Use of lactoferrin in the newborn: where do we stand?

Sharma, Deepak; Murki, Anuradha; Murki, Srinivas; Oleti, Tejo Pratap

doi:10.3109/14767058.2014.968548

Cited by 10 publications

(7 citation statements)

References 35 publications

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“…1 There are many interventions that have been implemented to decrease neonatal mortality and sepsis. [2][3][4][5][6][7][8][9] The majority of the neonatal deaths (99%) occur in low-and middle-income countries, out of which more than 50% neonatal deaths occur at homes, which lack adequate care. 10,11 The neonates of developing countries have intrauterine growth restriction too, which makes them further vulnerable to various neonatal morbidities and mortality.…”

Section: Introductionmentioning

confidence: 99%

Correlation of Apgar Score with Asphyxial Hepatic Injury and Mortality in Newborns: A Prospective Observational Study from India

Sharma

Choudhary

Lamba

et al. 2016

Clin Med Insights Pediatr

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OBJECTIVEThe objective of this study is to determine the correlation of Apgar score with asphyxial hepatic injury and neonatal mortality in moderately and severely asphyxiated newborns.MATERIAL AND METHODSThis is a secondary analysis of our prospective observational case-controlled study. Sixteen neonates with severe birth asphyxia (five-minute Apgar ≤3) were compared with either 54 moderate asphyxia neonates (five-minute Apgar >3) or 30 normal neonates. Liver function tests were measured on postnatal days 1, 3, and 10 in the study and control groups. Neonatal mortality was observed in the study and control population.RESULTSCorrelation of Apgar score in severely asphyxiated neonates compared with normal Apgar score neonates and moderately asphyxiated neonates for deranged hepatic function showed significant correlation (odds ratio [OR] 4.88, 95% CI 3.26–5.84, P = 0.01 and OR 2.46, 95% CI 1.94–3.32, P = 0.02, respectively). There was a significant increase in serum lactate dehydrogenase (LDH) and total bilirubin on day 1 and serum LDH at age of 10th postnatal life in severely asphyxiated neonates when compared to moderately asphyxiated neonates, whereas there was a significant decrease in total bilirubin and serum albumin on day 3 in severely asphyxiated neonates. There was a significant increase in serum alanine transaminase, serum LDH, and total bilirubin on day 1, serum aspartate transaminase, serum LDH, and total bilirubin on day 3, and International Normalized Ratio on day 10 of postnatal life when severely asphyxiated neonates were compared with normal neonates. There was a significant reduction in total protein and serum albumin on day 1 and direct bilirubin on day 3 in severely asphyxiated neonates when compared with normal neonates. There was a significant increase in neonatal mortality in severely asphyxiated neonates when compared to the other two groups. Correlation of Apgar score in severely asphyxiated neonates compared with normal Apgar score neonates and moderately asphyxiated neonates for neonatal mortality showed significant correlation (odds ratio [OR] 2.23, 95% CI 1.42–3.04, P = 0.03 and OR 1.87, 95% CI 1.64–2.02, P = 0.04, respectively).CONCLUSIONThe severity of hepatic dysfunction correlates well with increasing severity of asphyxia. The neonatal mortality also showed good correlation with Apgar score in our study, although we need a large multicentric trial to confirm our observations. Apgar score combined with hepatic dysfunction can be used as a prognostication marker for neonatal mortality.

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Section: Introductionmentioning

confidence: 99%

Correlation of Apgar Score with Asphyxial Hepatic Injury and Mortality in Newborns: A Prospective Observational Study from India

Sharma

Choudhary

Lamba

et al. 2016

Clin Med Insights Pediatr

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“…It has potent antimicrobial activity, can stimulate the innate immune system and promote epithelial proliferation and differentiation of the immature gut (213). Recent studies have identified LF supplementation as a promising agent for the reduction of late onset sepsis and necrotizing enterocolitis (214).…”

Section: Current Understanding Of Bpd Pathophysiology New Pathophysimentioning

confidence: 99%

The Future of Bronchopulmonary Dysplasia: Emerging Pathophysiological Concepts and Potential New Avenues of Treatment

Collins¹,

Tibboel²,

Kleer³

et al. 2017

Front. Med.

