Social defeat stimulates local glucocorticoid regeneration in lymphoid organs

Stress is an important risk factors for human diseases. It activates the hypothalamic–pituitary–adrenal (HPA) axis and increases plasma glucocorticoids, which are powerful regulators of immune system. The response of the target cells to glucocorticoids depends not only on the plasma concentrations of cortisol and corticosterone but also on their local metabolism. This metabolism is catalyzed by 11β-hydroxysteroid dehydrogenases type 1 and 2, which interconvert glucocorticoid hormones cortisol and corticosterone and their 11-oxo metabolites cortisone and 11-dehydrocorticosterone. The goal of this study was to determine whether stress modulates glucocorticoid metabolism within lymphoid organs – the structures where immune cells undergo development and activation. Using the resident-intruder paradigm, we studied the effect of social stress on glucocorticoid metabolism in primary and secondary lymphoid organs of Fisher 344 (F344) and Lewis (LEW) rats, which exhibit marked differences in their HPA axis response to social stressors and inflammation. We show that repeated social defeat increased the regeneration of corticosterone from 11-dehydrocorticosterone in the thymus, spleen and mesenteric lymphatic nodes (MLN). Compared with the F344 strain, LEW rats showed higher corticosterone regeneration in splenocytes of unstressed rats and in thymic and MLN mobile cells after stress but corticosterone regeneration in the stroma of all lymphoid organs was similar in both strains. Inactivation of corticosterone to 11-dehydrocorticosterone was found only in the stroma of lymphoid organs but not in mobile lymphoid cells and was not upregulated by stress. Together, our findings demonstrate the tissue- and strain-dependent regeneration of glucocorticoids following social stress.

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Dendritic Cell Migration Limits the Duration of CD8+ T-Cell Priming to Peripheral Viral Antigen

Journal of Virology ◽

10.1128/jvi.01975-09 ◽

2010 ◽

Vol 84 (7) ◽

pp. 3586-3594 ◽

Cited By ~ 7

Author(s):

Amanda M. Schell ◽

Erica L. Granger ◽

Frank Koczot ◽

Matthew A. Fischer ◽

Christopher C. Norbury

Keyword(s):

Natural Infection ◽

Lymphoid Organs ◽

Target Cells ◽

Virus Infections ◽

Dendritic Cell Migration ◽

Infected Cells ◽

Peptide Complexes ◽

Antigen Presenting ◽

Secondary Lymphoid Organs ◽

Experimental Virus

ABSTRACT CD8+ T cells (TCD8+ ) play a crucial role in immunity to viruses. Antiviral TCD8+ are initially activated by recognition of major histocompatibility complex (MHC) class I-peptide complexes on the surface of professional antigen-presenting cells (pAPC). Migration of pAPC from the site of infection to secondary lymphoid organs is likely required during a natural infection. Migrating pAPC can be directly infected with virus or may internalize antigen derived from virus-infected cells. The use of experimental virus infections to assess the requirement for pAPC migration in initiation of TCD8+ responses has proven difficult to interpret because injected virus can readily drain to secondary lymphoid organs without the need for cell-mediated transport. To overcome this ambiguity, we examined the generation of antigen-specific TCD8+ after immunization with recombinant adenoviruses that express antigen driven by skin-specific or ubiquitous promoters. We show that the induction of TCD8+ in response to tissue-targeted antigen is less efficient than the response to ubiquitously expressed antigen and that the resulting TCD8+ fail to clear all target cells pulsed with the antigenic peptide. This failure to prime a fully functional TCD8+ response results from a reduced period of priming to peripherally expressed antigen versus ubiquitously expressed antigen and correlated with a brief burst of pAPC migration from the skin, a requirement for induction of the response to peripheral antigen. These results indicate that a reduced duration of pAPC migration after virus infection likely reduces the amplitude of the TCD8+ response, allowing persistence of the peripheral virus.

