Altered Distribution of T Lymphocyte Subsets in Lithium-Treated Patients

Wåhlin, Anders; Knorring, Lars von; Roos, Göran

doi:10.1159/000118087

Cited by 16 publications

(7 citation statements)

References 5 publications

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“…Lithium has been demonstrated to have a consistent positive effect on lymphocyte-based host de fense systems [6], such as enhancing T-lymphocyte sub sets, T4T8 ratios, following administration in normal patients and those receiving lithium for manic depressive psychoses [6]; enhancing T-lymphocyte-derived colonystimulating activity through an effect upon T-suppressor cells [7]; and elevating the circulating granulocytes in clin ical conditions such as cyclic neutropenia [8][9][10] and con genital and acquired neutropenia [11][12][13]. It appears throughout many of the clinical studies performed that for lithium to be effective in neutropenic patients depends on the presence of a residual stem cell population capable of responding to lithium.…”

Section: Introductionmentioning

confidence: 99%

Effect of Lithium in Murine Immunodeficiency Virus Infected Animals

Gallicchio¹,

Cibull²,

Hughes³

et al. 1993

Pathobiology

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Murine AIDS (MAIDS) is a disease that shows many similarities to human HIV infection. The etiological agent of MAIDS is a defective murine leukemia virus that seems to be able to induce disease in the absence of viral replication. This animal model has been useful in stimulating the search of answers to questions and the formation of new hypotheses related to human AIDS. The monovalent cation lithium can influence a number of immunohematopoietic cell types and cellular processes where proliferation and differentiation occur. We describe here the result of in vivo studies investigating the effect of lithium treatment on MAIDS-infected mice. Viral control and lithium-treated animals were monitored for survival and development of MAIDS pathology. MAIDS animals treated with lithium demonstrated a marked reduction in their development of lymphadenopathy and splenomegaly. Both MAIDS control and lithium-treated virus-infected mice developed evidence of lymphoma; however, the involvement was much more massive both at the gross and microscopic levels in the MAIDS control compared with the lithium-treated mice. These data suggest that lithium may be effective in modulating murine immunodeficiency virus infection and raise important questions related to the potential role lithium may play in the pathophysiological processes associated with retroviral infections.

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Section: Introductionmentioning

confidence: 99%

Effect of Lithium in Murine Immunodeficiency Virus Infected Animals

Gallicchio¹,

Cibull²,

Hughes³

et al. 1993

Pathobiology

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“…The criteria for a diagnosis of depression were not stated in terms of RDC or DSM-111, and the medication status of the patients at the (13), using RDC criteria for major depression, found melancholic patients to have lower mitogen responses than controls, but the study lacked age-and sexmatched controls studied on the same day as the patients. Krueger et al (12) found decreases in the percentage of T-cell number and in T-cell function in patients who met DSM-111 criteria for major depression, but 5 of the 6 patients studied were o n psychotropic medicines known to alter immune function (16,21,29). This study also evaluated NK activity, and reported no significant change between depressed and control groups.…”

Section: Discussionmentioning

confidence: 75%

Lymphocyte function in major depression

Altshuler¹,

Plaeger-Marshall²,

Richeimer

et al. 1989

Acta Psychiatr Scand

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Immunologic function as measured by lymphocyte response to phytohemagglutinin (PHA) mitogen was evaluated in 8 psychiatric inpatients. All were less than 45 years of age and had a DSM-III diagnosis of major depression. When patient's immunologic responses were compared with healthy age- and sex-matched controls, a significant increase in PHA mitogen stimulation was observed in the depressed group. Further, a significantly greater variance in PHA response was observed in the patients compared with controls. The literature on depression and immunity is reviewed and the clinical implications of our findings are discussed.

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“…Concomitantly, lithium elevates the concentration of circulatory TNF-α (Beyaert, Schulze-Osthoff, Roy, & Fiers, 1991;El-Twab & Abdul-Hamid, 2016;Matsebatlela, Gallicchio, & Becker, 2012). This elevation might be attributed to the activation of the extracellular signal-regulated kinase (ERK) pathway (Kim et al, 2012;Sung et al, 2019), mitogen-activated protein kinases (MAPK)-ERKdependent pathway (Hull et al, 2014), nuclear factor-kappa B (NF-κB)-independent pathway (Schotte, Loo, Carpentier, Vandenabeele, & Beyaert, 2001;Sung et al, 2019), protein kinase C (PKC) (Young, Wang, Woods, & Robb, 1999), CD4 helper T-cell/CD8 suppressor (Wahlin, Knorring, & Roos, 1984) or initiation of granulocytosis (Kleinerman, Knowles, Blick, & Zwelling, 1989). Thus, lithium stimulates TNF-mediated cytotoxicity (Gallicchio, Hughes, Tse, Ling, & Birch, 1995).…”

Section: T a B L E 4 Maternal Administration Ofmentioning

confidence: 99%

Maternal lithium chloride exposure alters the neuroendocrine‐cytokine axis in neonatal albino rats

Mohammed

Ahmed

2020

Intl J of Devlp Neuroscience

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The aim of this work was to clarify whether maternal lithium chloride (LiCl) exposure disrupts the neonatal neuroendocrine‐cytokine axis. Pregnant Wistar rats were orally administrated 50 mg LiCl/kg b.wt. from gestational day (GD) 1 to postpartum day 28. Maternal administration of LiCl induced a hypothyroid state in both dams and their neonates compared to the control dams and neonates at lactation days (LDs) 14, 21 and 28, where the levels of serum free triiodothyronine (FT3) and free thyroxin (FT4) were decreased and the level of serum thyrotropin (TSH) level was increased. A noticeable depression in maternal body weight gain, neonatal body weight and neonatal serum growth hormone (GH) was observed on all examined postnatal days (PNDs; 14, 21 and 28). A single abortion case was recorded at GD 17, and three dead neonates were noted at birth in the LiCl‐treated group. Maternal administration of LiCl disturbed the levels of neonatal serum tumor necrosis factor‐alpha (TNF‐α), transforming growth factor‐beta (TGF‐β), interleukin‐1 beta (IL‐1β), interferon‐gamma (INF‐γ), leptin, adiponectin and resistin at all tested PNDs compared to the control group. This administration produced a stimulatory action on the level of neonatal cerebral serotonin (5‐HT) at PND 14 and on the level of neonatal cerebral norepinephrine (NE) at PNDs 21 and 28. However, this administration produced an inhibitory action on the level of neonatal cerebral dopamine (DA) at all examined PNDs and on the level of neonatal cerebral NE at PND 14 and the level of neonatal cerebral 5‐HT at PNDs 21 and 28 compared to the corresponding control group. Thus, maternal LiCl exposure‐induced hypothyroidism disrupts the neonatal neuroendocrine‐cytokine system, which delay cerebral development.

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Altered Distribution of T Lymphocyte Subsets in Lithium-Treated Patients

Cited by 16 publications

References 5 publications

Effect of Lithium in Murine Immunodeficiency Virus Infected Animals

Effect of Lithium in Murine Immunodeficiency Virus Infected Animals

Lymphocyte function in major depression

Maternal lithium chloride exposure alters the neuroendocrine‐cytokine axis in neonatal albino rats

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