Regulation of the mouse B lymphocyte cell cycle by substances raising intracellular cAMP and cGMP levels

Ado, A. D.; Dontsov, V. I.; Goldshtein, Matan

doi:10.1007/bf00842746

Cited by 4 publications

(7 citation statements)

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“…Acetylcholine and aceclidine st'unulated antibody production and ADCC, which is clearly explained by the mechanisms analyzed by other scientists [1,2,13,14] and confirmed in other experimental models [5]. One pathogenetic effect of ADCC activation may be an increased level of cGMP in these cells due to stimulation of their M-cholinoceptive structures [ 11].…”

Section: Resultsmentioning

confidence: 89%

“…There are different interpretations of the mechanisms lying at the basis of the radioprotective effect of cholinomimetics, but the immunological mechanisms of this phenomenon, specifically, during the use of cholinergic stimulants after irradiation, have been little studied. On the other hand, we know that agents stimulating M-cholinoreactive structures can activate some immune reactions [1,2,13]. Methods aimed at increasing radioresistance are based on the use of immunotropic agents (interleukin-1, tumor necrosis factor, etc.…”

mentioning

confidence: 99%

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Cholinomimetics boost the immunological mechanisms of radioresistance

Забродский

1996

Bull Exp Biol Med

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Acetylcholine and aceclidine reduce the mortality of mice after irradiation. This effect is evidently due to activation of M-cholinoreactive structures leading to an increase of the number of colony-forming units in the spleen, migration of T and B lymphocytes from lymphoid organs, and boosting of antibody production and of antibody-dependent cell cytotoxicity. Key Words: ionizing radiation; immunocyte migration; antibody production; antibodydependent cell cytotoxicityRadioresistance is known to appreciably increase under the effect of cholinergic stimulation prior to irradiation [10]. There are different interpretations of the mechanisms lying at the basis of the radioprotective effect of cholinomimetics, but the immunological mechanisms of this phenomenon, specifically, during the use of cholinergic stimulants after irradiation, have been little studied. On the other hand, we know that agents stimulating M-cholinoreactive structures can activate some immune reactions [1,2,13]. Methods aimed at increasing radioresistance are based on the use of immunotropic agents (interleukin-1, tumor necrosis factor, etc.), which are used both before and after exposure [3]. This study was carded out to investigate the immunological mechanisms of radioresistance boost under the effect of cholinomimetics used after ionizing radiation. MATERIALS AND METHODSExperiments were carded out with outbred and CBA mice weighing 18 to 22 g. Acetylcholine in a dose of 5 mg/kg three times a day and aceclidine in a single Toxicology Department, Saratov Medical Univemity dose of 1 mg/kg were used as cholinergic stimulants. The outbred animals were totally irradiated in a dose of 7 Gy. The lethality was assessed on day 9. Colony-forming splenocytes were determined by the endogenous colony formation method [7,15] aRer total exposure of outbred mice in a dose of 7 Gy.Migration of T cells from the thymus and of B lymphocy-tes from the bone marrow was assessed in CBA mice as described elsewhere [10], the index of migration being the content of antibody-producing cells in the spleens after 8 days, determined as described previously [ 12]. Cholinergic agonists were injected subcutaneously 30 to 60 min after exposure. Syngeneic T cells (2x107) or bone marrow cells (10 7 ) were administered simultaneously with sheep red cells (SRBC, 2x108) in a dose of 0.5 ml intravenously 1 day after irradiation. The migration of T and B cells was examined after exposure to 8 Gy with shielding of the thymus or hind limbs to the level of the knee joint, respectively. Antibody-producing cells in CBA mouse spleens were counted after 5 days as described previously [12] and antibody-dependent cell cytotoxicity (ADCC) was assessed in nonirradiated mice. These mice were immunized with sheep red cells (5x 10 s cells in 0.5 ml

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Section: Resultsmentioning

confidence: 89%

mentioning

confidence: 99%

Cholinomimetics boost the immunological mechanisms of radioresistance

Забродский

1996

Bull Exp Biol Med

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“…However, not much is known about second messenger signaling in B lymphocytes. Opposing results were reported depending on the nature of second messengers in B cell cycling (78). Treating murine B lymphocytes with the neurotransmitter acetylcholine indirectly increased the intracellular cGMP levels by stimulating the NO/cGMP pathway, consequently stimulating B cells to enter the cell cycling stages (78, 79).…”

Section: Inflammatory Damage Control In Active Ms Lesions By Inhibitimentioning

confidence: 96%

“…Opposing results were reported depending on the nature of second messengers in B cell cycling (78). Treating murine B lymphocytes with the neurotransmitter acetylcholine indirectly increased the intracellular cGMP levels by stimulating the NO/cGMP pathway, consequently stimulating B cells to enter the cell cycling stages (78, 79). In contrast, adrenaline-induced intracellular cAMP inhibited the entry of B lymphocytes into the DNA replication stage of the cell cycle (78).…”

Section: Inflammatory Damage Control In Active Ms Lesions By Inhibitimentioning

confidence: 96%

“…Treating murine B lymphocytes with the neurotransmitter acetylcholine indirectly increased the intracellular cGMP levels by stimulating the NO/cGMP pathway, consequently stimulating B cells to enter the cell cycling stages (78, 79). In contrast, adrenaline-induced intracellular cAMP inhibited the entry of B lymphocytes into the DNA replication stage of the cell cycle (78). The latter is consistent with the observations that forskolin, an activator of AC in the plasma membrane, arrested human B lymphocytes in the G1 phase of cell cycling and thereby inhibited B cell growth (80).…”

Section: Inflammatory Damage Control In Active Ms Lesions By Inhibitimentioning

confidence: 99%

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Targeting Phosphodiesterases—Towards a Tailor-Made Approach in Multiple Sclerosis Treatment

et al. 2019

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Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) characterized by heterogeneous clinical symptoms including gradual muscle weakness, fatigue, and cognitive impairment. The disease course of MS can be classified into a relapsing-remitting (RR) phase defined by periods of neurological disabilities, and a progressive phase where neurological decline is persistent. Pathologically, MS is defined by a destructive immunological and neuro-degenerative interplay. Current treatments largely target the inflammatory processes and slow disease progression at best. Therefore, there is an urgent need to develop next-generation therapeutic strategies that target both neuroinflammatory and degenerative processes. It has been shown that elevating second messengers (cAMP and cGMP) is important for controlling inflammatory damage and inducing CNS repair. Phosphodiesterases (PDEs) have been studied extensively in a wide range of disorders as they breakdown these second messengers, rendering them crucial regulators. In this review, we provide an overview of the role of PDE inhibition in limiting pathological inflammation and stimulating regenerative processes in MS.

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On the History of Immunophysiology

Корнева¹

2010

New Insights to Neuroimmune Biology

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Regulation of the mouse B lymphocyte cell cycle by substances raising intracellular cAMP and cGMP levels

Cited by 4 publications

References 5 publications

Cholinomimetics boost the immunological mechanisms of radioresistance

Cholinomimetics boost the immunological mechanisms of radioresistance

Targeting Phosphodiesterases—Towards a Tailor-Made Approach in Multiple Sclerosis Treatment

On the History of Immunophysiology

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