Inescapable footshock exposure differentially alters antigen- and mitogen-stimulated spleen cell proliferation in rats

Kusnecov, Alexander W.; Rabin, Bruce S.

doi:10.1016/0165-5728(93)90265-z

Cited by 31 publications

(15 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in accordance with the hypothesis of a lack of effect of stress on antigen-specific response when it is applied after priming. As hypothesized by Kusnecov and Rabin [8], this could result from a lower sensitivity to stress hormones of activated and memory T cells than naive cells.…”

Section: Discussionmentioning

confidence: 97%

“…In studies using dead antigens, it has been proposed that stress could only alter the response of T cells to molecules for which they do not have any specific memory. Accordingly, a stress occurring at the very beginning of a primary response could inhibit naive T cells, impairing the formation of memory T cells, but stress would be less effective if happening after priming [8]. Nevertheless, a stress can occur at any time of an infectious process.…”

Section: Introductionmentioning

confidence: 99%

“…The timing for applying stressor and primary immunization is known to influence the nature of the immune alterations induced by stress [8][9][10]. In studies using dead antigens, it has been proposed that stress could only alter the response of T cells to molecules for which they do not have any specific memory.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Immune Alterations Induced by Social Defeat Do Not Alter the Course of an On-Going BCG Infection in Mice

Merlot

Moze

Dantzer

et al. 2004

Neuroimmunomodulation

View full text Add to dashboard Cite

The timing for applying stressor and primary immunization is known to influence the nature of the immune alterations induced by stress. The aim of the present study was to investigate the consequences of a stress occurring several days after the beginning of a primary infection on the host resistance. For this purpose, we investigated the effects of repeated social defeat on the immune response of mice infected with BCG 11 days before. In vitro production of cytokines in response to LPS or tuberculin, and the sensitivity of spleen cells to corticosterone were assessed 8 days after the end of the stress. Bacterial growth was assessed in the spleen. We demonstrated that social defeat in BCG-infected mice induced a long-term increase in IL-6 and IL-10 production in response to LPS but did not modify the sensitivity of spleen cells to corticosterone. Stress did not affect the specific response to BCG, as shown by the production of cytokines in tuberculin-stimulated cultures. Accordingly, social defeat was unable to influence the mycobacterial growth in vivo. These results support the hypothesis postulating that stress does not affect antigen-specific response when it is applied after priming.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Immune Alterations Induced by Social Defeat Do Not Alter the Course of an On-Going BCG Infection in Mice

Merlot

Moze

Dantzer

et al. 2004

Neuroimmunomodulation

View full text Add to dashboard Cite

show abstract

“…For example, acute stress enhances the trafficking of lymphocytes and macrophages to the site of acute challenge through HPA axis stimulation; 7 the effects of stress are probably beneficial. By contrast, repeated stress induces a decrease or a disruption of cellular immunity, 6,8 , 9 a decrease of the different subsets of lymphoid cells in secondary lymphoid organs that correlates with a decrease of antibody levels, 10 and/or a disruption of cytokine secretion 11 …”

Section: Introductionmentioning

confidence: 99%

Chronic restraint stress induces severe disruption of the T‐cell specific response to tetanus toxin vaccine

Tournier¹,

Mathieu²,

Mailfert³

et al. 2001

Immunology

View full text Add to dashboard Cite

Summary Chronic stress is known to induce immunological disorders. In the present study we examined the consequences of chronic restraint stress on the immune response to tetanus toxin in mice. We investigated the repartition of subsets of lymphoid cells in blood and spleen, the functional ability of lymphocytes to proliferate and to produce cytokines, and antibody titres against tetanus toxin following stress. We report discordance of the stimulation index of lymphocytes in the restraint group: the proliferating rate severely decreased following stimulation with a relevant antigen, whereas it increased with mitogen. Thus, we report a decrease in cytokine production with relevant antigen (interferon‐γ and interleukin‐10), without a T helper type 1 and 2 secretion imbalance. Moreover, we observed an alteration in the humoral response, including a delay in isotype maturation and an immunoglobulin G1/G2a imbalance.

show abstract

“…This has been demonstrated for several quantitative and qualitative aspects of immune func tion, including nonspecific innate immune parameters [15][16][17][18][19][20][21], and specific T and B lymphocyte functions, including those against infectious and tumor antigens [22][23][24][25][26][27][28][29][30][31][32][33], How ever, there is a lack of consensus as to which types of stres sors are likely to promote specific types of alterations in a particular parameter of immune function. For example, whereas some researchers have found stressor-induced sup pression of antibody production in rats or mice [34][35][36], others find an enhancement in antibody formation [37,38].…”

Section: Modulation Of the Immune Function By Stressmentioning

confidence: 99%

Stressor-lnduced Alterations of Immune Function: Mechanisms and Issues

Kusnecov

Rabin²

1994

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

This paper reviews the role of catecholamines and the hypothalamic-pituitary-adrenal system in the mediation of stress-induced immune changes in both human and animal subjects. There is evidence to support the importance of these factors in mediating stressor effects on certain immune parameters, but further research is needed to define the specific circumstances in which they are relevant. Therefore, discussion of such issues as sex, genotype, stress history, environment, and stressor characteristics is provided to suggest possible ways to increase our understanding of stressor effects on immune function. Since the imposition of a stressor disrupts physiological homeostasis, understanding the capacity of the immune system to function under such conditions is of prime importance in predicting disease onset and outcome.

show abstract

Inescapable footshock exposure differentially alters antigen- and mitogen-stimulated spleen cell proliferation in rats

Cited by 31 publications

References 34 publications

Immune Alterations Induced by Social Defeat Do Not Alter the Course of an On-Going BCG Infection in Mice

Immune Alterations Induced by Social Defeat Do Not Alter the Course of an On-Going BCG Infection in Mice

Chronic restraint stress induces severe disruption of the T‐cell specific response to tetanus toxin vaccine

Stressor-lnduced Alterations of Immune Function: Mechanisms and Issues

Contact Info

Product

Resources

About