Eosinophil-Mediated Cholinergic Nerve Remodeling

Durcan, Niamh; Costello, Richard W.; McLean, W. Graham; Blusztajn, Jan Krzysztof; Madziar, Beata; Fenech, Anthony G.; Hall, Ian P.; Gleich, Gerald J.; McGarvey, Lorcan; Walsh, Marie Therese

doi:10.1165/rcmb.2005-0196oc

Cited by 44 publications

(29 citation statements)

References 53 publications

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“…The interaction of eosinophils with M2Rs is important to the pathogenesis of neuronal AHR. Eosinophils co-cultured with human Caucasian neruoblastoma cell line cell leads to increased expression of the M2R, which is mediated via an adhesion-dependent release of eosinophil proteins, including major basic protein and nerve growth factor, increasing acetylcholine release and potentiating vagally mediated bronchoconstriction [103].…”

Section: Inflammatory Cell Localisation To Airway Nervesmentioning

confidence: 99%

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

European Respiratory Journal

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Airway inflammation is a critical feature of the airway diseases asthma and chronic obstructive pulmonary disease (COPD). There is emerging evidence that structural cells play a key role in the development and perpetuation of the inflammatory response and are pivotal in the development of the changes in the airway structures that lead to airway remodelling.To date, little attention has been given to the localisation of inflammatory cells to airway structures or the potential interactions between these intimately located cells. However, it is likely that interactions between inflammatory and structural cells in the airway contribute enormously to the pathophysiology of asthma and COPD.Indeed, recent evidence suggests that mast cells localised to the airway smooth muscle bundle may be important in the development of airway hyperresponsiveness in asthma.In the present article, the authors aim to summarise: 1) the current understanding of which inflammatory cells locate to airway structures; 2) the proposed mechanisms that may be involved in mediating this microlocalisation; 3) the possible consequences of interactions between inflammatory and structural cells; and 4) the pressing need to investigate whether modulating these interactions is beneficial in asthma and chronic obstructive pulmonary disease.

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Section: Inflammatory Cell Localisation To Airway Nervesmentioning

confidence: 99%

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

European Respiratory Journal

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“…In seasonal exposure, unlike in our challenge model, there would be additional mechanisms involved in the process. Namely, the eosinophils recruited to the site of challenge can associate with nerves to increase their reactivity to a subsequent exposure to pollen (21,14). Nerve growth factor may contribute to this phenomenon as well as enhancing eosinophil recruitment (26).…”

Section: Discussionmentioning

confidence: 99%

Unilateral nasal allergic reactions increase bilateral sinus eosinophil infiltration

