Influence of maternal and neonatal factors on bronchopulmonary dysplasia development

Lima, Marcela Raquel de Oliveira; Andrade, Maria do Amparo; Araújo, Ana Paula G. de; Figueroa, José Natal; Andrade, Lívia Barboza de

doi:10.1016/s0104-4230(11)70083-5

Cited by 2 publications

(1 citation statement)

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“…Infection and Immunity: During pregnancy in utero exposures to infections, such as maternal vulvovaginitis (Candida albicans), chorioamnionitis (bacterial infection of the foetal membranes, amnion, and chorion), and Group B streptococcal (GBS) bacterial infection, negatively affect foetal pulmonary and immunological development and have been shown to associate with bronchopulmonary dysplasia [43] (BPD) and potentially childhood asthma [12], fig. 1.…”

Section: Environmental Stimulimentioning

confidence: 99%

Childhood asthma: causes, risks, and protective factors; a role of innate immunity

Noutsios¹,

Floros²

2014

Swiss Med Wkly

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Childhood asthma is an umbrella of multifactorial diseases with similar clinical features such as mast cell and eosinophil infiltration causing airway hyper responsiveness, inflammation, and airway obstruction. There are various factors that are implicated in childhood asthma pathogenesis. A combined contribution of genetic predisposition, environmental insults, and epigenetic changes account for polarisation of the immune system towards T helper (Th) type 2 cell responses that include production of pro-inflammatory cytokines, IgE, and eosinophil infiltrates, shown to associate with asthma. Environmental cues in prenatal, perinatal, and early childhood seem to determine development of asthma incidence or protection against it. Mode of birth delivery, use of antibiotics, oxidative stress, exposure to tobacco smoke and an industrialised lifestyle are significant contributors to childhood asthma exacerbation. Environmental stimuli such as exposure to maternal antibodies through breast milk, and certain early infections favour Th1 cell responses, leading to the production of anti-inflammatory cytokines that protect from asthma. Aside from the Th cell responses the role of innate immunity in the context of alveolar macrophages, dendritic cells, and surfactant protein A (SP-A) and SP-D is discussed. SP-A and SP-D enhance pathogen phagocytosis and cytokine production by alveolar macrophages, bind and clear pathogens, and interact with dendritic cells to mediate adaptive immunity responses. Further study of the interactions between genetic variants of genes of interest (SP-A and SP-D) and the environment may provide valuable knowledge about the underlying mechanisms of various interactions that differentially affect asthma susceptibility, disease severity, and reveal potential points for therapeutic interventions.

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Section: Environmental Stimulimentioning

confidence: 99%