Rodent Models of Stress-Induced Depression: The Link Between Stress and Immune System Related Changes

Author(s):  
Barry McGuinness ◽  
Andrew Harkin
Keyword(s):  
2021 ◽  
pp. 278-307
Author(s):  
Sheila Donnelly ◽  
Robin Flynn ◽  
Grace Mulcahy ◽  
Sandra O'Neill

Abstract This book chapter tests the immune system response in ruminants naturally infected with F. hepatica and compare the results of these research with research obtained through experiments of rodent models.


2002 ◽  
Vol 21 (9-10) ◽  
pp. 533-536 ◽  
Author(s):  
H J Rothkötter ◽  
E Sowa ◽  
R Pabst

There are many limitations to analyse the developing immune system in humans, thus there is need for experimental animal models to study the environmental influences during the ontogeny of the immune system. However, risk assessment is difficult in using rodent models alone, especially as the intrauterine period of development is much shorter than that of humans. In addition to studies in dogs, the pig provides a variety of experimental approaches for developmental immuno-toxicology. The gestation period is 115 days and the occurrence of the different lines of T and B lymphocytes in the blood and organs of the porcine embryo and fetus is well documented. Fetal porcine B cells represent a naïve population developing without maternal idiotypic–antiidiotypic influences. The postnatal development is highly correlated to sufficient uptake of colostrum during the first 48 hours. Although many immunotoxicological experiments have been performed, there is a limited number of original publications about these studies. With the different strains of standard pigs and miniature pigs available and the rapid growing amount of immunological reagents, the pig represents an important experimental model for cost-effective studies in developmental immunotoxicology to analyse the risk of environmental hazards.


2019 ◽  
Vol 317 (2) ◽  
pp. H279-H289 ◽  
Author(s):  
Niousha Ahmari ◽  
Monica M. Santisteban ◽  
Douglas R. Miller ◽  
Natalie M. Geis ◽  
Riley Larkin ◽  
...  

Increased sympathetic nervous system activity is a hallmark of hypertension (HTN), and it is implicated in altered immune system responses in its pathophysiology. However, the precise mechanisms of neural-immune interaction in HTN remain elusive. We have previously shown an association between elevated sympathetic drive to the bone marrow (BM) and activated BM immune cells in rodent models of HTN. Moreover, microglial-dependent neuroinflammation is also seen in rodent models of HTN. However, the cause-effect relationship between central and systemic inflammatory responses and the sympathetic drive remains unknown. These observations led us to hypothesize that increase in the femoral BM sympathetic nerve activity (fSNA) initiates a cascade of events leading to increase in blood pressure (BP). Here, we investigated the temporal relationship between the BM sympathetic drive, activation of the central and peripheral immune system, and increase in BP in the events leading to established HTN. The present study demonstrates that central infusion of angiotensin II (ANG II) induces early microglial activation in the paraventricular nucleus of hypothalamus, which preceded increase in the fSNA. In turn, activation of fSNA correlated with the timing of increased production and release of CD4+.IL17+ T cells and other proinflammatory cells into circulation and elevation in BP, whereas infiltration of CD4+ cells to the paraventricular nucleus marked establishment of ANG II HTN. This study identifies cellular and molecular mechanisms involved in neural-immune interactions in early and established stages of rodent ANG II HTN. NEW & NOTEWORTHY Early microglia activation in paraventricular nucleus precedes sympathetic activation of the bone marrow. This leads to increased bone marrow immune cells and their release into circulation and an increase in blood pressure. Infiltration of CD4+ T cells into paraventricular nucleus paraventricular nucleus marks late hypertension.


2019 ◽  
Author(s):  
Heath W. Shelton ◽  
Somasundar Prasad Gabbita ◽  
W. Drew Gill ◽  
Katherine C. Burgess ◽  
Wyatt S. Whicker ◽  
...  

