To study the effects of sheep red blood cells (SRBC), viable Escherichia coli inoculation and IL-6 administration on steroidogenesis, activities and expression of hydroxy steroid dehydrogenase enzymes (3βHSD and 17βHSD) were measured in lymphoid organs of control and infected mice after 3 weeks treatment. Serum testosterone and cytokine levels were also estimated. Reduced expression of 3βHSD4 was found in the spleen of treated groups as compared to control, whereas the 3βHSD4 expression was increased in the thymus and lymph gland after stimulation. Reduced serum testosterone level was observed after antigenic stimulation and also altered serum IL-12p70, TNF-α, IFN-γ, MCP-1 or IL-10 level. These studies provide the evidence of expression of 3βHSD4 enzyme in the murine lymphoid organs after particulate antigen stimulation along with a parallel alteration in endogenous cytokine level. © 2009 Elsevier Inc. All rights reserved.

BISWADEV BISHAYI

Physiology

R MUKHOPADHYAY

M K MISHRA

A BASU

University of Calcutta (informally known as Calcutta University or CU) is a collegiate public state university located in Kolkata, West Bengal, India.&nbsp;Within India it is recognized as a &quot;Five-Star University&quot; and accredited &quot;A&quot; Grade by National Assessment and Accreditation Council.

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The University of Calcutta has secured the Fifth position among the Universities of India in the prestigious &quot;Indian University Ranking 2019&quot; list, released by the NIRF of the Ministry of Human Resource Development, Government of India.

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It was established on 24 January 1857, and was one of the first institutions in Asia to be established as a multidisciplinary and Western-style university. Its alumni and faculty include several heads of state, heads of government, social reformers, prominent artists, only academy award winner and Dirac medal winner in India, many Fellows of the Royal Society and five Nobel laureates as of 2019 which is highest in South Asia.

University Of Calcutta

Cellular Immunology

Stress leads to immune malfunction and increased susceptibility to infection resulting in impaired cognitive behavior and depression. Working with an animal model of Staphylococcus aureus infection and restraint stress we demonstrated impaired immune response and altered behavior against the S. aureus infection after exposure to acute or chronic restraint stress. This enhanced the resistance of mice to S. aureus infection via inhibiting the production of pro-inflammatory cytokines, free radicals, and upregulating corticosterone and anti-inflammatory cytokine production, resulting in altered exploratory behavior, compared to non-stressed infected group (P < 0.05), thereby helping the animals to recover from depressive-like symptoms due to stress. © 2015 Elsevier B.V..

Journal of Neuroimmunology

Systemic Staphylococcus aureus infection in restraint stressed mice modulates impaired immune response resulting in improved behavioral activities

Immobilization is an easy and convenient method to induce both psychological and physical stress resulting in restricted motility and aggression and is believed to be the most severe type of stress in rodent models. Although it has been generally accepted that chronic stress often results in immunosuppression while acute stress has been shown to enhance immune responses, the effects of IS on the host resistance to Escherichia coli (E. coli) infection and associated behavioral changes are still not clear. In a series of experiments aimed at determining the level of hypothalamic COX-2, HSP-90, HSP-70, SOD-1 and plasma level of corticosterone, cytokine, antibody titer and their association with behavioral activities, mice were infected with viable E. coli during acute and chronic IS by taping their paws. In this study we show that acute and chronic IS enhances the resistance of mice to E. coli infection via inhibiting the production of pro-inflammatory cytokines, free radicals, and by improving the exploratory behavior. Altogether, our findings support the notion that cytokines released during immune activation and under the influence of corticosterone can modulate the open field behavior both in terms of locomotor activity as well as exploration. One of the features observed with chronic stressor was a lower ability to resist bacterial infection, although in case of acute stress, a better clearance of bacterial infection was observed in vivo with improvement of exploratory behavior and cognitive functions. © 2012 Elsevier Inc.

Brain, Behavior, and Immunity

Increased resistance of immobilized-stressed mice to infection: Correlation with behavioral alterations

To study the effects of immune cell activation by a protein antigen or lymphoid tissue derived cytokines on peripheral steroidogenesis activities of 3β HSD and 17β HSD was measured in lymphoid organs of control and BSA immunized mice after 3 weeks treatment. We demonstrated the presence of 3βHSD and 17βHSD in the lymphoid organs after active immunization. We found elevated serum corticosterone after 3 weeks of antigen administration in presence of CFA and a higher serum IL-6 level that also alter lymphoid tissue cytokine responses like TNF-α, IL-12p70, and IL-6, among which IL-12p70 and TNF-α down-regulate the activity of steroidogenic enzymes in the thymus during an immune response. Copyright © Informa Healthcare USA, Inc.

