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PubMed2006

[Psychological stress, immune function and disease development. The psychoneuroimmunologic perspective].

Interdisciplinary psychoneuroimmunological (PNI) research increasingly demonstrates clinically relevant interrelations between psychological stressors and the onset or progression of chronic diseases. Disturbances of the bi-directional interaction between the nervous system, the immune system and the endocrine system have been hypothesized to be implicated in several diseases. Here, we review evidence from psychoneuroimmunology within the theoretical framework of allostatic load to conceptualize some of these associations. Interdisciplinary PNI research investigating the importance of psychological stress for the higher incidence of infections, decreased responses to vaccinations and delayed wound healing is reviewed. Furthermore, the literature supporting similar associations with regard to progression of oncological diseases and autoimmune disorders is reviewed with a focus on breast cancer and multiple sclerosis. The accumulating evidence regarding the importance of neuroendocrine-immune interaction in these diseases may thus lead to novel insights into pathogenetic mechanisms and could contribute to the development of novel preventive and therapeutic strategies.

Chronic Disease↗
PubMed1995

Influence of age and health on immune functions and trace elements.

Apparently healthy elderly donors were screened according to a simple protocol that included clinical examination and the determination of hematological and biochemical values. This screening was performed to detect subclinical alterations which might interfere with immune responses and trace element status. The elderly were divided into two groups. The first group consisted of 22 (age 76 +/- 1 years) positively selected elderly (PSE), i.e. healthy subjects with no hematological and laboratory alterations, the second one comprised 13 (age 75 +/- 1 years) negatively selected elderly (NSE). Data were then compared with those obtained from 40 (age 35 +/- 2 years) healthy young controls. In both groups of elderly donors, plasma zinc levels were normal, while plasma copper concentrations were increased. Intracellular values of zinc and copper in mono- and polymorphonuclear cells from both groups of elderly were within reference limits. After in vitro activation, granulocyte chemiluminescence activity was impaired only in NSE. A decrement in the number of circulating CD3 lymphocytes and an increase in CD8d, CD57 cells were found in PSE, while NSE showed an increased number of CD3,DR cells and CD8d, CD57, CD8b,CD57 and CD16,CD56 positive cells. Our results indicate that only plasma copper levels were affected by age, whereas subclinical alterations in hematological or biochemical values appear to impair immune responses in the elderly.

Adult↗
PubMed1985

Alteration of bone marrow cell cycle kinetics by diphenylhydantoin: relationship to folate utilization and immune function.

Female B6C3F1 mice were administered the anticonvulsant drug diphenylhydantoin (DPH) for 1 to 4 weeks by gavage at doses of 25 to 200 mg/kg. None of the dosing regimens caused toxicological manifestations other than hepatomegaly. Evaluation of the immune status of the drug-treated mice revealed no alteration of cellular immunity, measured by delayed hypersensitivity response and lymphocyte responsiveness to mitogens or allogeneic leukocytes. Humoral immunity, as measured by serum immunoglobulin quantitation and plaque-forming cell response to sheep erythrocytes, was depressed by DPH at 100 mg/kg after 2 weeks, as was host resistance to infection with the parasite Plasmodium yoelii. The bone marrow was the most sensitive target organ with loss of the multipotent stem cell colony-forming unit-spleen occurring within 1 week at a dose of 50 mg/kg. The colony-forming unit-spleen suppression was the result of a selective loss of stem cells in S phase. Committed granulocyte macrophage progenitor cells, colony-forming unit-granulocyte macrophage, were also inhibited by DPH in vivo, as well as in vitro at concentrations as low as 0.2 microM. Bone marrow cells from DPH-treated mice were folate deficient, as determined by the inability of these cells to convert deoxyuridine to thymidine. However, these mice had normal serum folate levels, even after 4 weeks of treatment. Folic acid protected bone marrow stem cells after both in vivo and in vitro treatment with DPH. It is suggested that DPH inhibits folate utilization or metabolism at the cellular level, selectively affecting bone marrow stem cells and resulting in altered stem cell kinetics. This lesion ultimately results in altered humoral immunity and impaired host resistance.

Animals↗
PubMed1985

Evaluation of host resistance and immune function in cadmium-exposed mice.

