PGD--a model to evaluate efficacy?
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Abortion, Habitual↗
Biomedical subjects
Maas Jan Heineman
Publications and source records attributed to Maas Jan Heineman.
Species differences in the effect of pregnancy on lymphocyte cytokine production between human and rat.
In the present study, we evaluated whether lymphocyte cytokine production during human and rat pregnancy shifts toward T helper cell type 2 (Th2) cytokine production. Therefore, blood samples were taken during the follicular and luteal phase and during pregnancy in rats and humans. Whole blood was ex vivo-stimulated with phorbol 12-myristate 13-acetate and calcium ionophore and intracellular interferon-gamma (IFN-gamma) and interleukin (IL)-4 production, and the percentage of cells in the various lymphocyte populations was measured using flow cytometry. Rats and humans adapted their immune responses to pregnancy but have different strategies: During human pregnancy, the percentage of lymphocytes producing IFN-gamma was decreased, and the percentage IL-4-producing lymphocytes was not affected. The rat adapts its immune response to pregnancy by decreasing the total number of the various lymphocyte populations, and the percentage of IFN-gamma- or IL-4-producing lymphocytes was not affected or increased (% IFN-gamma-producing cytotoxic lymphocytes). It is speculated that during rat pregnancy, there is no need to decrease the number of IFN-gamma-producing lymphocytes, as in nonpregnant rats, the total number of IFN-gamma-producing lymphocytes after stimulation is relatively low, and there is no necessity for a further decrease. In nonpregnant humans, the percentage IFN-gamma-producing lymphocytes is much higher and probably dangerous for pregnancy, and therefore, this percentage needs to decrease during pregnancy. In conclusion, although the data from humans concur with the Th1/Th2 paradigm, the data from rats do not concur with this paradigm. The present studies therefore challenge the classical Th1/Th2 paradigm during pregnancy.
Animals↗
Sex hormones and the immune response in humans.
In addition to their effects on sexual differentiation and reproduction, sex hormones appear to influence the immune system. This results in a sexual dimorphism in the immune response in humans: for instance, females produce more vigorous cellular and more vigorous humoral immune reactions, are more resistant to certain infections, and suffer a higher incidence of autoimmune diseases. Disease expression is also affected by the reproductive status of the female. As sex steroids--estrogens, progesterone and testosterone--differ between gender and within different reproductive stages, a lot of research has focussed on the effects of sex hormones on immune responses. Although there is also a vast literature on the effects of sex hormones on immune responses in animals, in this review we will focus on the most intriguing effects and mechanisms by which sex hormones affect different components of the immune system in humans.
Female↗
Comment 1 on Staessen et al. (2004). Design and analysis of a randomized controlled trial studying preimplantation genetic screening.
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Aneuploidy↗
Altered monocyte function in experimental preeclampsia in the rat.
OBJECTIVES: In the present study, we evaluated functional activity of monocytes in experimental preeclampsia induced by low-dose endotoxin infusion. STUDY DESIGN: Pregnant (n = 12) and cyclic rats (n = 12) were equipped with a permanent jugular vein cannula and infused with either low-dose endotoxin or saline. One day before the infusion, and 4, 24, 72, and 168 hours after the infusion, blood samples (400 microL) were taken and white blood cell (WBC) and differential cell counts were measured. Samples were (re)stimulated with endotoxin, and the percentage of tumor necrosis factor-alpha (TNFalpha) producing monocytes was measured. RESULTS: During experimental preeclampsia, monocyte TNFalpha production is persistently decreased, while total WBC and granulocyte counts are persistently increased compared with normal pregnant rats. No persistent effect of endotoxin was found in cyclic rats. CONCLUSION: Because decreased endotoxin-induced TNFalpha production is a feature of activated monocytes, the present results indicate that monocytes are persistently activated in experimental preeclampsia. Increased WBC counts and granulocyte numbers in these rats also point to an activated inflammatory response.
Animals↗
17beta-estradiol and progesterone do not influence the production of cytokines from lipopolysaccharide-stimulated monocytes in humans.
OBJECTIVE: To test whether 17beta-estradiol or progesterone influence the cytokine productive capacity of lipopolysaccharide (LPS)-stimulated monocytes in humans. DESIGN: Prospective study. SETTING: Academic research institution. PATIENT(S): Seven women in the luteal phase of a normal ovarian cycle, 13 oral contraceptive users, 10 men, and 10 postmenopausal women. INTERVENTION(S): Blood samples collected from women in the luteal phase and from oral contraceptive users were used to study the in vivo effect of 17beta-estradiol and progesterone on monocyte cytokine production. Blood samples collected from men and postmenopausal women were used for in vitro incubation with 17beta-estradiol and progesterone. MAIN OUTCOME MEASURE(S): The percentage of monocytes producing tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) after in vitro LPS-stimulation was determined. RESULT(S): No in vivo relation in the productive capacities of LPS-stimulated monocytes in the luteal phase of the ovarian cycle was found between progesterone and TNF-alpha or IL-1beta; or between 17beta-estradiol and TNF-alpha or IL-1beta. Moreover, the production of TNF-alpha and IL-1beta by LPS-stimulated monocytes did not vary between periods of oral contraceptive use and nonuse. The production of TNF-alpha and IL-1beta by LPS-stimulated monocytes in the blood of men and postmenopausal women in vitro was not influenced by incubation with different concentrations of 17beta-estradiol or progesterone. CONCLUSION(S): We could not find evidence for a causal relationship between 17beta-estradiol or progesterone and TNF-alpha- or IL-1beta-production. We conclude that 17beta-estradiol and progesterone do not influence the cytokine-production capacity of LPS-stimulated monocytes in humans.