Abstract Background: Increased neuroinflammation has been shown in individuals diagnosed with schizophrenia (SCHZ). This study evaluated a novel immune modulator (PD2024) that targets the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) to alleviate sensorimotor gating deficits and microglial activation employing two different rodent models of SCHZ. Methods: In Experiment 1, rats were neonatally treated with saline or the dopamine D2-like agonist quinpirole (NQ; 1 mg/kg) from postnatal day (P) 1-21 which produces increases of dopamine D2 receptor sensitivity throughout the animal’s lifetime. In Experiment 2, rats were neonatally treated with saline or the immune system stimulant polyinosinic:polycytidylic acid (Poly I:C) from P5-7. Neonatal Poly I:C treatment mimics immune system activation associated with SCHZ. In both experiments, rats were raised to P30 and administered a control diet or a novel TNFα inhibitor PD2024 (10mg/kg) in the diet from P30 until P67. At P45-46 and from P60-67, animals were behaviorally tested on auditory sensorimotor gating as measured through prepulse inhibition (PPI). Results: NQ or Poly I:C treatment resulted in PPI deficits, and PD2024 treatment alleviated PPI deficits in both models. Results also revealed that hippocampal microglial activation produced by neonatal Poly I:C was significantly reduced to control levels by PD2024. In addition, a separate group of animals neonatally treated with saline or Poly I:C from P5-7 demonstrated increased TNFα protein levels in the hippocampus, verifying increased TNFα in the brain produced by Poly I:C. Conclusions: Results from this study suggests that that brain TNFα is a viable pharmacological target to treat the neuroinflammation known to be associated with SCHZ.


2014 ◽  
Author(s):  
Joanna Moreton ◽  
Sunir Malla ◽  
Aziz Aboobaker ◽  
Rachael Tarlinton ◽  
Richard D Emes

The immune system of the horse has not been well studied, despite the fact that the horse displays several features such as sensitivity to bacterial lipopolysaccharide that make them in many ways a more suitable model of some human disorders than the current rodent models. The difficulty of working with large animal models has however limited characterisation of gene expression in the horse immune system with current annotations for the equine genome restricted to predictions from other mammals and the few described horse proteins. This paper outlines sequencing of 184 million transcriptome short reads from immunologically active tissues of three horses including the genome reference “Twilight”. In a comparison with the Ensembl horse genome annotation, we found 8,763 potentially novel isoforms.


1998 ◽  
Vol 66 (11) ◽  
pp. 5224-5231 ◽  
Author(s):  
Rance K. Sellon ◽  
Susan Tonkonogy ◽  
Michael Schultz ◽  
Levinus A. Dieleman ◽  
Wetonia Grenther ◽  
...  

ABSTRACT Mice with targeted deletion of the gene for interleukin-10 (IL-10) spontaneously develop enterocolitis when maintained in conventional conditions but develop only colitis when kept in specific-pathogen-free (SPF) environments. This study tested the hypothesis that enteric bacteria are necessary for the development of spontaneous colitis and immune system activation in IL-10-deficient mice. IL-10-deficient mice were maintained in either SPF conditions or germfree conditions or were populated with bacteria known to cause colitis in other rodent models. IL-10-deficient mice kept in SPF conditions developed colitis in all segments of the colon (cecum and proximal and distal colon). These mice exhibited immune system activation as evidenced by increased expression of CD44 on CD4+ T cells; increased mesenteric lymph node cell numbers; and increased production of immunoglobulin A (IgA), IgG1, and IL-12 p40 from colon fragment cultures. Mice populated with bacterial strains, including Bacteroides vulgatus, known to induce colitis in other rodent models had minimal colitis. Germfree IL-10-deficient mice had no evidence of colitis or immune system activation. We conclude therefore that resident enteric bacteria are necessary for the development of spontaneous colitis and immune system activation in IL-10-deficient mice.


2002 ◽  
Vol 5 (4) ◽  
pp. 345-356 ◽  
Author(s):  
Brian E. Leonard ◽  
Cai Song
Keyword(s):  

2014 ◽  
Author(s):  
Joanna Moreton ◽  
Sunir Malla ◽  
Aziz Aboobaker ◽  
Rachael Tarlinton ◽  
Richard D Emes

The immune system of the horse has not been well studied, despite the fact that the horse displays several features such as sensitivity to bacterial lipopolysaccharide that make them in many ways a more suitable model of some human disorders than the current rodent models. The difficulty of working with large animal models has however limited characterisation of gene expression in the horse immune system with current annotations for the equine genome restricted to predictions from other mammals and the few described horse proteins. This paper outlines sequencing of 184 million transcriptome short reads from immunologically active tissues of three horses including the genome reference “Twilight”. In a comparison with the Ensembl horse genome annotation, we found 8,763 potentially novel isoforms.


2005 ◽  
Vol 173 (4S) ◽  
pp. 44-45
Author(s):  
Quan-Ming Zhu ◽  
Dong-Qing Hu ◽  
David R. Blue ◽  
Philip A. Nunn ◽  
Anthony P.D.W. Ford

2005 ◽  
Vol 173 (4S) ◽  
pp. 330-330
Author(s):  
Peter Zvara ◽  
Fabio Benigni ◽  
Enrico Baroni ◽  
Marija Zecevic ◽  
Antonia Monno ◽  
...  

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