Adult female B6C3F1 mice received distilled water only or water containing 10, 50, or 250 ppm of cadmium chloride (CdCl2) for 90 days. Body weights were measured weekly. On selected days during exposure and on Day 91, Cd tissue concentrations were measured along with changes in primary antibody responses. On Day 91 mice also received a primary challenge with various infectious agents. T- and B-cell mitogenesis, natural killer (NK) cell function, delayed type hypersensitivity (DTH) as well as macrophage bactericidal activity, and phagocytosis were measured. There was no change in body weight gain, organ weights, or in humoral immunity during treatment even though cadmium had accumulated in significant quantities in the tissues. Compared with controls, exposure to cadmium had no statistically significant effect on mortality and mean survival time following primary or secondary challenge with any of the infectious agents. However, there was a dose-related, increased susceptibility to Herpes simplex type 2 virus. T- and B-lymphocyte proliferation was significantly reduced, and macrophage phagocytosis was significantly increased following cadmium exposure. NK cell activity was augmented, but not significantly. Macrophage bactericidal activity and DTH were not significantly altered.

Animals↗
PubMed2001

Characterization of the cellular immune function of patients with chronic mucocutaneous candidiasis.

Chronic mucocutaneous candidiasis (CMC) is a rare syndrome characterized by persistent and refractory infections of the skin, nails and mucosal tissues by yeasts of the genus Candida. Defects in the cellular limb of the immune system are well documented in CMC patients, but non-specific immune defects, such as myeloperoxidase deficiency or phagocyte chemotaxis disorders, have also been described. Nonetheless, the underlying defect(s) remains poorly understood, and further studies are required. We studied eight CMC patients without endocrinopathies, who showed (i) low normal proliferative response to phytohaemagglutinin (PHA), (ii) partially defective response to pokeweed mitogen (PWM), and (iii) impaired response to Candida and PPD antigens. Furthermore, peripheral blood mononuclear cells (PBMC) from CMC patients produced lower levels of type-1 cytokines (IL-2 and interferon-gamma) in response to Candida antigens, compared with control individuals. Conversely, we did not observe an enhancement of IL-4 and IL-10 in the patients, suggesting that, even though Th1 cytokines are decreased, the Th2 response is not increased in CMC. Nevertheless, the synthesis of these cytokines was normal when induced by PHA. We also observed an increased antigen-induced apoptosis in lymphocytes from the patients compared with controls, and this applied both to Candida and PPD antigens. Lastly, innate immunity defects were investigated. We observed an impairment of natural killer activity against K-562 target cells in half of the studied patients. These findings corroborate the extensive clinical and laboratory variability of CMC, which requires further studies on a larger number of patients to be better understood.

Adolescent↗
PubMed1994

Immune function in mice lacking the perforin gene.

Mice lacking the perforin gene were generated by using targeted gene disruption in embryonal stem cells. When infected with lymphocytic choriomeningitis virus (LCMV), perforin-less (-/-) mice showed clear signs of having mounted an immune response based on activation of CD8 T cells but were unable to clear the LCMV infection. This failure to eliminate virus was accompanied by a failure to generate spleen cells capable of lysing LCMV-infected fibroblasts in vitro. Spleen cells from LCMV-infected -/- mice were able to lyse hematopoietic target cells after exposure to phorbol 12-myristate 13-acetate and ionomycin, provided the target cells expressed the Fas antigen. Spleen cells from -/- mice also responded to alloantigen in mixed leukocyte culture by blastogenesis and proliferation. The resulting cells were able to lyse hematopoietic target cells, although not as well as spleen cells from +/+ littermates sensitized in the same manner. However, lysis by -/- cells was again seen only if the target cells expressed Fas antigen. We conclude that perforin-less -/- mice retain and express the Fas lytic pathway as expressed in vitro but that this pathway is insufficient to clear an LCMV infection in vivo.

Animals↗
PubMed2006

Interactions of lactoferrin with cells involved in immune function.

The antimicrobial activities of lactoferrin (Lf) depend on its capacity to bind iron and on its direct interaction with the surface of microorganisms. Its protective effect also extends to the regulation of the host response to infections. Depending on the immune status of an individual, Lf can have anti-inflammatory properties that downregulate the immune response and prevent septic shock and damage to tissues. It also acts as a promoter of the activation, differentiation, and (or) proliferation of immune cells. Although most of the anti-inflammatory activities are correlated with the neutralization of proinflammatory molecules by Lf, the promoting activity seems to be related to a direct effect of Lf on immune cells. Although the mechanisms that govern these activities are not clearly defined, and probably differ from cell to cell, several cellular targets and possible mechanisms of action are highlighted. The majority of the molecular targets at the surface of cells are multiligand receptors but, interestingly, most of them have been reported as signaling, endocytosis, and nuclear-targeting molecules. This review focuses on the known and putative mechanisms that allow the immunoregulating effect of Lf in its interactions with immune cells.

Animals↗