Underlying inflammation has no impact on the oxidative stress response to acute mental stress

Introduction: Mental stress is considered to be a trigger for acute myocardial infarction (MI), with inflammation thought to provide a mechanism. Inflammation is reciprocally linked to oxidative stress, which h as also been implicated in MI. The purpose of this study was to assess the effects of experimentally-induced inflammation on the oxidative stress response to mental stress in healthy participants. Methods: Healthy males undertook one of two inflammatory stimuli: typhoid vaccination (Vaccination paradigm, N= 17) or eccentric exercise (Eccentric exercise paradigm, N= 17). All participants completed a mental arithmetic stress task twice (within-subject design): 6. h after the inflammatory stimulus, and during a control non-inflammation condition. Blood samples were taken before, immediately and 30. min after the stress task. Plasma was assessed for interleukin-6 (IL-6), protein carbonyls (PC), lipid hydroperoxides (LOOH), total antioxidant capacity (TAC) and nitric oxide metabolites (NOx). Results: Vaccination paradigm: IL-6, PC and NOx were significantly higher in the vaccination condition, relative to the control condition (p < .05). PC, TAC, LOOH and NOx were unchanged in response to mental stress in both the vaccination and control conditions. Eccentric Exercise paradigm: IL-6 and TAC were significantly higher in the eccentric exercise condition (p < .05), relative to the control condition. PC, TAC and NOx were unchanged in response to mental stress in both the eccentric exercise and control conditions. Conclusions: Two different inflammatory paradigms were successful in increasing selective plasma markers of inflammation and oxidative stress prior to a mental stress task. However, experimentally induced transient inflammation had no impact on mental stress-induced changes in plasma LOOH, PC, TAC or NOx in young healthy participants

Parental caregivers of children with developmental disabilities mount a poor antibody response to pneumococcal vaccination.

In older populations, caregiving for a spouse with dementia has been associated with a poor antibody response to vaccination. The present study examined whether younger caregivers, specifically the parents of children with developmental disabilities, would also show a diminished antibody response to vaccination. At baseline assessment, 30 parents of children with developmental disabilities and 29 parents of typically developing children completed standard measures of depression, perceived stress, social support, caregiver burden, and child problem behaviours. They also provided a blood sample and were then vaccinated with a pneumococcal polysaccharide vaccine. Further blood samples were taken at 1- and 6-month follow-ups. Caregivers mounted a poorer antibody response to vaccination than control parents at both follow-ups. This effect withstood adjustment for a number of possible confounders and appeared to be, at least in part, mediated by child problem behaviours. The negative impact of caregiving on antibody response to vaccination is not restricted to older spousal caregivers, but is also evident in younger parents caring for children with developmental disabilities. The behavioural characteristics of the care recipients may be a key consideration in whether or not immunity is compromised in this context

Caregiving for children with developmental disabilities is associated with a poor antibody response to influenza vaccination

Objective: Older spousal caregivers of dementia patients have been found to show a relatively poor antibody response to medical vaccination. The present case control study compared the antibody responses to vaccination of younger parental caregivers of children with developmental disabilities and parents of typically developing children. Methods: At baseline assessment, 32 parents of children with developmental disabilities and 29 parents of typically developing children completed standard measures of perceived stress and child problem behaviours. They also provided a blood sample and were then vaccinated with the thymus-dependent trivalent influenza vaccine. Further blood samples were taken at 1- and 6-month follow-ups. Results: Relative to parents of typically developing children (mean titre = 458, SD = 155.7 at 1-month and mean titre = 265, SD = 483.0 at 6-month followup) caregivers (mean titre = 219, SD = 528.4 at 1-month and 86, SD = 55.0 at 6- month) mounted a poorer antibody response than controls to the B/Malaysia strain of the vaccine. It was those caregivers reporting more child problem behaviours that tended to show the weakest antibody response. Conclusion: The negative impact of caregiving on antibody response to vaccination would not appear to be restricted to older spousal caregivers, but is also evident in younger parents caring for children with developmental disabilities. The behavioural characteristics of the care recipients may be a determinant of whether or not antibody response to vaccination is compromised

Relationship of (z scored) log sIgA secretion to respiratory mortality risk.

