The collectins family encompasses several collagenous Ca2+-dependent defense lectins that are described as pathogen recognition molecules. They play an important role in both adaptive and innate immunity. Surfactant protein A and D are two of these proteins which were initially discovered in association with surfactant in the pulmonary system. The structure, immune and inflammatory functions, and genetic variations have been well described in relation to their roles, function and pathophysiology in the pulmonary system. Subsequently, these proteins have been discovered in a wide range of other organs and organ systems. The role of these proteins outside the pulmonary system is currently an active area of research. This review intends to provide a current overview of the genetics, structure and extra-pulmonary functions of the surfactant collectin proteins.

Inhaled nitric oxide (iNO) use in premature newborns remains controversial among clinicians. In 2014, the American Academy of Pediatrics, Committee on Fetus and Newborn released a statement that the available data do not support routine iNO use in pre-term newborns. Despite the absence of significant benefits, 2016 California data showed that clinicians continue to utilize iNO in pre-term infants. With studies as recent as January 2017, the Cochrane review confirmed no major advantages of iNO in pre-term newborns. Still, it recognized that a subset of pre-term infants with pulmonary hypertension (PHTN) had not been separately investigated. Furthermore, recent non-randomized controlled trials have suggested that iNO may benefit specific subgroups of pre-term newborns, especially those with PHTN, prolonged rupture of membranes, and antenatal steroid exposure. Those pre-term infants who showed a clinical response to iNO had increased survival without disability. These findings underscore the need for future studies in pre-term newborns with hypoxemic respiratory failure and PHTN. This review will discuss the rationale for using iNO, controversies regarding the diagnosis of PHTN, and additional novel approaches of iNO treatment in perinatal asphyxia and neonatal resuscitation in the pre-term population < 34 weeks gestation.

Surfactant proteins are important collectin immune molecules with a wide distribution throughout the body, including the ocular system. Mice with gene deletions for the surfactant protein genes Sftpa1 and Sftpd were observed to have visual impairment and thinning of the outer nuclear layers of the retina. We hypothesized that gene deletion of Sftpa1 and Sftpd (Sftpa1tm1Kor/J and Sftpd-/-) results in early retinal degeneration in these mice. Sftpa1tm1Kor/J and Sftpd-/- retinas were evaluated by histopathology and optical coherence tomography (OCT). Retinas from Sftpa1tm1Kor/J and Sftpd -/- mice showed early retinal degeneration with loss of the outer nuclear layer. After screening of mice for known retinal degeneration mutations, the mice were found to carry a previously unrecognized Pde6brd1 genotype which resulted from earlier breeding of the strain with Black Swiss mice during their generation. The mutation was outbred and the genotype of Sftpa1tm1Kor/J and Sftpd-/- was confirmed. Outbreeding of the Pde6brd1 mutation resulted in restoration of normal retinal architecture confirmed by in vivo and in vitro examination. We can therefore conclude that loss of Sftpa1 and Sftpd do not result in retinal degeneration. We have now generated retinal Sftpa1 and Sftpd targeted mice that exhibit normal retinal histology.

Necrotizing enterocolitis (NEC) is a significant cause of morbidity and mortality in the neonatal population. Formula feeding is among the many risk factors for developing the condition, a practice often required in the cohort most often afflicted with NEC, preterm infants. While the virtues of many bioactive components of breast milk have been extolled, the ability to digest and assimilate the nutritional components of breast milk is often overlooked. The structure of formula differs from that of breast milk, both in lipid composition and chemical configuration. In addition, formula lacks a critical digestive enzyme produced by the mammary gland, bile salt-stimulated lipase (BSSL). The gastrointestinal system of premature infants is often incapable of secreting sufficient pancreatic enzymes for fat digestion, and pasteurization of donor milk (DM) has been shown to inactivate BSSL, among other important compounds. Incompletely digested lipids may oxidize and accumulate in the distal gut. These lipid fragments are thought to induce intestinal inflammation in the neonate, potentially hastening the development of diseases such as NEC. In this review, differences in breast milk, pasteurized DM, and formula lipids are highlighted, with a focus on the ability of those lipids to be digested and subsequently absorbed by neonates, especially those born prematurely and at risk for NEC.

Surfactant Protein D (SP-D), an essential protein related to innate immunity, is expressed in multiple tissue types throughout the body. A closely-related protein, Surfactant Protein A (SP-A), is present in the mouse retina and is associated with neovascularization (NV) in the Oxygen-Induced Retinopathy (OIR) mouse model, mimicking retinopathy of prematurity (ROP). We hypothesized that SP-D would be present in the retina and is also associated with OIR and ROP, which is one of the leading causes of pediatric blindness due to increasing survival rates of extremely preterm newborns. In our study, we did not detect SP-D in the mouse retina through proteomic and genomic investigation at baseline and in pathways known to up-regulate SP-D in other mammal tissues. It is therefore unlikely that SP-D participates in neovascularization in the mouse retina.

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Objective The aim of this study was to evaluate the effect of a policy to deliver at 39 weeks for class III obesity. Methods This was a retrospective cohort study of women with class III obesity delivering at ≥ 37 weeks before (May 2012 to April 2014) and after the policy (September 2014 to August 2016). The primary outcome was the cesarean rate. Secondary outcomes included maternal morbidities and a neonatal morbidity composite. Modified Poisson regression was used to adjust for demographic differences between groups. Results The study included a total of 1,210 patients, 580 before the policy and 630 after the policy. Before and after the policy, cesarean rates were similar (41.6% vs. 47.1%; risk ratio [RR]: 1.13 [95% CI: 1.00‐1.29]; adjusted RR [aRR]: 1.03 [95% CI: 0.92‐1.14]). In adjusted comparisons of women undergoing labor induction, parous women had lower cesarean rates (aRR: 0.62; 95% CI: 0.41‐0.94) but nulliparous women had higher cesarean rates (aRR: 1.32; 95% CI: 1.04‐1.68) after the policy (P for interaction = 0.01). Rates of chorioamnionitis, endometritis, and cesarean wound infection were not different between groups. Composite neonatal morbidity was not different between pre‐ and postpolicy groups. Conclusions A policy of delivery at 39 weeks for class III obesity did not affect overall cesarean rate or rates of maternal or neonatal morbidity. Further investigation should evaluate subsets of women who may have a higher cesarean rate with this policy.

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