Adult↗
Developing ovarian follicles inhibit the endotoxin-induced glomerular inflammatory reaction in pseudopregnant rats.
PROBLEM: We tested the hypothesis that developing ovarian follicles produce factors inhibiting the endotoxin induced inflammatory response. METHOD OF STUDY: Pseudopregnant rats were treated with FSH to induced follicular development (FSH-rats). For control we used untreated pseudopregnant rats (PSP-rats) and rats in the follicular phase of the ovarian cycle (C-rats). All rats were infused with either saline or endotoxin. Three days after the infusion rats were sacrificed and kidney specimens were snapfrozen. Cryostat kidney sections were stained for the presence of monocytes, granulocytes, CD11a- and CD11b-positive cells and for ICAM-1 expression. RESULTS: The results show that induction of follicular development in pseudopregnant rats inhibited glomerular infiltration of monocytes and CD11b(+) cells, while it did not affect the other parameters, i.e. glomerular granulocyte number, CD11a(+) cells and glomerular ICAM-1 expression. CONCLUSION: Developing ovarian follicles produce factors inhibiting monocyte responses to endotoxin.
Animals↗
Gender difference in the non-specific and specific immune response in humans.
PROBLEM: The purpose of this present ex vivo study is to get insight in the sex differences of the basic non-specific and specific immune response. METHOD OF STUDY: Intracellular types 1 and 2 cytokine production by stimulated male and female lymphocytes and monocytes in a whole blood preparation was measured by flow cytometry. RESULTS: Increased percentage interleukin (IL)-12, IL-1 beta and tumor necrosis factor (TNF)-alpha producing monocytes and decreased percentage IL-2 producing lymphocytes, i.e. type 1 cytokine, were found in men as compared with women. CONCLUSION: These results suggest a gender difference in the balance between the specific and non-specific immune response, i.e. a more profound and higher state of excitation of the non-specific immune response and relative suppression of the cellular immune response of the specific immune system in men as compared with women.
Adult↗
The effect of testosterone on cytokine production in the specific and non-specific immune response.
PROBLEM: Cytokine production of monocytes and lymphocytes differs between males and females. This difference is characterized by a decreased percentage of interleukin (IL)-2-producing lymphocytes and an increased percentage of IL-12, IL-1beta and tumour necrosis factor (TNF)-alpha-producing monocytes in males compared with females. In the present study, we investigated whether testosterone may explain these differences. METHOD OF STUDY: Stimulated whole blood of healthy woman was incubated with different concentrations of testosterone. Intracellular lymphocyte production of IL-2 and interferon (IFN)-gamma, as well as intracellular monocyte production of IL-12, IL-1beta and TNF-alpha were measured using flow cytometry. RESULTS: A significant increased percentage of IL-12- and IL-1beta-producing monocytes was found after incubation with physiological concentrations of testosterone. No effect of testosterone was found on IL-2- and IFN-gamma-producing lymphocytes and TNF-alpha-producing monocytes. CONCLUSIONS: The increased percentage of IL-12- and IL-1beta-producing monocytes in males compared with females in vivo may be induced by testosterone, as the in vitro percentage of IL-12- and IL-1beta-producing monocytes is increased after incubation with physiological concentrations of testosterone.
Cytokines↗
Endotoxin-induced cytokine production of monocytes of third-trimester pregnant women compared with women in the follicular phase of the menstrual cycle.
OBJECTIVE: Little is known about the function of the innate immune response during pregnancy. We therefore investigated monocyte cytokine production, as a measure of monocyte function, in pregnant women compared with nonpregnant women. STUDY DESIGN: Whole blood of women in the follicular phase (day 5-6) and of healthy pregnant women (30 weeks) was collected and stimulated with endotoxin (2 microg/mL). After incubation for 4 hours (37 degrees C, 5% carbon dioxide), red blood cells were lysed and white blood cells were permeabilized, followed by staining with anti-CD14 (fluorescein isothiocyanate labeled) and with phycoerythrin-labeled tumor necrosis factor-alpha, interleukin-1beta, or interleukin-12. The cells were analyzed by flow cytometry after fixation. Results are expressed as a percentage cytokine producing cells after endotoxin stimulation. Statistical analysis was performed with the Mann-Whitney U test (P <.05). RESULTS: Compared with the percentage endotoxin-induced cytokine producing peripheral monocytes in women in the follicular phase, this percentage in pregnancy was decreased for interleukin-12 (mean 6.63 +/- 1.34 vs 3.34 +/- 0.87, P <.05) and tumor necrosis factor-alpha (mean 50.20 +/- 5.80 vs 31.29 +/- 5.57, P >.05). No significant difference was seen in the production of interleukin-1beta (mean 58.22 +/- 11.09 vs 47.18 +/- 7.88, P >.05). CONCLUSION: The percentage of interleukin-12 and tumor necrosis factor-alpha producing monocytes is decreased in pregnant women compared with nonpregnant women, suggesting that pregnancy is a proinflammatory state.
Adult↗