve stimulation, and were thereby stained with Monastral blue B, were found to be exclusively postcapillary venules. 2) Disodium cromoglycate (DSCG), a mast cell stabilizing compound, inhibited the cutaneous vascular permeability induced by intradermal injections of anti-IgE in a dose-dependent manner. By contrast, vascular permeability induced by ENS was not influenced by disodium cromoglycate treatment. 3) ENS and i.v. substance P both induced cutaneous vascular permeability in mast cell-deficient W/Wv mice, despite the fact that their skin contained only 4.7% of the mast cells present in their normal +/+ litter mates. The magnitude of ENS-induced vascular permeability responses in W/Wv mice were similar to control +/+ and BALB/c mice. This study supports our earlier observations suggesting that mast cell activation is not essential for the initial, vascular permeability phase of neurogenic inflammation in rodent skin.

Animals↗

PubMed1997

Neurogenic inflammation in cholecystitis.

Neurogenic inflammation implies stimulation of nerves with resultant inflammation in tissue surrounding the nerve terminals. We hypothesized that neurogenic inflammation has a role in cholecystitis. Capsaicin (stimulant of afferent, nociceptive neurons), 6-hydroxydopamine (stimulates release of peptides from sympathetic nerve terminals), bradykinin, lipopolysaccharide, and saline were instilled into guinea pig gallbladders for 24 hr (N = 5 in each group). In parallel, test agents were instilled with 1% Iidocaine. Water transport across gallbladder mucosa, myeloperoxidase and interluekin-1 release from gallbladder tissue, and prostaglandin E2 in luminal fluid were measured. Capsaicin caused water secretion and significant release of myeloperoxidase, interleukin-1, and prostaglandin-E2, effects that were blocked by Iidocaine. 6-Hydroxydopamine did not affect water transport or prostaglandin E2, but did cause myeloperoxidase and interleukin-1 release. Bradykinin- and lipopolysaccharide-induced inflammation were partially inhibited by lidocaine. Taken together, these results suggest that neurogenic inflammation has a role in the pathophysiology of cholecystitis.

Animals↗

PubMed1993

Cyclooxygenase inhibitors acetylsalicylic acid and indomethacin do not affect capsaicin-induced neurogenic inflammation in human skin.

Neurogenic inflammation is evoked by neuropeptides released from primary afferent terminals and, presumably, by other secondarily released inflammatory mediators. This study examines whether prostaglandins might participate in the development of neurogenic inflammation in humans and whether cyclooxygenase inhibitors have any anti-inflammatory effect on this type of inflammation. In healthy volunteers, neurogenic inflammation was elicited by epicutaneously applied capsaicin (1%), after systemic pretreatment with acetylsalicylic acid, or topically applied indomethacin compared to pretreatment with saline or vehicle, respectively. The extent of neurogenic inflammation was quantified by planimetry of visible flare size and recording the increase of superficial cutaneous blood flow (SCBF) with a laser Doppler flowmeter. Capsaicin-induced flare sizes and outside SCBF (both representing neurogenically evoked inflammation) were unaffected by acetylsalicylic acid or indomethacin. Only the capsaicin-induced increase of inside SCBF was attenuated by local pretreatment with indomethacin, reflecting the participation of prostaglandins in the inflammatory response of those areas which were in direct contact with capsaicin.

Adult↗

PubMed1991

Neurogenic inflammation in airways.

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) and calcitonin-gene-related peptide released from airway sensory nerves may cause bronchoconstriction, vasodilatation, plasma exudation and mucus secretion. Sensory nerves may become sensitised by inflammatory products and triggered by mediators such as bradykinin, resulting in exaggerated inflammation. The effects of tachykinins may be further amplified by loss of the major degrading enzyme, neutral endopeptidase, from epithelial cells. Several strategies for reducing neurogenic inflammation are possible.

Animals↗

PubMed2002

[Neurogenic inflammation. II. pathophysiology and clinical implications].

Neurogenic inflammation is elicited by activation of unmyelinated sensory neurons through noxious stimuli and subsequent release of neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) from peripheral nerve endings. The nerve-mediated inflammatory responses in the tissue consist of hyperaemia and oedema which under some circumstances may be accompanied by pain. Neurogenic inflammation has been implicated in the pathophysiology of various human diseases with uncertain etiology. Signs of inflammation and hyperalgesia associated with chronic pain syndromes such as migraine, arthritis and complex regional pain syndrome resemble the characteristics of neurogenic inflammation. By extrapolation of convincing evidence obtained in rodent models, neurogenic inflammation is assumed to contribute to diseases of the respiratory system, gastrointestinal tract, urogenital tract, and skin in humans. Since, however, highly selective substance P receptor antagonists, found to be effective against inflammation in rodents, failed to inhibit inflammatory processes in clinical trials, the hypothesis of an involvement of neurogenic inflammation in human diseases is discussed critically in this review. Beyond its primarily inflammatory character neurogenic inflammation can be regarded as a mechanism that activates protective responses, thus bringing about a first line of defence to maintain the integrity of the tissue and to contribute to tissue repair.

