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Intrauterine infection/inflammation during pregnancy and offspring brain damages: possible mechanisms involved.

Huleihel M, Golan H, Hallak M - Reprod. Biol. Endocrinol. (2004)

Bottom Line: Effects on the fetal, newborn, and adult central nervous system (CNS) may include signs of neurological problems, developmental abnormalities and delays, and intellectual deficits.However, the mechanisms or pathophysiology that leads to permanent brain damage during development are complex and not fully understood.This damage may affect morphogenic and behavioral phenotypes of the developed offspring, and that mice brain damage could be mediated through a final common pathway, which includes over-stimulation of excitatory amino acid receptor, over-production of vascularization/angiogenesis, pro-inflammatory cytokines, neurotrophic factors and apoptotic-inducing factors.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Microbiology and Immunology and the BGU Cancer Research Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. huleihel@bgumail.bgu.ac.il

ABSTRACT
Intrauterine infection is considered as one of the major maternal insults during pregnancy. Intrauterine infection during pregnancy could lead to brain damage of the developmental fetus and offspring. Effects on the fetal, newborn, and adult central nervous system (CNS) may include signs of neurological problems, developmental abnormalities and delays, and intellectual deficits. However, the mechanisms or pathophysiology that leads to permanent brain damage during development are complex and not fully understood. This damage may affect morphogenic and behavioral phenotypes of the developed offspring, and that mice brain damage could be mediated through a final common pathway, which includes over-stimulation of excitatory amino acid receptor, over-production of vascularization/angiogenesis, pro-inflammatory cytokines, neurotrophic factors and apoptotic-inducing factors.

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Possible mechanisms involved in the effect of intrauterine infection during pregnancy and offspring brain damage and development.
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Figure 1: Possible mechanisms involved in the effect of intrauterine infection during pregnancy and offspring brain damage and development.

Mentions: In summary, it is possible to hypotheses that intrauterine infection/inflammation during pregnancy may lead to newborn, adult and aged offspring brain damages (Fig. 1). This may affect morphogenic and behavioral phenotypes of the developed offspring. The offspring brain damage could be mediated through up-regulation of pro-inflammatory cytokine production in the circulation and in the brain of the fetal/offspring. These pro-inflammatory cytokines could, by one hand, decrease the production of neurotrophic factors such as NGF and BDNF and, by other hand, to increase the production of NO, VEGF and PGE. These factors increase apoptosis and also may lead to vascularization/angiogenesis defects. Affecting these functions in the brain may lead to compartment/site brain damage, which may, during a developmental window, lead to some neurological diseases and/or cognitive defects.


Intrauterine infection/inflammation during pregnancy and offspring brain damages: possible mechanisms involved.

Huleihel M, Golan H, Hallak M - Reprod. Biol. Endocrinol. (2004)

Possible mechanisms involved in the effect of intrauterine infection during pregnancy and offspring brain damage and development.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC411057&req=5

Figure 1: Possible mechanisms involved in the effect of intrauterine infection during pregnancy and offspring brain damage and development.
Mentions: In summary, it is possible to hypotheses that intrauterine infection/inflammation during pregnancy may lead to newborn, adult and aged offspring brain damages (Fig. 1). This may affect morphogenic and behavioral phenotypes of the developed offspring. The offspring brain damage could be mediated through up-regulation of pro-inflammatory cytokine production in the circulation and in the brain of the fetal/offspring. These pro-inflammatory cytokines could, by one hand, decrease the production of neurotrophic factors such as NGF and BDNF and, by other hand, to increase the production of NO, VEGF and PGE. These factors increase apoptosis and also may lead to vascularization/angiogenesis defects. Affecting these functions in the brain may lead to compartment/site brain damage, which may, during a developmental window, lead to some neurological diseases and/or cognitive defects.

Bottom Line: Effects on the fetal, newborn, and adult central nervous system (CNS) may include signs of neurological problems, developmental abnormalities and delays, and intellectual deficits.However, the mechanisms or pathophysiology that leads to permanent brain damage during development are complex and not fully understood.This damage may affect morphogenic and behavioral phenotypes of the developed offspring, and that mice brain damage could be mediated through a final common pathway, which includes over-stimulation of excitatory amino acid receptor, over-production of vascularization/angiogenesis, pro-inflammatory cytokines, neurotrophic factors and apoptotic-inducing factors.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Microbiology and Immunology and the BGU Cancer Research Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. huleihel@bgumail.bgu.ac.il

ABSTRACT
Intrauterine infection is considered as one of the major maternal insults during pregnancy. Intrauterine infection during pregnancy could lead to brain damage of the developmental fetus and offspring. Effects on the fetal, newborn, and adult central nervous system (CNS) may include signs of neurological problems, developmental abnormalities and delays, and intellectual deficits. However, the mechanisms or pathophysiology that leads to permanent brain damage during development are complex and not fully understood. This damage may affect morphogenic and behavioral phenotypes of the developed offspring, and that mice brain damage could be mediated through a final common pathway, which includes over-stimulation of excitatory amino acid receptor, over-production of vascularization/angiogenesis, pro-inflammatory cytokines, neurotrophic factors and apoptotic-inducing factors.

Show MeSH
Related in: MedlinePlus