Social stress alters the severity and onset of the chronic phase of Theiler's virus infection

Johnson, Robin; Prentice, Thomas W.; Bridegam, Patrick; Young, Colin R.; Steelman, Andrew J.; Welsh, T. H.; Welsh, C. Jane; Meagher, Mary W.

doi:10.1016/j.jneuroim.2006.02.014

Cited by 33 publications

(72 citation statements)

References 41 publications

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“…In our study, we focused on the risk for autoimmune disorders in individuals with PTSD. The hypothesis that trauma exposure and PTSD may increase risk for the development of autoimmune disorders is supported by some non-human experimental stress studies (58, 59). However, other investigators have proposed that stress may actually protect against the development of specific autoimmune disorders under some circumstances (60).…”

Section: Discussionmentioning

confidence: 91%

Elevated Risk for Autoimmune Disorders in Iraq and Afghanistan Veterans with Posttraumatic Stress Disorder

O’Donovan

Cohen

Seal

et al. 2015

Biological Psychiatry

224

173

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BACKGROUND Posttraumatic stress disorder (PTSD) is associated with endocrine and immune abnormalities that could increase risk for autoimmune disorders. However, little is known about the risk for autoimmune disorders among individuals with PTSD. METHODS We conducted a retrospective cohort study of 666,269 Iraq and Afghanistan veterans under age 55 who were enrolled in the Department of Veterans Affairs (VA) healthcare system between October 7, 2001 and March 31, 2011. Generalized linear models were used to examine if PTSD, other psychiatric disorders, and military sexual trauma exposure (MST) increase risk for autoimmune disorders, including thyroiditis, inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, and lupus erythematosus, adjusting for age, gender, race, and primary care visits. RESULTS PTSD was diagnosed in 203,766 (30.6%) veterans, and psychiatric disorders other than PTSD were diagnosed in an additional 129,704 (19.5%) veterans. Veterans diagnosed with PTSD had significantly higher adjusted relative risk (ARR) for diagnosis with any of the autoimmune disorders alone or in combination compared to veterans with no psychiatric diagnoses (ARR = 2.00, 95% CI, 1.91, 2.09), and compared to veterans diagnosed with psychiatric disorders other than PTSD (ARR = 1.51, 95% CI, 1.43, 1.59, p < .001). The magnitude of the PTSD-related increase in risk for autoimmune disorders was similar in women and men, and MST was independently associated with increased risk in both women and men. CONCLUSIONS Trauma exposure and PTSD may increase risk for autoimmune disorders. Altered immune function, lifestyle factors, or shared etiology may underlie this association.

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Section: Discussionmentioning

confidence: 91%

Elevated Risk for Autoimmune Disorders in Iraq and Afghanistan Veterans with Posttraumatic Stress Disorder

O’Donovan

Cohen

Seal

et al. 2015

Biological Psychiatry

224

173

View full text Add to dashboard Cite

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“…Our laboratory has previously demonstrated that chronic social disruption (SDR) prior to TMEV infection exacerbates both the acute and chronic phases of the disease (Johnson et al, 2004, 2006; Meagher et al, 2007; Young et al, 2008). Specifically, SDR has been shown to enhance functional impairment and increase CNS inflammatory lesions during the acute phase of disease.…”

Section: Introductionmentioning

confidence: 99%

Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release

Vichaya

Young

Frazier

et al. 2011

Journal of Neuroimmunology

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Chronic social disruption stress (SDR) exacerbates acute and chronic phase Theiler’s murine encephalomyelitis virus (TMEV) infection, a mouse model of multiple sclerosis. However, the precise mechanism by which this occurs remains unknown. The present study suggests SDR exacerbates TMEV disease course by priming virus-induced neuroinflammation. It was demonstrated that IL-1β mRNA expression increases following acute SDR; however, IL-6 mRNA expression, but not IL-1β, is upregulated in response to chronic SDR. Furthermore, this study demonstrated SDR prior to infection increases infection related central IL-6 and IL-1β mRNA expression, and administration of IL-6 neutralizing antibody during SDR reverses this increase in neuroinflammation.

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“…Although recent studies in both humans and experimental animals suggest that PS compromises host defenses against bacterial and viral infections (13)(14)(15)(16)(17)(18)(19)(20)(21), the pathogenic mechanisms remain unknown. Three potentially interconnected mechanisms have been proposed to explain the negative impact of PS on host defenses against infection and neoplasia: (a) psychoneuroimmunoendocrine dysfunction, which leads to increased proinflammatory neuropeptide and cytokine production in a manner either dependent or independent of the hypothalamic-pituitary-adrenal (HPA) axis (18)(19)(20)(21)(22)(23)(24); (b) increased plasma levels of endogenous glucocorticoid (GC) caused by activation of the HPA axis (16, 18-21, 24, 25); and (c) a cutaneous steroidogenic system, with localized production of corticotropin-releasing factor (CRF) (26,27), which could mediate the adverse effects of PS on skin.…”

Section: Introductionmentioning

confidence: 99%

Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice

Åberg

Radek

Choi³

et al. 2007

J. Clin. Invest.

209

187

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The skin is the first line of defense against microbial infection, and psychological stress (PS) has been shown to have adverse effects on cutaneous barrier function. Here we show that PS increased the severity of group A Streptococcus pyogenes (GAS) cutaneous skin infection in mice; this was accompanied by increased production of endogenous glucocorticoids (GCs), which inhibited epidermal lipid synthesis and decreased lamellar body (LB) secretion. LBs encapsulate antimicrobial peptides (AMPs), and PS or systemic or topical GC administration downregulated epidermal expression of murine AMPs cathelin-related AMP and β-defensin 3. Pharmacological blockade of the stress hormone corticotrophin-releasing factor or of peripheral GC action, as well as topical administration of physiologic lipids, normalized epidermal AMP levels and delivery to LBs and decreased the severity of GAS infection during PS. Our results show that PS decreases the levels of 2 key AMPs in the epidermis and their delivery into LBs and that this is attributable to increased endogenous GC production. These data suggest that GC blockade and/or topical lipid administration could normalize cutaneous antimicrobial defense during PS or GC increase. We believe this to be the first mechanistic link between PS and increased susceptibility to infection by microbial pathogens.

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Social stress alters the severity and onset of the chronic phase of Theiler's virus infection

Cited by 33 publications

References 41 publications

Elevated Risk for Autoimmune Disorders in Iraq and Afghanistan Veterans with Posttraumatic Stress Disorder

Elevated Risk for Autoimmune Disorders in Iraq and Afghanistan Veterans with Posttraumatic Stress Disorder

Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release

Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice

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