Animals↗

PubMed1997

Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation.

The Working Group on Neurogenic Inflammation proposed 11 testable hypotheses in the three domains of neurogenic inflammation, perceptual and central integration, and nonneurogenic inflammation. The working group selected the term people reporting chemical sensitivity (PRCS) to identify the primary subject group. In the domain of neurogenic inflammation, testable hypotheses included: PRCS have an increased density of c-fiber neurons in symptomatic tissues; PRCS produce greater quantities of neuropeptides and prostanoids than nonsensitive subjects in response to exposure to low-level capsaicin or irritant chemicals; PRCS have an increased and prolonged response to exogenously administered c-fiber activators such as capsaicin; PRCS demonstrate augmentation of central autonomic reflexes following exposure to agents that produce c-fiber stimulation; PRCS have decreased quantities of neutral endopeptidase in their mucosa; exogenous neuropeptide challenge reproduces symptoms of PRCS. In the domain of perceptual and central integration, testable hypotheses included: PRCS have alterations in adaptation, habituation, cortical representation, perception, cognition, and hedonics compared to controls; the qualitative and quantitative interactions between trigeminal and olfactory systems are altered in PRCS; higher integration of sensory inputs is altered in PRCS. In the domain of nonneurogenic inflammation, testable hypotheses included: increased inflammation is present in PRCS in symptomatic tissues and is associated with a heightened neurosensory response; PRCS show an augmented inflammatory response to chemical exposure. The working group recommended that studies be initiated in these areas.

Chemoreceptor Cells↗

PubMed1993

Neurogenic inflammation and sensitivity to environmental chemicals.

Neurogenic inflammation as a pathway distinct from antigen-driven, immune-mediated inflammation may play a pivotal role in understanding a broad class of environmental health problems resulting from chemical exposures. Recent progress in understanding the mediators, triggers, and regulation of neurogenic inflammation is reviewed. Evidence for and speculations about a role for neurogenic inflammation in established disorders such as asthma, rhinitis, contact dermatitis, migraine headache, and rheumatoid arthritis are presented. The sick building syndrome and multiple chemical sensitivity syndrome have been defined as clinical entities in which exposure to chemical inhalants gives rise to disease. Current data on the existence of chemical irritant receptors in the airway and skin are discussed; neurogenic inflammation arising from stimulation of chemical irritant receptors is a possible model to explain many of the aspects of chemical sensitivities.

Air Pollutants↗

PubMed1989

Inhibition of neutral endopeptidase potentiates neurogenic inflammation in the rat trachea.

The present study was performed to determine whether neurogenic inflammation in the rat trachea can be exaggerated by inhibiting neutral endopeptidase, an enzyme that degrades tachykinins that are believed to mediate neurogenic inflammation. Neurogenic inflammation was produced by antidromic electrical stimulation of one vagus nerve (2.5 Hz, 1 ms, 5 V for 5 min) in the presence of atropine or by an intravenous injection of capsaicin (100 micrograms/kg). Neutrophils that adhered to the endothelium of venules were visualized and counted in tracheal whole mounts that were stained by a histochemical reaction for myeloperoxidase. Neural inflammation increased the number of adherent neutrophils. Pretreatment with the neutral endopeptidase inhibitor phosphoramidon (1.0 or 2.5 mg/kg iv) increased neutrophil adhesion induced by neural inflammation. As assessed by the amount of extravasation of Monastral blue pigment, neural inflammation also increased vascular permeability, and this change was potentiated by phosphoramidon. These results are consistent with the concept that neuropeptides released from sensory nerves in the tracheal mucosa cause neutrophils to adhere to venules and increase vascular permeability and that these effects are modulated by neutral endopeptidase.

Animals↗

PubMed1998

Regulation of airway neurogenic inflammation by neutral endopeptidase.

