Stress-induced cytokine changes in rats

Himmerich, Hubertus; Fischer, Johannes; Bauer, Katrin; Kirkby, Kenneth C.; Sack, Ulrich; Krügel, Ute

doi:10.1684/ecn.2013.0338

Cited by 83 publications

(66 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These deficits were reversed through administration of the immunomodulatory drug glatiramer acetate (Copaxone), a “universal antigen” that weakly activates a wide spectrum of self-reactive T cells and confers neuroprotective effects (Chen et al, 2015; Kipnis and Schwartz, 2002). Other studies of chronic stress in rodents also found altered cytokines in blood, reflective of a reduced Th1/Th2 ratio (Frick et al, 2009a; Himmerich et al, 2013; Hou et al, 2013); however, this profile was not always consistent (Schmidt et al, 2010; Voorhees et al, 2013). It is important to note that the cytokine profile observed from blood is a composite result of both adaptive and innate immune cell output, so meaningful conclusions about the relative contributions of each may not be possible.…”

Section: Adaptive Immunity In Affective Disordersmentioning

confidence: 88%

Contributions of the adaptive immune system to mood regulation: Mechanisms and pathways of neuroimmune interactions

Herkenham

Kigar

2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

Clinical and basic studies of functional interactions between adaptive immunity, affective states, and brain function are reviewed, and the neural, humoral, and cellular routes of bidirectional communication between the brain and the adaptive immune system are evaluated. In clinical studies of depressed populations, lymphocytes—the principal cells of the adaptive immune system—exhibit altered T cell subtype ratios and CD4+ helper T cell polarization profiles. In basic studies using psychological stress to model depression, T cell profiles are altered as well, consistent with stress effects conveyed by the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. Lymphocytes in turn have effects on behavior and CNS structure and function. CD4+ T cells in particular appear to modify affective behavior and rates of hippocampal dentate gyrus neurogenesis. These observations force the question of how such actions are carried out. CNS effects may occur via cellular and molecular mechanisms whereby effector memory T cells and the cytokine profiles they produce in the blood interact with the blood-brain barrier in ways that remain to be clarified. Understanding the mechanisms by which T cells polarize and interact with the brain to alter mood states is key to advances in the field, and may permit development of therapies that target cells in the periphery, thus bypassing problems associated with bioavailability of drugs within the brain.

show abstract

Section: Adaptive Immunity In Affective Disordersmentioning

confidence: 88%

Contributions of the adaptive immune system to mood regulation: Mechanisms and pathways of neuroimmune interactions

Herkenham

Kigar

2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

show abstract

“…Post-mortem samples from patients with a history of depression express elevated levels of pro-inflamatory cytokines in the frontal cortex [253]. Rodents exposed to chronic mild stress exhibit neuroinflammatory markers [254] while administration of cytokine or lipoipolysaccharide (a cytokine inducer) induced depressive-like behaviour [255, 256]. Extracellular signal regulated kinase (ERK1/2) is one of several mitogen-activated protein kinases (MAPK) involved in numerous cellular processes including long-term neural plasticity, maintenance, survival and immune responses[257–259].…”

Section: Immune Responsementioning

confidence: 99%

Neuronal correlates of depression

Chaudhury

Liu

Han

2015

Cell. Mol. Life Sci.

121

View full text Add to dashboard Cite

Major depressive disorder (MDD) is a common psychiatric disorder effecting approximately 121 million people worldwide and recent reports from the World Health Organization (WHO) suggest that it will be the leading contributor to the global burden of diseases. At present the most commonly used treatment strategies are still based on the monoamine hypothesis that has been the predominant theory in the last 60 years. Clinical observations that only a subset of depressed patients exhibits full remission when treated with classical monoamine-based antidepressants together with the fact that patients exhibit multiple symptoms suggest that the pathophysiology leading to mood disorders may differ between patients. Accumulating evidence indicates that depression is a neural circuit disorder and that onset of depression may be located at different regions of the brain involving different transmitter systems and molecular mechanisms. This review synthesizes findings from rodent studies from which emerges a role for different, yet interconnected, molecular systems and associated neural circuits to the etiology of depression.

show abstract

“…TNFα production was detected in both FCoV-positive and negative cohorts. The production of this cytokine in the control cats could be due to an inflammatory process unrelated to FCoV infection, such as physiological stress [28]. In addition, the pro-inflammatory cytokine IL-18 was not consistently detected in both serum and PES.…”

Section: Expression Profiles Of Immune-related Proteins In Serum and mentioning

confidence: 85%

Expression profiles of immune mediators in feline Coronavirus-infected cells and clinical samples of feline Coronavirus-positive cats

Safi

Haghani

et al. 2017

BMC Vet Res

View full text Add to dashboard Cite

BackgroundThere are two biotypes of feline coronavirus (FCoV): the self-limiting feline enteric coronavirus (FECV) and the feline infectious peritonitis virus (FIPV), which causes feline infectious peritonitis (FIP), a fatal disease associated with cats living in multi-cat environments. This study provides an insight on the various immune mediators detected in FCoV-positive cats which may be responsible for the development of FIP.ResultsIn this study, using real-time PCR and multiplex bead-based immunoassay, the expression profiles of several immune mediators were examined in Crandell-Reese feline kidney (CRFK) cells infected with the feline coronavirus (FCoV) strain FIPV 79–1146 and in samples obtained from FCoV-positive cats. CRFK cells infected with FIPV 79–1146 showed an increase in the expression of interferon-related genes and pro-inflammatory cytokines such as MX1, viperin, CXCL10, CCL8, RANTES, KC, MCP1, and IL8. In addition, an increase in the expression of the above cytokines as well as GM-CSF and IFNγ was also detected in the PBMC, serum, and peritoneal effusions of FCoV-positive cats. Although the expression of MX1 and viperin genes was variable between cats, the expression of these two genes was relatively higher in cats having peritoneal effusion compared to cats without clinically obvious effusion. Higher viral load was also detected in the supernatant of peritoneal effusions compared to in the plasma of FCoV-positive cats. As expected, the secretion of IL1β, IL6 and TNFα was readily detected in the supernatant of peritoneal effusions of the FCoV-positive cats.ConclusionsThis study has identified various pro-inflammatory cytokines and interferon-related genes such as MX1, viperin, CXCL10, CCL8, RANTES, KC, MCP1, IL8, GM-CSF and IFNγ in FCoV-positive cats. With the exception of MX1 and viperin, no distinct pattern of immune mediators was observed that distinguished between FCoV-positive cats with and without peritoneal effusion. Further studies based on definitive diagnosis of FIP need to be performed to confirm the clinical importance of this study.

show abstract

Stress-induced cytokine changes in rats

Cited by 83 publications

References 0 publications

Contributions of the adaptive immune system to mood regulation: Mechanisms and pathways of neuroimmune interactions

Contributions of the adaptive immune system to mood regulation: Mechanisms and pathways of neuroimmune interactions

Neuronal correlates of depression

Expression profiles of immune mediators in feline Coronavirus-infected cells and clinical samples of feline Coronavirus-positive cats

Contact Info

Product

Resources

About