Lymphocyte Subpopulations in Bronchopulmonary Dysplasia

Ballabh, Praveen; Simm, Maciej; Kumari, Jaishree; Krauss, Alfred N.; Jain, Ajey; Auld, Peter A. M.; Cunningham‐Rundles, Susanna

doi:10.1055/s-2003-45387

Cited by 23 publications

(6 citation statements)

References 25 publications

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“…More activated T cells in those who go on to develop BPD may reflect sequestration and activation of cells within the lung. 142 , 143 CD4+ T-cell percentage continued to decrease with postnatal age. Berrington and colleagues 144 measured lymphocyte subclasses in premature infants just before first immunizations.…”

Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 87%

“… 140 Significant infiltrates of T cells were noted in distal lung of infants who died with BPD as compared with gestational age–matched infants without lung disease. 141 In serial blood samples from premature infants with RDS born 1200 g and less than 30 weeks’ gestation, Ballabh and colleagues 142 demonstrated a reduction in absolute lymphocyte count, as well as the percentage and the absolute number of CD4+ T cells, in those who progressed to BPD ( P <.03), significant even on day 1 of life. More activated T cells in those who go on to develop BPD may reflect sequestration and activation of cells within the lung.…”

Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 99%

“… 146 Several reports now demonstrate a correlation between T-cell activation, as measured by CD45RO expression, and premature infants’ adverse outcomes, such as BPD, necrotizing enterocolitis, and periventricular leukomalacia. 25 , 142 , 147 CD4+ and CD8+ T cells at lower gestational age are also shown to have enhanced cytokine production with in vitro stimulation, suggesting that enhanced CD45RO expression in preterms is accompanied by inducible effector functions that may contribute to the severity of lung disease. 146 , 148 A report that regulatory CD4+ T cells (CD4+CD25 hi FoxP3+CD127Dim) were significantly reduced in cord blood of preterm infants who developed BPD further raises the potential for enhanced inflammation due to reduced inhibitory control.…”

Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 99%

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Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Pryhuber

2015

Clinics in Perinatology

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Synopsis Premature infants suffer significant respiratory morbidity during infancy with long-term negative consequences on health, quality of life, and health care costs. Enhanced susceptibility to a variety of infections and inflammation play a large role in early and prolonged lung disease following premature birth, though the mechanisms of susceptibility and immune dysregulation are active areas of research. This chapter will review aspects of host-pathogen interactions and immune responses that are altered by preterm birth and that impact chronic respiratory morbidity in these children.

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Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 87%

Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 99%

Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 99%

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Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Pryhuber

2015

Clinics in Perinatology

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“…Lymphocyte activation is further increased in preterm infants that develop BPD (Turunen et al, 2009). However, the absolute lymphocyte number is decreased in preterm neonates with BPD, contributed to by a decrease in circulating CD4 cells (Ballabh et al, 2003). …”

Section: Mechanical Ventilationmentioning

confidence: 99%

The immune consequences of preterm birth

Melville¹,

Moss²

2013

Front. Neurosci.

292

243

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Preterm birth occurs in 11% of live births globally and accounts for 35% of all newborn deaths. Preterm newborns have immature immune systems, with reduced innate and adaptive immunity; their immune systems may be further compromised by various factors associated with preterm birth. The immune systems of preterm infants have a smaller pool of monocytes and neutrophils, impaired ability of these cells to kill pathogens, and lower production of cytokines which limits T cell activation and reduces the ability to fight bacteria and detect viruses in cells, compared to term infants. Intrauterine inflammation is a major contributor to preterm birth, and causes premature immune activation and cytokine production. This can induce immune tolerance leading to reduced newborn immune function. Intrauterine inflammation is associated with an increased risk of early-onset sepsis and likely has long-term adverse immune consequences. Requisite medical interventions further impact on immune development and function. Antenatal corticosteroid treatment to prevent newborn respiratory disease is routine but may be immunosuppressive, and has been associated with febrile responses, reductions in lymphocyte proliferation and cytokine production, and increased risk of infection. Invasive medical procedures result in an increased risk of late-onset sepsis. Respiratory support can cause chronic inflammatory lung disease associated with increased risk of long-term morbidity. Colonization of the infant by microorganisms at birth is a significant contributor to the establishment of the microbiome. Caesarean section affects infant colonization, potentially contributing to lifelong immune function and well-being. Several factors associated with preterm birth alter immune function. A better understanding of perinatal modification of the preterm immune system will allow for the refinement of care to minimize lifelong adverse immune consequences.

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“…Activation of circulating CD4 + and CD8 + T cells occurs in preterm infants with BPD [7], however, the absolute lymphocyte number is decreased, owing to a decrease in circulating CD4 + cells [8]. This initial inflammatory response to ventilation may influence development of lung injury [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Human amnion epithelial cells modulate the inflammatory response to ventilation in preterm lambs

et al. 2017

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Ventilation of preterm neonates causes pulmonary inflammation that can contribute to lung injury, propagate systemically and result in long-term disease. Modulation of this initial response may reduce lung injury and its sequelae. We aimed to determine the effect of human amnion epithelial cells (hAECs) on immune activation and lung injury in preterm neonatal lambs. Preterm lambs received intratracheal hAECs (90x106) or vehicle, prior to 2 h of mechanical ventilation. Within 5 min of ventilation onset, lambs also received intravenous hAECs (90x106) or vehicle. Lung histology, bronchoalveolar lavage (BAL) cell phenotypes, and cytokine profiles were examined after 2 h of ventilation, and in unventilated controls. Histological indices of lung injury were higher than control, in vehicle-treated ventilated lambs but not in hAEC-treated ventilated lambs. Ventilation-induced pulmonary leukocyte recruitment was greater in hAEC-treated lambs than in vehicle-treated lambs. Lung IL-1β and IL-6 mRNA expression was higher in vehicle- and hAEC-treated ventilated lambs than in controls but IL-8 mRNA levels were greater than control only in vehicle-treated ventilated lambs. Numbers of CD44+ and CD21+ lymphocytes and macrophages from the lungs were altered in vehicle- and hAEC-treated ventilated lambs. Numbers of CD8+ macrophages were lower in hAEC-treated ventilated lambs than in vehicle-treated ventilated lambs. Indices of systemic inflammation were not different between vehicle- and hAEC-treated lambs. Human amnion epithelial cells modulate the pulmonary inflammatory response to ventilation in preterm lambs, and reduce acute lung injury. Immunomodulatory effects of hAECs reduce lung injury in preterm neonates and may protect against longer-term respiratory disease.

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Lymphocyte Subpopulations in Bronchopulmonary Dysplasia

Cited by 23 publications

References 25 publications

Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

The immune consequences of preterm birth

Human amnion epithelial cells modulate the inflammatory response to ventilation in preterm lambs

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