Airway neurogenic inflammation is caused by tachykinins released from peripheral nerve endings of sensory neurons within the airways, and is characterized by plasma protein extravasation, airway smooth muscle contraction and increased secretion of mucus. Tachykinins are degraded and inactivated by neutral endopeptidase (NEP), a membrane-bound metallopeptidase, which is located mainly at the surface of airway epithelial cells, but is also present in airway smooth muscle cells, submucosal gland cells and fibroblasts. The key role of NEP in limiting and regulating the neurogenic inflammation provoked by different stimuli has been demonstrated in a large series of studies published in recent years. It has also been shown that a variety of factors, which are relevant for airway diseases, including viral infections, allergen exposure, inhalation of cigarette smoke and other respiratory irritants, is able to reduce NEP activity, thus enhancing the effects of tachykinins within the airways. On the basis of these observations, the reduction of neutral endopeptidase activity may be regarded as a factor that switches neurogenic airway responses from their physiological and protective functions to a detrimental role that increases and perpetuates airway inflammation. However, further studies are needed to assess the role of neutral endopeptidase down regulation in the pathogenesis of asthma and other inflammatory airway diseases.

Animals↗

PubMed1997

Neurogenic inflammation in skin and airways.

Neurogenic inflammation, in its original definition, the plasma leakage induced by stimulation of peripheral sensory nerves, occurs in the postcapillary venules of the skin and airways. Plasma leakage is accompanied by increased blood flow, which results from dilatation of arterioles. In skin, these phenomena are manifested as wheal and flare, respectively. Both phenomena are mediated by neuropeptides released from capsaicin-sensitive unmyelinated sensory nerve fibers. Substance P is the primary mediator responsible for plasma leakage, acting via tachykinin NK-1 receptors, whereas both calcitonin gene-related peptide and substance P induce vasodilatation. Sensory nerve transmitters also cause release of histamine from mast cells, which contributes substantially to plasma leakage in the skin, but less so in the airways. Substance P causes an increase in vascular permeability as a result of the focal, transient, and fully reversible formation of gaps, approximately 0.5 to 1.5 microns in diameter, located in the intercellular junctions of endothelial cells. The gaps can be visualized by silver nitrate staining of the endothelial cell borders, by lectin staining, or by scanning and transmission electron microscopy. Neurogenic inflammation can be inhibited by preventing the stimulation of sensory nerves, by presynaptic inhibition of neuropeptide release from sensory nerves, or by blocking neuropeptide receptors. The formation of endothelial gaps can also be inhibited by anti-inflammatory drugs that stabilize endothelial cells, such as beta-adrenergic agonists and steroids.

Animals↗

PubMed2002

Activation of spinal ORL-1 receptors prevents acute cutaneous neurogenic inflammation: role of nociceptin-induced suppression of primary afferent depolarization.

Neurogenic inflammation is an inflammatory response of peripheral tissue to vasoactive substances released from sensory afferent terminals. It can be triggered via a local axon reflex and by dorsal root reflex (DRR) activity involving the spinal cord. Nociceptin, an endogenous ligand for the opioid receptor-like (ORL-1) G-protein coupled receptor, has been found to inhibit the local axon reflex-mediated neurogenic inflammation by suppressing the release of vasoactive neuropeptides from sensory afferent terminals. The present study was to explore the role of spinal ORL-1 receptors in the modulation of DRR-induced neurogenic inflammation. We first examined the effect of nociceptin on DRR by recording dorsal root potentials (DRPs) and the associated antidromic discharges, evoked by electrical stimulation of an adjacent dorsal root in an in vitro neonatal rat spinal cord preparation. Nociceptin reversibly inhibited the DRP in a concentration-dependent manner (IC50: approximately 45 nM, maximal inhibition: approximately 50%), an effect that was antagonized by the ORL-1 receptor antagonist, J-113397. Neurochemical studies demonstrated that nociceptin (10 microM) also produced an approximately 40% reduction in gamma amino butyric acid (GABA) release evoked by electrical stimulation of neonatal rat spinal cord slices. On the other hand, nociceptin had no effect on exogenous GABA-evoked DRP. These findings suggest that the nociceptin-induced inhibition of the DRP is most likely due to the suppression of GABA release, the principle transmitter mediating DRP, from GABAergic neurons that are pre-synaptic to primary afferent terminals. Finally, in order to explore the physiological significance of such modulation in a fully integrated system, we evaluated the effect of intrathecally administered nociceptin on capsaicin-induced acute cutaneous neurogenic inflammation in rat hind paw, quantified by examining the degree of paw edema in anesthetized rats. The magnitude of capsaicin-induced increase of paw thickness was reduced by approximately 50% from 31+/-1.34% (n=6) to 15+/-1.63% (n=8; P<0.05) by nociceptin (10 micromol). We conclude that spinal ORL-1 receptors can modulate neurogenic inflammation by suppressing the GABAergic neuronal activity in the dorsal horn that is responsible for generating DRRs.

Acute Disease↗

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↗