Gender Difference in Cytokine Secretion on Immune Stimulation with LPS and LTA

Aulock, Sonja von; Deininger, Susanne; Draing, Christian; Gueinzius, Katja; Dehus, Oliver; Hermann, Corinna

doi:10.1089/jir.2006.26.887

Cited by 105 publications

(70 citation statements)

References 21 publications

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“…This assumption is in line with observations that healthy males produce higher serum levels of pro-inflammatory cytokines, e.g. tumor necrosis factor-alpha (TNF-α ), interleukin-1beta (IL-1 β ), IL-6, and IL-8, to different stimuli (Aulock et al ., 2006). TNF-α levels, in particular, have been shown to inversely correlate with T-cell telomere length (Panossian et al ., 2003).…”

Section: Resultssupporting

confidence: 88%

Different rates of telomere attrition in peripheral lymphocytes in a pair of dizygotic twins with hematopoietic chimerism

Brüderlein

Müller²,

Melzner

et al. 2008

Aging Cell

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SummaryHematopoietic chimerism in dizygotic twins is due to placental vascular anastomoses and arises when hematopoietic stem cells from one twin home to the bone marrow of the other. We report a case of hematopoietic chimerism in a pair of 27-year-old dizygotic twins who each had a mixture of 46,XX and 46,XY blood lymphocytes, both with 98% male (XY) lymphocytes and 2% female (XX) lymphocytes. Analysis of telomere length by T/C FISH revealed that the female twin generally had longer telomeres than the male twin. Moreover, in the male sibling, the telomeres within the female lymphocytes were shortened to 87% of their original length, while the telomeres within the male lymphocytes were 33% longer in the female sibling. Thus, telomere length attrition in peripheral lymphocytes is determined mainly by the environment of the cell and less by intracellular factors.

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Section: Resultssupporting

confidence: 88%

Different rates of telomere attrition in peripheral lymphocytes in a pair of dizygotic twins with hematopoietic chimerism

Brüderlein

Müller²,

Melzner

et al. 2008

Aging Cell

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“…The effect is dose dependent and associated with increased expression of markers of inflammation [10][11][12]. Similar effects have also been seen in humans, where LPS induces a hypotensive response, associated with an increase in circulating cytokines [13], although females are more resistant, with a lesser increase in temperature, fall in blood pressure, and in vitro release of cytokines [14][15][16]. Few studies have investigated differences in the peripheral blood mononuclear cells responses in pregnant and NP individuals and found that the cytokine (interleukin (IL)-6, IL-10, and IL-17) response was increased in the cells from pregnant women exposed to a variety of agents (umbilical cord blood (UCB) of the mother's own child, third-party UCB, phytohemagglutinin, and anti-CD3 antibody) [17].…”

Section: Introductionmentioning

confidence: 61%

The response of the innate immune and cardiovascular systems to LPS in pregnant and nonpregnant mice†

Zöllner

Howe

Edey

et al. 2017

Biology of Reproduction

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Sepsis is the leading cause of direct maternal mortality, but there are no data directly comparing the response to sepsis in pregnant and nonpregnant (NP) individuals. This study uses a mouse model of sepsis to test the hypothesis that the cardiovascular response to sepsis is more marked during pregnancy. Female CD1 mice had radiotelemetry probes implanted and were time mated. NP and day 16 pregnant CD-1 mice received intraperitoneal lipopolysaccharide (LPS; 10 μg, serotype 0111: B4). In a separate study, tissue and serum (for RNA, protein and flow cytometry studies), aorta and uterine vessels (for wire myography) were collected after LPS or vehicle control administration. Administration of LPS resulted in a greater fall in blood pressure in pregnant mice compared to NP mice. This occurred with similar changes in the circulating levels of cytokines, vasoactive factors, and circulating leukocytes, but with a greater monocyte and lesser neutrophil margination in the lungs of pregnant mice. Baseline markers of cardiac dysfunction and apoptosis as well as cytokine expression were higher in pregnant mice, but the response to LPS was similar in both groups as was the ex vivo assessment of vascular function. In pregnant mice, nonfatal sepsis is associated with a more marked hypotensive response but not a greater immune response. We conclude that endotoxemia induces a more marked hypotensive response in pregnant compared to NP mice. These changes were not associated with a more marked systemic inflammatory response in pregnant mice, although monocyte lung margination was greater. The more marked hypotensive response to LPS may explain the greater vulnerability to some infections exhibited by pregnant women. Pregnancy enhances LPS-induced hypotension, 2017, Vol. 97, No. 2 Summary SentenceIn pregnant mice, nonfatal sepsis is associated with a more marked hypotensive response but not a greater immune response.

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“…Female myelin-specific T cells produce more IFNγ and less Th2 cytokines than male T cells and are more encephalitogenic upon adoptive transfer (9)(10)(11). However, despite numerous attempts to explore this issue in humans (12)(13)(14)(15)(16), conclusive evidence in support of a Th1 bias in women is lacking.…”

mentioning

confidence: 99%

Peroxisome proliferator-activated receptor (PPAR)α and -γ regulate IFNγ and IL-17A production by human T cells in a sex-specific way

Zhang

Rego

Moshkova

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

199

177

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Women develop certain autoimmune diseases more often than men. It has been hypothesized that this may relate to the development of more robust T-helper (Th)1 responses in women. To test whether women exhibit a Th1 bias, we isolated naïve cluster of differentiation (CD)4 + T cells from peripheral blood of healthy women and men and measured the proliferation and cytokine production by these cells in response to submaximal amounts of anti-CD3 and anti-CD28. We observed that CD4 + T cells from women produced higher levels of IFNγ as well as tended to proliferate more than male CD4 + T cells. Intriguingly, male CD4 + T cells instead had a predilection toward IL-17A production. This sex dichotomy in Th cytokine production was found to be even more striking in the Swiss/Jackson Laboratory (SJL) mouse. Studies in mice and humans indicated that the sexual dimorphism in Th1 and Th17 cytokine production was dependent on the androgen status and the T-cell expression of peroxisome proliferator activated receptor (PPAR)α and PPARγ. Androgens increased PPARα and decreased PPARγ expression by human CD4 + T cells. PPARα siRNA-mediated knockdown had the effect of increasing IFNγ by male CD4 + T cells, while transfection of CD4 + T cells with PPARγ siRNAs increased IL-17A production uniquely by female T cells. Together, our observations indicate that human T cells exhibit a sex difference in the production of IFNγ and IL-17A that may be driven by expressions of PPARα and PPARγ. autoimmunity | cytokines | experimental autoimmune encephalomyelitis | gender | nuclear receptor

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Gender Difference in Cytokine Secretion on Immune Stimulation with LPS and LTA

Cited by 105 publications

References 21 publications

Different rates of telomere attrition in peripheral lymphocytes in a pair of dizygotic twins with hematopoietic chimerism

Different rates of telomere attrition in peripheral lymphocytes in a pair of dizygotic twins with hematopoietic chimerism

The response of the innate immune and cardiovascular systems to LPS in pregnant and nonpregnant mice†

Peroxisome proliferator-activated receptor (PPAR)α and -γ regulate IFNγ and IL-17A production by human T cells in a sex-specific way

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