Ureaplasma spp. is detected in the urogenital tract, including the vagina, cervix, chorioamnion, and placenta. Their colonization is associated with histologic chorioamnionitis (CAM), often observed in placentas from preterm delivery. We isolated Ureaplasma spp. from 63 preterm placentas among 151 specimens, which were delivered at Ͻ32 wk of gestation. Of the 63 placentas, 52 (83%) revealed CAM in cultures positive for Ureaplasma spp., however, CAM was observed only in 30% (26/88) of cultures negative for Ureaplasma spp. (p Ͻ 0.01). Colonization by Ureaplasma spp. was an independent risk factor for CAM (OR, 11.27; 95% CI,). Characteristic neutrophil infiltration was observed in the amnion and subchorion (bistratified pattern) in cultures positive for Ureaplasma spp. FISH analysis of CAM placenta with male infant pregnancy indicated that bistratified infiltrated neutrophils showed the XX karyotype and umbilical vein infiltrated neutrophils showed XY karyotype. The distribution of sulfoglycolipid, the receptor of Ureaplasma spp., was mainly detected in the amnion. Ureaplasmal urease D protein and ureB gene were both detected in the amnion, indicating direct colonization by Ureaplasma spp. U reaplasma spp. is the smallest self-replicating organism, both in genome size and in cellular dimensions. It lacks cell walls and exists in association with eukaryotic cells, mainly colonizing mucosal surfaces of the respiratory and urogenital tracts (1). Ureaplasma spp. is a common inhabitant of the lower genital tract and isolated from 40 to 80% women of child-bearing age (2). However, once Ureaplasma spp. spreads from the lower genital tract into the body, this microorganism exerts widespread pathogenic effects, such as chorioamnionitis (CAM), urinary tract infections, preterm labor, and spontaneous abortion. On the other hand, Ureaplasma spp. infection is also reported as a risk factor for lethal pneumonia, chronic lung disease, and meningitis of fetuses and neonates (3).CAM is a placental finding associated with premature rupture of membranes (PROM) and preterm birth, which are the most important causes of perinatal morbidity and mortality (4,5). Previous studies showed that CAM was positively related to the isolation of Ureaplasma spp (6,7). Although many researchers reported the detection of Ureaplasma spp. from specimens of vagina, cervix, chorioamnion, and placenta using culture or PCR methods (8 -12), the precise pathologic findings of CAM with Ureaplasma spp. remain unclear.A variety of infectious microorganisms use specific host cell surface molecules as receptors. Such receptors provide a mechanism for intimate interaction with the host cell membrane and in some cases may facilitate the subsequent entry of the organism into the cell (13). Ureaplasma spp. and Mycoplasma hominis were shown to specifically recognize host cell surface glycolipids (sulfogalactoglycerolipid and the sphingolipid counterpart, sulfogalactosyl ceramide), which have been implicated in spermegg interactions (14). This glycolipid rec...
BackgroundNeonatal hypoxia-ischemia induces massive brain damage during the perinatal period, resulting in long-term consequences to central nervous system structural and functional maturation. Although neural progenitor cells (NPCs) migrate through the parenchyma and home in to injury sites in the rodent brain, the molecular mechanisms are unknown. We examined the role of chemokines in mediating NPC migration after neonatal hypoxic-ischemic brain injury.MethodsNine-day-old mice were exposed to a 120-minute hypoxia following unilateral carotid occlusion. Chemokine levels were quantified in mouse brain extract. Migration and proliferation assays were performed using embryonic and infant mouse NPCs.ResultsThe neonatal hypoxic-ischemic brain injury resulted in an ipsilateral lesion, which was extended to the cortical and striatal areas. NPCs migrated toward an injured area, where a marked increase of CC chemokines was detected. In vitro studies showed that incubation of NPCs with recombinant mouse CCL11 promoted migration and proliferation. These effects were partly inhibited by a CCR3 antagonist, SB297006.ConclusionsOur data implicate an important effect of CCL11 for mouse NPCs. The effective activation of NPCs may offer a promising strategy for neuroregeneration in neonatal hypoxic-ischemic brain injury.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-017-0474-9) contains supplementary material, which is available to authorized users.
Skull development after eye migration was studied in a bothid flounder Bothus myriaster (Bothidae). In the stage immediately following the migration, skull ossification was apparently weaker on the blind side than on the ocular side, such being related to the extensive dorsally directed shift of the blind side eye. The blind side frontal had two initial ossification sites; below ("pseudomesial bar" in Psettodes) and behind ("frontal" in bothids) the blind side eye. In bothids, the former was fused with the lateral ethmoid but autogenous to the latter during ontogeny. With increased eye size with growth, the otic region became progressively narrower. The late ossification of the region was considered to provide flexibility for cranial modifications owing to rapid eye enlargement.
Regenerative medicine using umbilical cord blood (UCB) cells shows promise for the treatment of cerebral palsy. Although the efficacy of this therapy has been seen in the clinic, the mechanisms by which UCB cells interact and aid in the improvement of symptoms are not clear. We explored the chemokine expression profile in damaged brain tissue in the neonatal mouse ischemia-reperfusion (IR) brain injury model that was infused with human UCB (hUCB) cells. IR brain injury was induced in 9-day-old NOD/SCID mice. hUCB cells were administered 3 weeks post brain injury. Chemokine expression profiles in the brain extract were determined at various time points. Inflammatory chemokines such as CCL1, CCL17, and CXCL12 were transiently upregulated by 24 hours post brain injury. Upregulation of other chemokines, including CCL5, CCL9, and CXCL1 were prolonged up to 3 weeks post brain injury, but most chemokines dissipated over time. There were marked increases in levels of CCL2, CCL12, CCL20, and CX3CL1 in response to hUCB cell treatment, which might be related to the new recruitment and differentiation of neural stem cells, leading to the induction of tissue regeneration. We propose that the chemokine expression profile in the brain shifted from responding to tissue damage to inducing tissue regeneration. hUCB cell administration further enhanced the production of chemokines, and chemokine networks may play an active role in tissue regeneration in neonatal hypoxic-ischemic brain injury.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.