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Yearly more than 15 million babies are born premature (<37 weeks gestational age), accounting for more than 1 in 10 births worldwide. Lung injury caused by maternal chorioamnionitis or preeclampsia, postnatal ventilation, hyperoxia, or inflammation can lead to the development of bronchopulmonary dysplasia (BPD), one of the most common adverse outcomes in these preterm neonates. BPD patients have an arrest in alveolar and microvascular development and more frequently develop asthma and early-onset emphysema as they age. Understanding how the alveoli develop, and repair, and regenerate after injury is critical for the development of therapies, as unfortunately there is still no cure for BPD. In this review, we aim to provide an overview of emerging new concepts in the understanding of perinatal lung development and injury from a molecular and cellular point of view and how this is paving the way for new therapeutic options to prevent or treat BPD, as well as a reflection on current treatment procedures.

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“…Lactoferrin is an iron-binding glycoprotein typically found in human milk, saliva and other mucosal secretions and is produced by multiple cells, including neutrophils, during inflammation [ 5 , 6 ]. This apparent enrichment in secretions has been postulated to be related to lactoferrin’s broad antimicrobial properties [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…Historically, these defense mechanisms were ascribed to lactoferrin’s iron sequestration properties [ 8 , 9 ]. However, more recent evidence suggests that lactoferrin may play a direct antimicrobial role by preventing bacterial biofilm formation, activating proteolysis of bacterial virulence factors and blocking the adhesion of bacteria to host immune cell membranes [ 6 , 10 ]. In fact, lactoferrin’s non-iron binding protein domains have exhibited frequent evolvement of polymorphisms, suggesting an importance of lactoferrin’s other moieties [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Lactoferrin is a dynamic protein in human melioidosis and is a TLR4-dependent driver of TNF-α release in Burkholderia thailandensis infection in vitro

et al. 2020

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Melioidosis is an often-severe tropical infection caused by Burkholderia pseudomallei (Bp ) with high associated morbidity and mortality. Burkholderia thailandensis ( Bt ) is a closely related surrogate that does not require BSL-3 conditions for study. Lactoferrin is an iron-binding glycoprotein that can modulate the innate inflammatory response. Here we investigated the impact of lactoferrin on the host immune response in melioidosis. Lactoferrin concentrations were measured in plasma from patients with melioidosis and following ex vivo stimulation of blood from healthy individuals. Bt growth was quantified in liquid media in the presence of purified and recombinant human lactoferrin. Differentiated THP-1 cells and human blood monocytes were infected with Bt in the presence of purified and recombinant human lactoferrin, and bacterial intracellular replication and cytokine responses (tumor necrosis factor-α (TNF-α), interleukin-1β and interferon-γ) were measured. In a cohort of 49 melioidosis patients, non-survivors to 28 days had significantly higher plasma lactoferrin concentrations compared to survivors (median (interquartile range (IQR)): 326 ng/ml (230–748) vs 144 ng/ml (99–277), p<0.001). In blood stimulated with heat-killed Bp , plasma lactoferrin concentration significantly increased compared to unstimulated blood (median (IQR): 424 ng/ml (349–479) vs 130 ng/ml (91–214), respectively; p<0.001). Neither purified nor recombinant human lactoferrin impaired growth of Bt in media. Lactoferrin significantly increased TNF-α production by differentiated THP-1 cells and blood monocytes after Bt infection. This phenotype was largely abrogated when Toll-like receptor 4 (TLR4) was blocked with a monoclonal antibody. In sum, lactoferrin is produced by blood cells after exposure to Bp and lactoferrin concentrations are higher in 28-day survivors in melioidosis. Lactoferrin induces proinflammatory cytokine production after Bt infection that may be TLR4 dependent.

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Use of lactoferrin in the newborn: where do we stand?

Cited by 10 publications

References 35 publications

Correlation of Apgar Score with Asphyxial Hepatic Injury and Mortality in Newborns: A Prospective Observational Study from India

Correlation of Apgar Score with Asphyxial Hepatic Injury and Mortality in Newborns: A Prospective Observational Study from India

The Future of Bronchopulmonary Dysplasia: Emerging Pathophysiological Concepts and Potential New Avenues of Treatment

Lactoferrin is a dynamic protein in human melioidosis and is a TLR4-dependent driver of TNF-α release in Burkholderia thailandensis infection in vitro

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