<p><b>Fractional polynomial</b> model adjusted for assay batch and sex.</p

Psychosocial factors are associated with the antibody response to both thymus-dependent and thymus-independent vaccines

The present study examined the association between psychological stress, social support and antibody response to both thymus-dependent and thymus-independent vaccinations. Stressful life events in the previous year and customary social support were measured by standard questionnaires at baseline in 75 (41 females) healthy students. Antibody status was assessed at baseline, 4 and 18 weeks following vaccination with formaldehyde inactivated hepatitis A virus and pneumococcal polysaccharides, which induce thymus-dependent and -independent antibody responses respectively. Controlling for baseline antibody status, life event stress was negatively associated with antibody response to the hepatitis A vaccine at the 18-week follow-up; participants reporting a greater number of stressful life events had a poorer antibody response. There was no relationship between psychological stress and antibody response to pneumococcal vaccination. Social support was not associated with the antibody response to hepatitis A vaccination. However, there was a significant association between support and the antibody response to the thymus-independent pneumococcal vaccine at 4-week followup; participants with larger social networks mounted a better response. These relationships could not be accounted for by age and sex, or by variations in health behaviours. Psychosocial factors would appear to influence the response to both thymusdependent and thymus-independent vaccines, but not in the same manner

Detection of IFNγ-producing lymphocytes by flow cytometry following stimulation with <i>Salmonella</i>.

<p>Dot plots of CD4⁺-T cells (A, C and E) and γδ-T cells (B, D and F) from human peripheral blood from one healthy adult, either unstimulated (A and B), or stimulated with PMA (C and D) or <i>S</i>. Typhimurium D23580 homogenate (E and F), showing intracellular production of IFNγ and expression of CD69. Numbers within gates indicate percentage of IFNγ-producing cells. Each dot represents one cell.</p

Effect of plasma from <i>Salmonella</i> stimulation of whole peripheral blood on monocyte CD38 expression.

<p>Plasma from <i>S</i>. Typhimurium-stimulated whole blood (NTS stimulated) was separated and filter-sterilized prior to adding to fresh blood for five hours followed by measurement of CD38 expression on monocytes. CD38 expression was significantly higher than for blood incubated with plasma taken from unstimulated blood (NC) or for blood incubated with plasma stimulated with NTS in the absence of cells (plasma control). <i>P</i> values are from Student's t test. Data are from four experiments.</p

Percentage and absolute numbers of IFNγ-producing cells in different lymphocyte subsets in peripheral blood from ten healthy adults following stimulation with <i>Salmonella</i>.

<p>For each lymphocyte subset in the peripheral blood of each subject, the absolute concentration of cells (Count; cells/µl), percentage of IFNγ-producing cells (%IFNγ⁺) and absolute numbers of IFNγ-producing cells (IFNγ⁺ Count; cells/µl) following stimulation for six hours with live <i>S</i>. Typhimurium D23580 were determined by intracellular cytokine staining and a hematological analyzer. All adaptive lymphocytes (Acq lymph; CD4⁺-and CD8⁺-T cells), innate lymphocytes (Innate lymp; γδ-T cells, NK cells and NK-like T cells), together with total numbers of IFNγ-producing lymphocytes are shown in the right-hand columns. Geometric means are for average percentages and absolute numbers of cells across all subjects.</p

Kinetics of IFNγ production by peripheral blood lymphocytes in response to stimulation with <i>Salmonella</i>.

<p>Percentage of IFNγ-producing CD69⁺ (A) CD4⁺-T cells, (B) CD8⁺-T cells, (C) γδ-T cells and (D) NK cells over an eight hour time course following stimulation with <i>S</i>. Typhimurium D23580 homogenate added at 0 hours with addition of Brefeldin A at 2 hours. Data are mean ± sd of three experiments.</p

Anti-<i>Salmonella</i> antibody content and <i>Salmonella</i>-killing ability of serum from peripheral adult blood.

<p>(A) Anti-<i>S</i>. Typhimurium D23580 IgG and (B) anti-D23580 IgM titers determined by flow cytometry compared with <i>Salmonellae</i> D23580-killing ability determined by serum bactericidal assay at 180 minutes using serum prepared from peripheral blood from ten healthy adults. Negative values on y axis indicate reduction in viable <i>Salmonellae</i> with -1.0 corresponding to a 90% reduction in viable <i>Salmonellae </i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0013667#pone.0013667-MacLennan1" target="_blank">[3]</a>. Each symbol corresponds to serum from one individual.</p