BackgroundHofbauer cells (HBCs) are macrophages of the feto-placental unit. Despite the general view that these cells have an anti-inflammatory M2 phenotype, recent studies have claimed that pregnancy pathologies—e.g., gestational diabetes mellitus (GDM)—cause a switch from an M2 to an M1 pro-inflammatory phenotype in HBCs. The pilot-study presented here challenges this claim, showing that HBCs maintain anti-inflammatory properties in spite of the hyperglycemic, low-grade inflammatory environment of GDM.MethodsHBCs were isolated from placentae of healthy women (N = 5) and women with GDM (N = 6) diagnosed in the second trimester. FACS was used to measure surface markers associated with either M1 or M2 phenotype on the cells. In addition, placental tissue sections were subjected to immune histochemical imaging to assess the phenotype within the tissue context. Supernatant from control and GDM HBCs was collected at defined time points and used in a multiplex ELISA-on-beads approach to assess secretion of cytokines, chemokines, and growth factors. The effect of HBC cell culture supernatant on placental endothelial activation was investigated.ResultsFACS and immune staining showed that, indeed, M2 markers, such as CD206 and CD209, are increased in HBCs isolated from GDM placentae. Also, the M1 marker CD86 was increased, but only by trend. Secretion of numerous cytokines, chemokines and growth factors was not changed; pro-inflammatory interleukin (IL)-1β and IL-6 release form GDM HBC was increased but not significant. Exposure to GDM HBC supernatant did not induce cell adhesion molecules (VCAM-1, selectins, vascular endothelial-cadherin) in placental endothelial cells compared to supernatant from control HBCs, an induction of intracellular adhesion molecule 1 was observed however.ConclusionOur study—although performed in a small set of patients—shows that placental macrophages maintain their anti-inflammatory, tissue remodeling M2 phenotype even in pregnancies affected by gestational diabetes. This consistent phenotype might be important for propagation of maternal tolerance toward the fetus and for protection of the fetus from a low-grade inflammatory environment.

Aneuploidies involving chromosomes 21, 18, 13, X and Y account for over 95% of all chromosomal abnormalities in live-born infants. Prenatal diagnosis of these disorders is usually accomplished by cytogenetic analysis of amniotic or chorionic cells but this is a lengthy procedure requiring great technical expertise. In this paper, we assess the diagnostic value of using a quantitative fluorescent polymerase chain reaction (PCR) suitable for the simultaneous and rapid diagnosis of trisomies 21 and 18 together with the detection of DNA sequences derived from the X and Y chromosomes. Samples of DNA, extracted from amniotic fluid, fetal blood or tissues, and peripheral blood from normal adults were investigated by quantitative fluorescent PCR amplification of polymorphic small tandem repeats (STRs) specific for two loci on each of chromosomes 21 and 18. Quantitative analysis of the amplification products allowed the diagnosis of trisomies 21 and 18, while sexing was performed simultaneously using PCR amplification of DNA sequences derived from the chromosomes X and Y. These results indicate the advantages of using two sets of STR markers for the detection of chromosome 21 trisomies and confirmed the usefulness of quantitative fluorescent multiplex PCR for the rapid prenatal diagnosis of selected chromosomal abnormalities.

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Background Necrotizing soft tissue infections (NSTI) require immediate radical debridement, broad-spectrum antibiotics and intensive care. Hyperbaric oxygen therapy (HBOT) may be performed adjunctively, but unequivocal evidence for its benefits is still lacking. Methods We performed a retrospective single-center study including 192 patients with necrotizing fasciitis or Fournier's gangrene to assess in-hospital mortality and outcome dependent on patient, disease and treatment characteristics with or without HBOT. Results The in-hospital mortality rate was 27.6%. Factors associated with increased mortality according to multivariate analysis were higher age, affection of multiple or problem localizations (odds ratio (OR) = 2.88, P = 0.003), ineligibility for HBOT despite clinical indication (OR = 8.59, P = 0.005), pathogens in blood cultures (OR = 3.36, P = 0.002), complications (OR = 10.35, P < 0.001) and sepsis/organ dysfunction (OR = 19.58, P < 0.001). Factors associated with better survival included vacuum-assisted wound closure (OR = 0.17, P < 0.001), larger number of debridements (OR = 0.83, P < 0.001) and defect closure with mesh graft (OR = 0.06, P < 0.001) or flap (OR = 0.09, P = 0.024). When participants were stratified into subgroups without requirement of HBOT (n = 98), treated with HBOT (n = 83) and ineligible for HBOT due to contraindications (n = 11), the first two groups had similar survival rates (75.5% vs. 73.5%) and comparable outcome, although patients with HBOT suffered from more severe NSTI, reflected by more frequent affection of multiple localizations (P < 0.001), sepsis at admission (P < 0.001) and intensive care treatment (P < 0.001), more debridements (P < 0.001) and a larger number of antibiotics (P = 0.001). In the subgroup ineligible for HBOT, survival was significantly worse (36.4%, P = 0.022). Conclusion These results point to a benefit from HBOT for treatment of NSTI in critically ill patients.