Stimulation of in vivo antibody production and concanavalin-A-induced mouse spleen cell mitogenesis by prolactin

Spangelo, Bryan L.; Hall, Nicholas R.; Ross, Philip C.; Goldstein, Allan L.

doi:10.1016/0162-3109(87)90004-x

Cited by 115 publications

(43 citation statements)

References 19 publications

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“…These findings provide biologic plausibility for the potential of prolactin and prolactin secretalogues to help reverse susceptibility to lymphoid depletion and nosocomial infection in critically ill patients. However, it is important to note that in vitro and animal studies suggest a biphasic effect of prolactin on the immune system similar to that seen in other target organs (40,41). Hypoprolactinemia (in humans, Ͻ2.5 ng/ml; Ref.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Lymphopenia, Lymphoid Depletion, and Hypoprolactinemia in Children with Nosocomial Sepsis and Multiple Organ Failure

Felmet¹,

Hall

Clark³

et al. 2005

The Journal of Immunology

226

200

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Lymphopenia and lymphoid depletion occur in adults dying of sepsis. Prolactin increases Bcl-2 expression, suppresses stress-induced lymphocyte apoptosis, and improves survival from experimental sepsis. We hypothesized that prolonged lymphopenia, lymphoid depletion, and hypoprolactinemia occur in children dying with sepsis and multiple organ failure (MOF). Fifty-eight critically ill children with and 55 without MOF admitted to a university hospital pediatric intensive care unit were enrolled in a prospective, longitudinal, observational clinical study. Prolactin levels and absolute lymphocyte count were measured on days 1, 3, 7, 14, and 21. Lymph node, thymus, and spleen autopsy specimens were examined for lymphoid depletion, with immunohistochemical staining for CD4, CD20, and CD21 and for lymphoid apoptosis. Prolonged lymphopenia (absolute lymphocyte count < 1000 for >7 days) occurred only in children with MOF (29 vs 0%, p < 0.05) and was associated independently with nosocomial infection (odds ratio (OR), 5.5, 95% confidence interval (CI), 1.7–17, p < 0.05), death (OR, 6.8, 95% CI, 1.3–34, p < 0.05), and splenic and lymph node hypocellularity (OR, 42, 95% CI, 3.7–473, p < 0.05). Lymphocyte apoptosis and ante/postmortem infection were observed only in children with lymphoid depletion. Prolonged hypoprolactinemia (>7 days) was more common in children with MOF (17 vs 2%, p < 0.05) and was associated independently with prolonged lymphopenia (OR, 8.3, 95% CI, 2.1–33, p < 0.05) and lymphoid depletion (OR, 12.2, 95% CI, 2.2–65, p < 0.05). Prolonged lymphopenia and apoptosis-associated depletion of lymphoid organs play a role in nosocomial sepsis-related death in critically ill children. Prolonged hypoprolactinemia is a previously unrecognized risk factor for this syndrome.

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Section: Discussionmentioning

confidence: 99%

Prolonged Lymphopenia, Lymphoid Depletion, and Hypoprolactinemia in Children with Nosocomial Sepsis and Multiple Organ Failure

Felmet¹,

Hall

Clark³

et al. 2005

The Journal of Immunology

226

200

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“…Prolactin (PRL), a neuroendocrine peptide hormone (24 kDa single structure) produced by the pituitary gland, has been suggested to play an important role in the regulation of the immune system because it stimulates lymphocyte proliferation and macrophage function (Spangelo et al 1987, Gala 1991. For example, PRL has been reported to cause a significant elevation of cytokine gene expression in macrophages, after the onset of sepsis (Zhu et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Prolactin protects against diabetes induced by multiple low doses of streptozotocin in mice

Holstad

Sandler²

1999

Journal of Endocrinology

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In earlier studies it has been shown that prolactin (PRL) is a stimulating factor for the immune system, and it has been suggested that PRL might antagonize immunosuppressive effects of glucocorticoids. PRL has been reported to affect the cytokine secretion pattern, by elevating cytokine gene expression in macrophages, after the onset of sepsis. It also promotes the antibody response in mice where it increases the production of interferon-(IFN-) and inhibits interleukin-1 (IL-1) production. Due to these properties, PRL might influence the development of autoimmune type 1 diabetes. The aim of the present study was to examine the effects of two drugs; PRL and bromocriptine (BC) in vivo on the development of hyperglycemia and pancreatic insulitis in mice treated with multiple doses of streptozotocin (STZ) (40 mg/kg body weight, i.p.). The dopaminergic agonist BC is known to inhibit PRL secretion. In another set of experiments, the direct effects of PRL on the function of pancreatic islets exposed to STZ in vitro were studied. Mice treated with STZ became gradually hyperglycemic, and concomitant treatment with PRL (4 mg/kg body weight) for 21 days significantly reduced the elevation in blood glucose levels from day 10 onwards (P<0·05). Morphologic examinations of the pancreas on day 21 of mice receiving STZ injections revealed a marked insulitis, but only moderate insulitis in the STZ treated animals given PRL. BC administration (10 mg/kg body weight) in combination with STZ did not significantly affect the elevation in blood glucose levels or the insulitis. PRL or BC administration alone did not change the serum glucose concentration. This study indicates that PRL may affect hyperglycemia in the early phase of autoimmune diabetes. We suggest that it might be due to counteraction of autoimmune immunologic mechanisms and/or enhancement of -cell regeneration.

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“…In vitro, costimulation with PRL has been reported to enhance lectin and alloantigen mitogenic responses by 30-80% (13,14). In ovariectomized female rats (15) and in an estrogen-induced T-lymphoma cell line (16), PRL directly stimulates a large proliferative response.…”

mentioning

confidence: 99%

Prolactin-immunoglobulin G complexes from human serum act as costimulatory ligands causing proliferation of malignant B lymphocytes.

Walker

Montgomery

Saraiya

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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Several lines of evidence indicate that immunoglobulin-bound prolactin found in human serum is not a conventional complex between an anti-prolactin antibody and prolactin but a different type of association of prolactin with the Fab portion of IgG heavy chains. The complex of prolactin with IgG was purified from serum by anti-human prolactin affinity chromatography and was shown to contain close to 1 mole of N8-(ryglutamyl)lysine crosslinks per mole of complex, a characteristic feature in structures crosslinked by transglutaminase. Interestingly, the complex caused a proliferation of cells from a subset of patients with chronic lymphocytic leukemia, while it was inactive in a cell proliferation prolactin bioassay. By contrast, human prolactin stimulated the proliferation of cells in the bioassay but had no effect on the complex-responsive cells from the patients. Competition studies with prolactin and free Fc fragment of IgG demonstrated a necessity for engaging both the prolactin and the immunoglobulin receptors for proliferation. More importantly, competition for the growth response by free prolactin and IgG suggests both possible reasons for the slow growth of this neoplasm as well as avenues for control of the disease.

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Stimulation of in vivo antibody production and concanavalin-A-induced mouse spleen cell mitogenesis by prolactin

Cited by 115 publications

References 19 publications

Prolonged Lymphopenia, Lymphoid Depletion, and Hypoprolactinemia in Children with Nosocomial Sepsis and Multiple Organ Failure

Prolonged Lymphopenia, Lymphoid Depletion, and Hypoprolactinemia in Children with Nosocomial Sepsis and Multiple Organ Failure

Prolactin protects against diabetes induced by multiple low doses of streptozotocin in mice

Prolactin-immunoglobulin G complexes from human serum act as costimulatory ligands causing proliferation of malignant B lymphocytes.

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