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Effects of interleukin-2 on the expression of corticotropin-releasing hormone in nerves and lymphoid cells in secondary lymphoid organs from the Fischer 344 rat

Journal of Neuroimmunology ◽

10.1016/s0165-5728(01)00362-9 ◽

2001 ◽

Vol 119 (1) ◽

pp. 37-50 ◽

Cited By ~ 8

Author(s):

Denise L. Bellinger ◽

David L. Felten ◽

Dianne Lorton ◽

Sabine Brouxhon

Keyword(s):

Interleukin 2 ◽

Lymphoid Organs ◽

Lymphoid Cells ◽

Corticotropin Releasing Hormone ◽

Releasing Hormone ◽

Fischer 344 ◽

Fischer 344 Rat ◽

Secondary Lymphoid Organs

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Single exposure to social defeat or immobilization stress fails to induce lasting alterations in general anxiety and hippocampal neurogenesis in Wistar and wild-type Groningen rats

10.1101/2020.02.12.946186 ◽

2020 ◽

Author(s):

Deepika Patel ◽

Ioannis Koutlas ◽

Sebastiaan H. de Waard ◽

Bauke Buwalda

Keyword(s):

Social Stress ◽

Wistar Rats ◽

Immobilization Stress ◽

Strain Difference ◽

Social Defeat ◽

Hippocampal Neurogenesis ◽

Coping With Stress ◽

Social Stressors ◽

General Anxiety ◽

Anxiety Behavior

ABSTRACTSuppression of hippocampal neurogenesis is a readout for stress-induced alterations in neuroplasticity. In this study, we hypothesized that a single episode of severe social or non-social stress would differentially suppress neurogenesis in the dentate gyrus (DG) 10 days later in two rat strains. We anticipated that the suppression following social stress would be less severe in wildtype Groningen (WTG) rats, a rat strain considered relatively resilient to social stressors. Male Wistar and WTG were subjected to either social defeat or to immobilization stress. Behavioral response to social defeat and acute corticosterone response to both stressors was measured as well as anxiety behavior 10 days later on the elevated plus maze. Subsequently, brains were collected following cardiac aldehyde perfusion. The behavioral freezing response to defeat was much stronger in Wistar rats as compared to WTG rats. Acute corticosteroid response was similar in both strains although Wistar rats more rapidly resumed baseline values. There was no significant effect of both stressors on hippocampal DG cell proliferation and differentiation as well as on anxiety behavior. However, a striking strain difference appeared in anxiety behavior and both markers of neurogenesis. The WTG strain exhibiting much lower anxiety as well as reduced rate of hippocampal neurogenesis under all treatments. The results in this study suggest that both short-lasting acute stressors failed to induce lasting anxiety or decreased neurogenesis in the DG. Future studies could explore if and how rate of hippocampal neurogenesis is related with behavioral coping with stress.

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Innate lymphoid cells in secondary lymphoid organs

Immunological Reviews ◽

10.1111/imr.12407 ◽

2016 ◽

Vol 271 (1) ◽

pp. 185-199 ◽

Cited By ~ 42

Author(s):

Yotam E. Bar-Ephraïm ◽

Reina E. Mebius

Keyword(s):

Innate Lymphoid Cells ◽

Lymphoid Organs ◽

Lymphoid Cells ◽

Secondary Lymphoid Organs

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Faculty Opinions recommendation of Autotaxin, an ectoenzyme that produces lysophosphatidic acid, promotes the entry of lymphocytes into secondary lymphoid organs.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1104852.560937 ◽

2008 ◽

Author(s):

Vassilis Aidinis

Keyword(s):

Lysophosphatidic Acid ◽

Lymphoid Organs ◽

Secondary Lymphoid Organs

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Ingestion of probiotic (Lactobacillus helveticus and Bifidobacterium longum) alters intestinal microbial structure and behavioral expression following social defeat stress

Scientific Reports ◽

10.1038/s41598-021-83284-z ◽

2021 ◽

Vol 11 (1) ◽

Cited By ~ 2

Author(s):

Katherine A. Partrick ◽

Anna M. Rosenhauer ◽

Jérémie Auger ◽

Amanda R. Arnold ◽

Nicole M. Ronczkowski ◽

...