Immunological Investigations

Modulation of steroidogenic enzymes in murine lymphoid organs after immune activation

Whether endogenous deficiency of adrenal corticosteroid by unilateral adrenalectomy leads to any modulation of macrophage response is not clear and needs investigation in detail. We performed unilateral adrenalectomy on male Swiss albino rats. Fractions of splenic macrophages were isolated and their functional activities were determined. To test the effect of adrenal hormone insufficiency (after unilateral adrenalectomy) on the cell mediated and humoral immune response, sheep red blood cells were injected, then the delayed type hypersensitivity (DTH) response and the number of antibody secreting plasma cells were determined. Studies reported herein indicate that in vivo glucocorticoid (GC) insufficiency due to unilateral adrenalectomy decreases chemotactic migration, myeloperoxidase enzyme release, and lysozyme release from rat splenic macrophages that were also related to the induction of cell mediated and humoral immune responses. The maximum number of plaque was obtained from control cells isolated from spleen after 10 days from the control rats, whereas the number of plaque was decreased in spleens isolated 20 days after unilateral adrenalectomy. Our study also showed time dependent decrease in foot pad swelling in the unilaterally adrenalectomized rats where endogenous GC was reduced with respect to control indicating reduced DTH response in case of GC insufficiency. We found slower clearance of bacterial burden from the blood and spleen isolated from unilaterally adrenalectomized rats with respect to control. Thus on one hand partially GC insufficient animals show altered macrophage response and on the other hand it heightens the persistence (in vivo) of Staphylococus aureus. The study may be helpful in understanding that adrenal corticosteroid insufficiency due to adrenalectomy interferes with immune functions, which may also support the hypothesis that endogenous GC plays a role in regulating immune response. © 2006 Elsevier GmbH. All rights reserved.

Immunobiology

Immunobiological changes of in vivo glucocorticoid depleted male Swiss albino rats

The study is undertaken to determine the effect of adrenal corticosteriod depletion after adrenalectomy on carbohydrate, protein and fat metabolism as well as maturation and functional efficacy of the immunocompetent cells. Beside biochemical and hematological parameters, whether in vivo glucocorticoid depletion has any modulatory effects on splenic macrophage responses to bacterial challenge with regards to intracellular killing, nitric oxide release and cellular integrity, were determined. Major findings of our study indicate that blood glucose, urea and total inorganic phosphate levels showed a time dependent increase in adrenalectomized rats compared to control. Total glycogen content in liver was decreased gradually due to adrenal corticosteroid insufficiency. Hematological parameters like hemoglobin concentration, hematocrit value, total leukocyte count and differential count were also found to increase in the adrenalectomized group with respect to intact group. From the functional study of immunocompetent cells, intracellular killing capacity of splenic macrophages recovered from control and adrenalectomized rats after 10 and 20 days of adrenalectomy showed no significant alteration; however, the function of splenic macrophages recovered from rats after 30 days of adrenalectomy showed altered response. Nitric oxide released from splenic macrophages of adrenalectomized rats was less than that of control animal even after stimulation with lipopolysaccharide. DNA fragmentation assay showed a lesser degree of fragmentation of splenic macrophages obtained from adrenalectomized rats indicating, apoptotic death of cells in this group decreases. Adrenal corticosteroid insufficiency due to adrenalectomy interferes with metabolic and hematopoietic functions and modulates the development and maintenance of normal immunitary status, which in turn influences the inflammatory response. © 2003 Elsevier Inc. All rights reserved.

Life Sciences

Metabolic and immunological responses associated with in vivo glucocorticoid depletion by adrenalectomy in mature Swiss albino rats

Glia

Proinflammatory mediators released by activated microglia induces neuronal death in Japanese encephalitis

Nature Reviews Immunology

Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens

Effect of particulate antigenic stimulation or in vivo administration of interleukin-6 on the level of steroidogenic enzymes in adrenal glands and lymphoid tissues of mice with parallel alteration in endogenous inflammatory cytokine level

Journal	Data powered by TypesetCellular Immunology
Publisher	Data powered by TypesetACADEMIC PRESS INC ELSEVIER SCIENCE
ISSN	0008-8749
Open Access	No