Effect of sympathectomy on lymphopoiesis in anterior eye chamber thymic explants

Singh, Upendra; Goldowitz, Dan

doi:10.1016/0192-0561(82)90218-1

Cited by 14 publications

(13 citation statements)

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“…First, adrenalectomy completely removes all adrenal products including corticosterone by surgically removing the production of corticosterone. This poses a problem since other adrenal products besides corticosterone (e.g., catecholamines) have been shown to modulate thymic cellularity (Singh, 1979;Durant, 1986). In order to verify that corticosterone was the likely mediator of the effect, a corticosterone synthesis inhibitor, aminoglutethimide was utilized.…”

Section: Discussionmentioning

confidence: 99%

Sodium Methyldithiocarbamate Causes Thymic Atrophy by an Indirect Mechanism of Corticosterone Up-Regulation

Myers

Fan

Zheng

et al. 2005

Journal of Immunotoxicology

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Sodium methyldithiocarbamate (SMD) is an agricultural fumigant-type pesticide commonly used as a pre-plant biocide. SMD is currently listed by the US Environmental Protection Agency (EPA) as the third most commonly used conventional pesticide. Previously, SMD has been shown to be immunotoxic in mice. Initial immunotoxicological studies indicated that thymocytes are major targets of SMD or its breakdown products in mice. The purpose of the present study was to determine if this effect was mediated by an SMD-induced stress response. The decrease in thymus weight correlated to a decrease in all thymocyte subpopulations. However, as seen in earlier studies, the double positive (CD4 + CD8 + ) thymocyte subpopulation was more selectively decreased than the other subpopulations. The double negative (CD4 − CD8 − ) and single positive (CD4 + CD8 − or CD4 − CD8 + ) thymocyte subpopulations decreased in absolute numbers while increasing in percentage of the remaining cells in the thymus after SMD intoxication. In the current study, SMD caused an increase in serum corticosterone, a stress-related hormone. Blocking corticosterone either by 1) adrenalectomy or by 2) chemically blocking synthesis of nascent corticosterone in adrenal-competent animals abrogated the thymocyte atrophy caused by SMD. However, an additional stressor (restraint) did not act additively or synergistically to increase atrophy. Therefore, it is likely that SMD causes thymic atrophy by increasing serum corticosterone.

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Section: Discussionmentioning

confidence: 99%

Sodium Methyldithiocarbamate Causes Thymic Atrophy by an Indirect Mechanism of Corticosterone Up-Regulation

Myers

Fan

Zheng

et al. 2005

Journal of Immunotoxicology

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“…Early studies in the 1970s and 1980s allude to β-AR-induced enhancement of thymocyte differentiation and suppression of thymocyte proliferation in the presence of intact NA innervation [58][59][60][61][62][63]. Isoproterenol exposure in vivo reduces thymic weight and thymocyte number in mice [64].…”

Section: Sympathetic Neurotransmission In the Thymusmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

223

185

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Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease-or injury-induced 'fight' responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.

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“…Given that (1) NA levels in rodent thymi increase with age [42][43][44] and (2) CAs have been suggested to exert an inhibitory influence on thymus via ␤ -and ␣ -adrenoceptors [46,48,49,[272][273][274][275][276] , a causal link between the ageassociated rise in thymic NA level and thymic involution has been suggested [42][43][44]49] . These data, taken together with the findings indicating that peripubertal gonadectomy significantly diminishes NA levels in thymus [38] , indicate that CAs may be considered as one of the putative mediators of sex steroid hormone action on the thymus.…”

Section: Cas and Thymus Agingmentioning

confidence: 99%

Age-Associated Remodeling of Thymopoiesis: Role for Gonadal Hormones and Catecholamines

Leposavić

Perišić

2008

Neuroimmunomodulation

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The present review summarizes recent data on age-related thymic changes termed thymic involution, and highlights the putative role of perturbances in extrathymical and, possibly, intrathymical production of gonadal steroids and catecholamines in this process. Thymic involution has been envisaged as an extremely complex process involving multifactorial mechanisms along the bone marrow-thymic axis that accounts for the major manifestations of immunosenescence. These mechanisms include basic cell aging processes (for example, cell replication and programmed cell death) and processes unique to the immune system (such as generation of the T cell receptor repertoire and control of potentially autoreactive cells). Given that the onset of age-associated thymic involution coincides with the rise in gonadal steroid levels at puberty, a causal link between these events has been suggested. It has been shown that: (1) peripubertal gonadectomy causes substantial decrease in the level of noradrenaline in adult male and female thymus and (2) catecholamines, acting via α- and β-adrenoceptor, produce suppressive effects on the thymic cellularity and production of both effector and regulatory T cells. Furthermore, the possibility that gonadal steroids contribute to thymic involution is discussed in this paper. In light of recent data indicating that effects of gonadal hormone deprivation on the thymic cellularity and function are long lasting but transitory, a putative role for the intrathymic sex steroid/catecholamine production in assuring the organ involution, under conditions of their limited supply by extrathymic sources, is also considered.

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Effect of sympathectomy on lymphopoiesis in anterior eye chamber thymic explants

Cited by 14 publications

References 0 publications

Sodium Methyldithiocarbamate Causes Thymic Atrophy by an Indirect Mechanism of Corticosterone Up-Regulation

Sodium Methyldithiocarbamate Causes Thymic Atrophy by an Indirect Mechanism of Corticosterone Up-Regulation

Sympathetic modulation of immunity: Relevance to disease

Age-Associated Remodeling of Thymopoiesis: Role for Gonadal Hormones and Catecholamines

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