Keyword(s):

Social Stress ◽

Bifidobacterium Longum ◽

Social Defeat ◽

Lactobacillus Helveticus ◽

Rrna Gene ◽

Social Avoidance ◽

Social Defeat Stress ◽

Microbial Structure ◽

Microbial Composition ◽

Anti Inflammatory

AbstractSocial stress exacerbates anxious and depressive behaviors in humans. Similarly, anxiety- and depressive-like behaviors are triggered by social stress in a variety of non-human animals. Here, we tested whether oral administration of the putative anxiolytic probiotic strains Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 reduces the striking increase in anxiety-like behavior and changes in gut microbiota observed following social defeat stress in Syrian hamsters. We administered the probiotic at two different doses for 21 days, and 16S rRNA gene amplicon sequencing revealed a shift in microbial structure following probiotic administration at both doses, independently of stress. Probiotic administration at either dose increased anti-inflammatory cytokines IL-4, IL-5, and IL-10 compared to placebo. Surprisingly, probiotic administration at the low dose, equivalent to the one used in humans, significantly increased social avoidance and decreased social interaction. This behavioral change was associated with a reduction in microbial richness in this group. Together, these results demonstrate that probiotic administration alters gut microbial composition and may promote an anti-inflammatory profile but that these changes may not promote reductions in behavioral responses to social stress.

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Neutrophils in secondary lymphoid organs

Immunology ◽

10.1111/imm.13406 ◽

2021 ◽

Author(s):

Laurence S. C. Lok ◽

Menna R. Clatworthy

Keyword(s):

Lymphoid Organs ◽

Secondary Lymphoid Organs

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Non invasive in vivo monitoring of dimethyl fumarate treatment in EAE by assessing the glucose metabolism in secondary lymphoid organs

European Journal of Immunology ◽

10.1002/eji.202048879 ◽

2020 ◽

Author(s):

Jürgen Brück ◽

Carsten Calaminus ◽

Sabrina H.L. Hoffmann ◽

Johannes Schwenck ◽

Julia Holstein ◽

...

Keyword(s):

Glucose Metabolism ◽

Dimethyl Fumarate ◽

Lymphoid Organs ◽

In Vivo Monitoring ◽

Non Invasive ◽

Secondary Lymphoid Organs

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Childhood Adversities and Salivary Cortisol Responses to the Trier Social Stress Test: A Systematic Review of Studies Using the Children Trauma Questionnaire (CTQ)

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph18010029 ◽

2020 ◽

Vol 18 (1) ◽

pp. 29

Author(s):

Chuk Ling Julian Lai ◽

Daryl Yu Heng Lee ◽

Monique On Yee Leung

Keyword(s):

Salivary Cortisol ◽

Social Stress ◽

Stress Test ◽

Trier Social Stress Test ◽

Future Research ◽

Cortisol Response ◽

Childhood Adversities ◽

Social Stressors ◽

Childhood Trauma Questionnaire ◽

Cortisol Responses

Alteration in cortisol response to acute social stressors has been hypothesized to mediate childhood adversities (CA) and increased morbidity in adulthood. However, the evidence supporting an association between CA and cortisol response to social stressors is inconclusive. The present review addressed this issue by reviewing the literature on CA and cortisol response to acute social stressors, with a focus on studies with adolescents or adults, using the Childhood Trauma Questionnaire (CTQ) to assess CA, and examining salivary cortisol response to the Trier Social Stress Test (TSST). Systematic searches of relevant articles in PsycINFO, PubMed, Web of Science and ScienceDirect in February and March 2020 identified 12 articles including 1196 participants with mean ages ranging from 15.3 to 52.3 yrs. across studies. CTQ scores were significantly associated with cortisol response in 2 studies. In addition, the physical abuse and emotional neglect subscales were associated with cortisol response respectively in 2 separate studies. The lack of association between CA and cortisol response calls for more longitudinal studies, and the use of formal records of maltreatment or informant reports in future research to complement information collected by retrospective measures. In addition, increased attention to biological mechanisms other than that associated with the regulation of cortisol in explaining the connection between CA and psychiatry morbidity is warranted.

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