The fetal inflammatory response syndrome.

The molecular basis of lung morphogenesis

▪ Abstract Endoderm, one of the three principal germ layers, contributes to all organs of the alimentary tract. For simplicity, this review divides formation of endodermal organs into four fundamental steps: (a) formation of endoderm during gastrulation, (b) morphogenesis of a gut tube from a sheet of cells, (c) budding of organ domains from the tube, and (d) differentiation of organ-specific cell types within the growing buds. We discuss possible mechanisms that regulate how undifferentiated endoderm becomes specified into a myriad of cell types that populate the respiratory and gastrointestinal tracts.

Vertebrate endoderm development

The fetal inflammatory response syndrome (FIRS) is a condition characterized by systemic inflammation and an elevation of fetal plasma interleukin-6. This syndrome has been observed in fetuses with preterm labor with intact membranes, preterm prelabor rupture of the membranes, and also fetal viral infections such as cytomegalovirus. FIRS is a risk factor for short-term perinatal morbidity and mortality after adjustment for gestational age at delivery and also for the development of long-term sequelae such as bronchopulmonary dysplasia and brain injury. Multiorgan involvement in FIRS has been demonstrated in the hematopoietic system, thymus, adrenal glands, skin, kidneys, heart, lung, and brain. This article reviews the fetal systemic inflammatory response as a mechanism of disease. Potential interventions to control an exaggerated inflammatory response in utero are also described.

Wnt2/2b and β-Catenin Signaling Are Necessary and Sufficient to Specify Lung Progenitors in the Foregut

We are interested in determining whether premature birth alters expression of counterregulatory cytokines which modulate lung inflammation Production of proinflammatory cytokines tumor necrosis factor alpha IL-1 beta, and IL-8 is regulated in part by the antiinflammatory cytokine IL-10 For preterm newborns with hyaline membrane disease, deficiencies in the ability of lung macrophages to express antiinflammatory cytokines may predispose to chronic lung inflammation We compared the expression of pro- and antiinflammatory cytokines at the mRNA and protein level in the lungs of preterm and term newborns with acute respiratory failure from hyaline membrane disease or meconium aspiration syndrome Four sequential bronchoalveolar lavage (BAL) samples were obtained during the first 96 h of life from all patients All patients rapidly developed an influx of neutrophils and macrophages Over time, cell populations in both groups became relatively enriched with macrophages The expression of proinflammatory cytokine mRNA and/or protein was present in all samples from both patient groups In contrast, IL-10 mRNA was undetectable in most of the cell samples from preterm infants and present in the majority of cell samples from term infants IL-10 concentrations were undetectable in lavage fluid from preterm infants with higher levels in a few of the BAL samples from term infants These studies demonstrate that 1) IL-10 mRNA and protein expression by lung inflammatory cells is related to gestational age and 2) during the first 96 h of life neutrophil cell counts and IL-8 expression decrease in BAL from term infants, but remain unchanged in BAL samples from preterm infants

/pdf/undetectable-interleukin-il-10-and-persistent-il-8-1tmjbze7ir.pdf

Undetectable Interleukin (IL)-10 and Persistent IL-8 Expression Early in Hyaline Membrane Disease: A Possible Developmental Basis for the Predisposition to Chronic Lung Inflammation in Preterm Newborns

TTF-1 regulates lung epithelial morphogenesis.

TTF-1 Is an Epithelial Morphoregulatory Transcriptional Factor

Structure of the human Nkx2.1 gene.

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Undetectable Interleukin (IL)-10 and Persistent IL-8 Expression Early in Hyaline Membrane Disease: A Possible Developmental Basis for the Predisposition to Chronic Lung Inflammation in Preterm Newborns

TTF-1 regulates lung epithelial morphogenesis.

TTF-1 Is an Epithelial Morphoregulatory Transcriptional Factor

Structure of the human Nkx2.1 gene.