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Carter Roberts
Carter Roberts

Why The Immune Systems Of Prematurely Born Babies Are Susceptible To Deadly Infections - Mr Validity WORK

Even as the premature newborn grows, it remains at increased risk for significant problems related to respiratory infections, particularly those of viral origin. Although immunization strategies such as Palivizumab, which aims to prevent serious and often life-threatening lung infections caused by respiratory syncytial virus (RSV), target premature newborns and at-risk newborns with significant lung disease, the growing premature newborn remains at an increased risk for RSV infection, particularly in the lower respiratory tract of the lung (American Academy of Pediatrics 2009; Hall et al. 2009). Furthermore, children born prematurely continue to be at increased risk for severe influenza infections, which adversely affect their long term prognosis (Izurieta et al. 2000; Louie et al. 2006).

Why the immune systems of prematurely born babies are susceptible to deadly infections - Mr Validity

Research in both humans and animals suggest that zinc depletion also may play a role in dampening immunity in alcohol exposed infants. Zinc is an essential cofactor in approximately 300 enzyme-dependent processes involved in immunity, growth, cell differentiation, and metabolism (Chandra 2002; Uriu-Adams et al. 2010). Studies of global disease burden for 2010 found that a primary risk factor for death in early infancy was bacterial infection linked to zinc insufficiency (Chaffee and King 2012; Lim et al. 2012; Mori et al. 2012). Indeed, zinc is essential for innate and adaptive immune responses (Knoell and Liu 2010; Maggini et al. 2007), and suboptimal concentrations of zinc result in an increased susceptibility to infection as well as exacerbation of existing infections (Prasad 2013). Newborns are at an increased risk for suboptimal zinc concentrations if their mothers have suboptimal zinc pools, and women who abuse alcohol during pregnancy tend to have suboptimal zinc pools (Keen et al. 2010; Picciano 2003). In addition, researchers have shown that decreases in zinc are a potential relative risk factor for FASD, and zinc supplements may protect against some of the adverse effects of prenatal alcohol exposure (Keen et al. 2010; Picciano 2003). Because approximately 50 percent of pregnancies are unintended (Finer and Henshaw 2006), some mothers may continue drinking during at least part of their pregnancy, resulting in significant fetal alcohol exposure and risk of suboptimal zinc concentrations in newborns. Furthermore, because the majority of zinc is transported across the placenta in the third trimester of pregnancy, newborns born prematurely, before zinc transport is complete, also are zinc deficient (Giles and Doyle 2007), which suggests that premature newborns exposed to alcohol in utero may be at an even higher risk of zinc deficiency.

In particular, researchers need more specific and accurate assays for identifying which newborns have been exposed to alcohol in utero, along with methods to determine the extent and timing of such exposure. Such approaches will allow researchers to determine and more precisely measure the influence of alcohol on infections and diseases related to immune system dysfunction. In addition, continued research is needed to clarify the potential link between alcohol and premature birth, particularly extreme premature delivery.

The Y-chromosome in boys increases their vulnerability. Biologically, males and females are differentiated by chromosomes: females have two X chromosomes (XX) and males one X and one Y chromosome (XY). Having two X chromosomes means that the newborn has a stronger immune system because X chromosomes contain a larger number of immune-related genes.107108 This means that, since females have two X chromosomes, they have a stronger immune response; boys on the other hand, are more vulnerable to X-linked infections.109

Neonates, especially those born prematurely, are at high risk of morbidity and mortality from sepsis. Multiple factors, including prematurity, invasive life-saving medical interventions, and immaturity of the innate immune system, put these infants at greater risk of developing infection. Although advanced neonatal care enables us to save even the most preterm neonates, the very interventions sustaining those who are hospitalized concurrently expose them to serious infections due to common nosocomial pathogens, particularly coagulase-negative staphylococci bacteria (CoNS). Moreover, the health burden from infection in these infants remains unacceptably high despite continuing efforts. In this paper, we review the epidemiology, immunological risk factors, diagnosis, prevention, treatment, and outcomes of neonatal infection due to the predominant neonatal pathogen CoNS.

While definitive data are yet to be produced, experimental HRV infections in adult volunteers initially suggested that asthmatics were more likely to develop lower respiratory infections (LRI) than healthy adults, i.e. less likely to be able to limit viral replication to the upper airways [19, 20]. Subsequent in vitro infection of primary airway epithelial cells from asthmatic and healthy adults with HRV have demonstrated that asthmatic cells produce less IFN-β [21] and IFN-λ [22] making them potentially more susceptible to infection, slower to clear infection, and more susceptible to virus-induced cell cytotoxicity. Deficiencies in the IFN-α response of peripheral blood mononuclear cells and plasmacytoid dendritic cells from asthmatic adults and children has also been observed, in these particular studies, in response to RSV, HRV [14, 15] and Influenza A [23]. It is likely that the overall impaired innate immune response of the asthmatic airway epithelium is a result of deficiencies in the antiviral response of both epithelial cells and immune cells. Childhood, especially infancy, is characterized by developmentally-regulated deficiencies in innate and adaptive immunity [24]. Such deficiencies are likely to increase the risk of viral LRI in children, especially in those at high risk for asthma and allergies. 041b061a72


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