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Published on: January 27, 2019
Defective production of interleukin-6 in very small premature infants in response to bacterial pathogens
1Department of Pediatrics, School of Medicine, Kanazawa University, Japan.
Insights
Preterm infants show reduced interleukin-6 (IL-6) production in response to bacterial pathogens and lipopolysaccharide. This diminished immune response in premature babies may increase their susceptibility to infections.
Area of Science:
- Neonatal immunology
- Infectious disease research
Background:
- Preterm infants exhibit increased susceptibility to bacterial infections.
- Interleukin-6 (IL-6) is a key cytokine in the immune response to pathogens.
Purpose of the Study:
- To investigate the capacity of preterm and term newborns to produce IL-6.
- To compare IL-6 production in response to bacterial pathogens and lipopolysaccharide (LPS).
Main Methods:
- Whole-blood cultures from preterm and term infants.
- Stimulation with major bacterial pathogens (Group B Streptococcus, E. coli, L. monocytogenes, S. pneumoniae).
- Stimulation with lipopolysaccharide (LPS).
Main Results:
- Term newborns and adults effectively produced IL-6 in response to all tested pathogens and LPS.
- Preterm infants, particularly those born before 30 weeks gestation, demonstrated significantly decreased IL-6 production in response to bacterial pathogens.
- IL-6 responses to LPS were also reduced in preterm newborns compared to term infants.
Conclusions:
- Preterm infants exhibit an impaired ability to produce IL-6.
- This diminished IL-6 production suggests potential monocyte abnormalities in preterm neonates.
- Reduced IL-6 may contribute to the heightened susceptibility of preterm infants to bacterial infections.
Abstract:
In the present study, a whole-blood culture was employed to examine the ability of preterm and term newborn infants to produce interleukin-6 (IL-6) in response to major bacterial pathogens such as group B streptococci, Escherichia coli, Listeria monocytogenes, and Streptococcus pneumoniae. Similarly, in response to stimulation with lipopolysaccharide, a potent stimulant for monocyte cytokine production, appreciable levels of IL-6 activity in the stimulated whole blood from term newborns as well as adults was effectively induced by all of these pathogens. In contrast to that of term infants, the bacteria-induced IL-6 production of preterm infants, especially those born before 30 weeks of gestation, was somewhat decreased (P less than 0.01 for each pathogen). It was also demonstrated that IL-6 responses to lipopolysaccharide stimulation were reduced in preterm newborns (for term versus preterm newborns less than 30 weeks of gestation, P was less than 0.01). These findings imply some inherent abnormality of monocytes in preterm babies. The diminished IL-6 production may be partly responsible for the susceptibility of preterm newborn infants to bacterial infections.
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