Thymocytes and Cultured Thymic Epithelial Cells Express Transcripts Encoding α‐3, α‐5, and β‐4 Subunits of Neuronal Nicotinic Acetylcholine Receptors: Preferential Transcription of the α‐3 and β‐4 Genes by Immature CD4+8+ Thymocytes and Evidence for Response to Nicotine in Thymocytes<sup>a</sup>

Mihovilovic, Mirta; Denning, Stephen M.; Mai, Yun; Fisher, Clare; Whichard, Leona P.; Patel, Dhavalkumar D.; Roses, Allen D.

doi:10.1111/j.1749-6632.1998.tb10951.x

Cited by 16 publications

(4 citation statements)

References 9 publications

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“…Biological actions of acetylcholine in the thymus are mediated through its interactions with cholinergic receptors. Rat thymocytes express on their surface nicotinic and muscarinic cholinergic receptors (Maslinski, Grabczewska, Laskowska‐Bozek & Ryzewski, 1987; Maslinski, Kullberg, Nordstrom & Bartfai, 1988; Rinner, Porta & Schauenstein, 1990; Tominaga, Hato, Kinoshita, Tominaga & Yamada, 1992; Mihovilovic et al. , 1997; Yamada, Murayama & Nomura, 1997).…”

Section: Catecholamines and Acetylcholinementioning

confidence: 99%

Autonomic innervation of immune organs and neuroimmune modulation

Mignini

Streccioni

Amenta

2003

Auton Autocoid Pharmacol

183

147

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1. Increasing evidence indicates the occurrence of functional interconnections between immune and nervous systems, although data available on the mechanisms of this bi-directional cross-talking are frequently incomplete and not always focussed on their relevance for neuroimmune modulation. 2. Primary (bone marrow and thymus) and secondary (spleen and lymph nodes) lymphoid organs are supplied with an autonomic (mainly sympathetic) efferent innervation and with an afferent sensory innervation. Anatomical studies have revealed origin, pattern of distribution and targets of nerve fibre populations supplying lymphoid organs. 3. Classic (catecholamines and acetylcholine) and peptide transmitters of neural and non-neural origin are released in the lymphoid microenvironment and contribute to neuroimmune modulation. Neuropeptide Y, substance P, calcitonin gene-related peptide, and vasoactive intestinal peptide represent the neuropeptides most involved in neuroimmune modulation. 4. Immune cells and immune organs express specific receptors for (neuro)transmitters. These receptors have been shown to respond in vivo and/or in vitro to the neural substances and their manipulation can alter immune responses. Changes in immune function can also influence the distribution of nerves and the expression of neural receptors in lymphoid organs. 5. Data on different populations of nerve fibres supplying immune organs and their role in providing a link between nervous and immune systems are reviewed. Anatomical connections between nervous and immune systems represent the structural support of the complex network of immune responses. A detailed knowledge of interactions between nervous and immune systems may represent an important basis for the development of strategies for treating pathologies in which altered neuroimmune cross-talking may be involved.

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Section: Catecholamines and Acetylcholinementioning

confidence: 99%

Autonomic innervation of immune organs and neuroimmune modulation

Mignini

Streccioni

Amenta

2003

Auton Autocoid Pharmacol

183

147

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“…62 , 83 Both thymic epithelium and thymocytes 84 express nAChR as do mature lymphocytes. 85 , 86 It has also been established that macrophages and dendritic cells also possess nAChR subunits.…”

Section: Immune Systemmentioning

confidence: 99%

Neuronal nicotinic acetylcholine receptor expression and function on nonneuronal cells

Gahring

Rogers

2005

AAPS J

135

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“…Although it is difficult to ascribe all of these effects to the actions of nicotine as compared with other tobacco components (Hockertz et al, 1994;Johnson et al, 1990;, some of the effects of smoking on immune function are clearly attributable to the direct actions of nicotine (Geng, Savage, Johnson, Seagrave, & Sopori, 1995;Geng, Savage, Razani-Boroujerdi, & Sopori, 1996;McAllister-Sistilli et al, 1998;, and the degree of immunosuppression is directly related to the nicotine content of the cigarettes (McAllister-Sistilli et al, 1998;. Human lymphocytes and polymorphonuclear cells contain mRNA encoding the subunits of the nicotinic acetylcholine receptor (Benhammou et al, 2000;Hiemke et al, 1996;Mihovilovic et al, 1998), and radioligand binding confirms that nicotinic acetylcholine receptors are present on lymphocytes in humans and rodents (Benhammou et al, 2000;Maslinski, Grabczewska, & Ryzewski, 1980;Maslinski, Laskowska-Bozek, & Ryzewski, 1992;Toyabe et al, 1997). The receptors are upregulated in smokers (Benhammou et al, 2000) and are increased when lymphocytes undergo mitogenic stimulation in accord with involvement in lymphocyte activation (Paldi-Haris, Szelenyi, Nguyen, & Hollan, 1990;Szelenyi, Paldi-Haris, & Hollan, 1987), and indeed, nicotine elicits mobilization of intracellular calcium in lymphocytes, leading T-cells to release cytokines (Goud, Zhang, & Kaplan, 1993;Petro, Schwartzbach, & Zhang, 1999;Zhang, & Petro, 1996).…”

Section: Introductionmentioning

confidence: 98%

Short-term adolescent nicotine exposure in rats elicits immediate and delayed deficits in T-lymphocyte function: Critical periods, patterns of exposure, dose thresholds

Navarro

Basta

Seidler

et al. 2003

Nicotine & Tobacco Research

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Prenatal nicotine exposure elicits lasting deficiencies in T-lymphocyte mitogenesis, and the period of vulnerability extends into adolescence, the stage at which smoking typically commences. We explored the importance of nicotine exposure patterns (continuous infusion vs. repeated subcutaneous injections), dose-effect relationships, and specificity of the effects. Adolescent rats were given nicotine infusions for 1 week beginning on postnatal day (PN) 30, using a regimen (6 mg/kg/day) that produces plasma nicotine levels (25 ng/ml) similar to those in smokers; another group received 2 mg/kg/day. At the end of the infusion period (PN37), T-lymphocyte mitogenic responses to concanavalin A were deficient in the group receiving 6 mg/kg/day; values for the 2 mg/kg/day group were intermediate between controls and the 6 mg/kg/day group. One week after the termination of nicotine treatment, responses returned to normal, only to reemerge in young adulthood (PN65), at which stage adverse effects were significant even for the group that received 2 mg/kg/day. In contrast to the T-cell alterations, B-lymphocyte responses were unaffected. Administering the same total doses of nicotine by twice-daily subcutaneous injections over the 1-week treatment period (1 or 3 mg/kg per injection) did not evoke deficits in responses of either T-cells or B-cells, even though the high dose produced overt systemic toxicity and persistent weight loss. Our results indicate that adolescent nicotine exposure, even at levels below those associated with active smoking, elicits selective deficits in T-lymphocyte function. Although short-term adaptations may correct the effects, deficits reemerge in young adulthood despite cessation of nicotine exposure.

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Cited by 16 publications

References 9 publications

Autonomic innervation of immune organs and neuroimmune modulation

Autonomic innervation of immune organs and neuroimmune modulation

Neuronal nicotinic acetylcholine receptor expression and function on nonneuronal cells

Short-term adolescent nicotine exposure in rats elicits immediate and delayed deficits in T-lymphocyte function: Critical periods, patterns of exposure, dose thresholds

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