This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Infants with NEC present with varying degrees of severity and in some cases NEC appears to be progressive in nature. Most epidemiological studies suggest that the overarching risk factor for NEC is prematurity combined with hypoxic insults and enteral feeding. Given our inability to predict which infants will develop NEC despite common risk factors, we believe that some infants will develop NEC as a maladaptive inflammatory response in the setting of gram-negative bacterial colonization. Since the hallmark of NEC is intestinal inflammation and a systemic inflammatory response, we propose the following working hypothesis for Study Arm I: the pattern of serum protein mediators in infants with NEC will differ between infants with medically stable NEC and progressive NEC.
The Specific Aims of this study are to use proteomic and bioinformatics technologies to: 1.) Determine the molecular signature of progressive NEC. 2.) Identify plasma proteins that participate in the pathogenesis of NEC and therefore will allow a distinct diagnosis of NEC. The working hypothesis for study Arm II is that neonates susceptible to developing NEC have a genotype that predisposes them to an over-exuberant pro-inflammatory cytokine response and or a depressed counter-regulatory anti-inflammatory cytokine response.Given this, we propose the following Specific Aim(s):
Specific Aim 1. Correlate the incidence of TNF-a, IFN-g, IL-6, IL-10, and TGFb polymorphisms with the severity of NEC.
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