Baroody

deTineo

Naclerio

2013

Journal of Applied Physiology

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Baroody FM, deTineo M, Naclerio RM. Unilateral nasal allergic reactions increase bilateral sinus eosinophil infiltration. J Appl Physiol 115: 1262-1267, 2013. First published August 22, 2013 doi:10.1152/japplphysiol.00547.2013We have previously shown that unilateral nasal challenge with antigen causes an increase in the number of eosinophils in the ipsilateral maxillary sinus. Here we aimed to determine whether there was an eosinophil response in the contralateral maxillary sinus after unilateral nasal challenge with antigen. Twenty subjects with a history of seasonal allergic rhinitis and a positive nasal challenge to ragweed or grass allergens were studied outside of their allergy season. Catheters were placed in both maxillary sinuses and the subjects were challenged with antigen via the left nostril. The subjects recorded nasal symptoms before and after each allergen challenge and hourly for 8 h afterward. We performed nasal lavages of the nose and sinuses at the same time as symptoms were recorded. The lavages were analyzed for the number of eosinophils and levels of albumin. Subjects showed a symptomatic response to challenge accompanied by an influx of eosinophils into the nose and increased vascular permeability. The number of eosinophils increased in both maxillary sinuses. The total change from diluent in eosinophils during the late phase response was higher in the ipsilateral maxillary sinus (median ϭ 8,505; range ϭ 0 -100,360) compared with the contralateral sinus (median ϭ 1,596; range ϭ Ϫ13,527-93,373; P ϭ 0.03). We conclude that eosinophils increase in both maxillary sinuses after unilateral nasal challenge. We speculate that a central neurologic reflex initiated in the nose by the nasal challenge contributes to the bilateral eosinophil response in the maxillary sinuses. We further speculate that, since there are more eosinophils in the ipsilateral compared with the contralateral maxillary sinus, there is also an axonal reflex into the ipsilateral maxillary sinus that contributed to the eosinophil response. maxillary sinus; nasal allergen challenge; eosinophils THE NOSE IS RICHLY INNERVATED by sensory fibers from the second division of the trigeminal nerve and sympathetic and parasympathetic fibers that pass through the sphenopalatine ganglion. Whereas the sympathetic fibers merely pass through the ganglion, the parasympathetic fibers synapse sending efferent fibers to the nasal cavity, the paranasal sinuses, and the eye (2).Numerous neural reflexes originating inside and outside the nose affect nasal pathophysiology. The nasonasal reflex results from stimulation of one nasal cavity with a stimulus such as allergen or histamine. It produces a bilateral secretory response with the contralateral response being blocked by topical atropine administration (8, 3). Stimulation of the nose with allergen also induces bilateral ocular symptoms, the nasal ocular reflex (4). The nasal cycle, the process by which airway resistance of the two nasal cavities fluctuates in a cyclic manner, also involves neural m...

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“…Eosinophil infiltration is a common feature in many inflammatory pathological conditions, such as asthma, eosinophilic gastroenteritis, and inflammatory bowel disease. In these pathologies, eosinophils have been shown to localize in close apposition to cholinergic nerves, where they promote nerve remodeling through the release of mediators such as the eosinophil cationic protein and NGF (Lee et al 2001;Kingham et al 2003;Durcan et al 2006). In our immunofluorescence preparations, we have observed many eosinophils apposed to myometrial and perivascular sympathetic nerve fibers following estrogen treatment (Fig.…”

Section: Effects Of Dex On Pregnancy-induced Degeneration Of Uterine mentioning

confidence: 99%

Effects of dexamethasone on estrogen- and pregnancy-induced plasticity in rat uterine sympathetic nerves

et al. 2007

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Estrogen and glucocorticoids are known to evoke opposing effects on the uterus. We analyzed the effects of dexamethasone (DEX) on uterine sympathetic denervation elicited by short- and long-term exposure to estrogen of intact prepubertal rats. We also studied the effects of DEX on the physiological degeneration of uterine sympathetic nerves at term pregnancy. Changes in innervation were assessed quantitatively by using computer-assisted methods on uterine cryostat tissue sections stained for tyrosine hydroxylase. At 24 h following treatment of prepubertal rats (25 days of age) with 1 microg or 2.5 microg estrogen, marked increases in uterine size and reductions in the percentage nerve area were observed. Co-administration of DEX (4 mg/kg) attenuated both these short-term estrogen-induced effects. Treatment of 19-day-old rats with a single dose of 25 mug estrogen provoked, at 26 days of age, a 54% reduction in the total nerve area. This reduction was abolished by the co-administration of nine doses of DEX (0.5 mg/kg) at 18-26 days of age. Treatment of rats with the same regime of DEX alone increased the total nerve area by 46% of the control values. Studies of control pregnant rats revealed the unexpected presence of intrauterine nerve fibers at term. Treatment of pregnant rats with six doses of DEX (4 mg/kg) at 16-21 days of age had no effects on the density of uterine sympathetic nerves. These results suggest that DEX has growth-promoting effects on immature uterine sympathetic nerves and may antagonize the degenerative effects elicited by long-term exposure to estrogen.

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Eosinophil-Mediated Cholinergic Nerve Remodeling

Cited by 44 publications

References 53 publications

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Unilateral nasal allergic reactions increase bilateral sinus eosinophil infiltration

Effects of dexamethasone on estrogen- and pregnancy-induced plasticity in rat uterine sympathetic nerves

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