Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute chorioamnionitis is a well-established lesion of the placenta in cases with intra-amniotic infection. In contrast, the clinicopathological significance of chronic chorioamnionitis is unclear. This study was conducted to determine the frequency and severity of chronic chorioamnionitis in normal pregnancy and in various pregnancy complications. Placentas from the following patient groups were studied: (1) term not in labor (n=100), (2) term in labor (n=100), (3) preterm labor (n=100), (4) preterm prelabor rupture of membranes (n=100), (5) preeclampsia at term (n=100), (6) preterm preeclampsia (n=100), and (7) small-for-gestational-age at term (n=100). Amniotic fluid CXCL10 concentration was measured in 64 patients. CXCL9, CXCL10, and CXCL11 mRNA expressions in the chorioamniotic membranes were assessed using real-time quantitative reverse transcription-PCR. The frequency of chronic chorioamnionitis in the preterm labor group and the preterm prelabor rupture of membranes group was 34 and 39%, respectively, which was higher than that of normal-term placentas (term not in labor, 19%; term in labor, 8%; P<0.05 each). The frequency of chronic chorioamnionitis in the preeclampsia at term group, preterm preeclampsia group, and small-for-gestational-age group was 23, 16, and 13%, respectively. Concomitant villitis of unknown etiology was found in 38 and 36% of preterm labor cases and preterm prelabor rupture of membranes cases with chronic chorioamnionitis, respectively. Interestingly, the median gestational age of preterm chronic chorioamnionitis cases was higher than that of acute chorioamnionitis cases (P<0.05). The median amniotic fluid CXCL10 concentration was higher in cases with chronic chorioamnionitis than in those without, in both the preterm labor group and preterm prelabor rupture of membranes group (P<0.05 and P<0.01, respectively). CXCL9, CXCL10, and CXCL11 mRNA expression in the chorioamniotic membranes was also higher in cases with chronic chorioamnionitis than in those without chronic chorioamnionitis (P<0.05). We propose that chronic chorioamnionitis defines a common placental pathological lesion among the preterm labor and preterm prelabor rupture of membranes groups, especially in cases of late preterm birth. Its association with villitis of unknown etiology and the chemokine profile in amniotic fluid suggests an immunological origin, akin to transplantation rejection and graft-versus-host disease in the chorioamniotic membranes.
 ...
PMID:The frequency, clinical significance, and pathological features of chronic chorioamnionitis: a lesion associated with spontaneous preterm birth. 2034 84

Chronic placental inflammatory lesions lead to poor obstetric outcomes. These lesions often proceed undetected until examination of placental tissues after delivery and are mediated by CXCR3, a seven-transmembrane G protein-coupled receptor, and its chemokine ligands - CXCL9, CXCL10 and CXCL11. CXCR3-chemokine ligand interaction disrupts feto-maternal immune tolerance and activate obnoxious immunological responses similar to transplant rejection and graft-versus-host disease. The resultant chronic inflammatory responses manifest in different parts of the placenta characterised by the presence of incompatible immunocompetent cells from the feto-maternal unit i.e. maternal CD8+ T cells in the chorionic membrane or plate (chronic chorioamnionitis); foetal Hofbauer cells and maternal CD8+ T cells in the chorionic villous tree (villitis of unknown aetiology); maternal CD8+ T and plasma cells in the basal plate (chronic deciduitis); and maternal CD8+ T cells, histiocytes and T regulatory cells in the intervillous space (chronic intervillositis). This review critically examines how the CXCR3-chemokine ligand interaction disrupts feto-maternal immune tolerance, initiates a series of chronic placental inflammatory lesions, and consequently activates the pathways to intrauterine growth restriction, stillbirth, spontaneous abortion, preterm prelabour rupture of membranes, preterm labour and birth. The possibility of interrupting these signalling pathways through the use of CXCR3 chemokine inhibitors to prevent adverse reproductive sequelae as well as the potential clinical utility of CXCR3 chemokines as non-invasive predictive clinical biomarkers are also highlighted.
 ...
PMID:The transmembrane G protein-coupled CXCR3 receptor-ligand system and maternal foetal allograft rejection. 3329 35