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Bronchopulmonary Dysplasia and Innate Immunity: A Narrative Review of the Roles of IL-1β and IL-8 (CXCL8)

Dubravka Bačaj Ivanić1, Štefan Grosek2,3, Andreja Nataša Kopitar4

  • 1Department of Gynecology and Obstetrics, Clinical Hospital Sveti Duh, 10000 Zagreb, Croatia.

Children (Basel, Switzerland)
|July 28, 2026
PubMed

Insights

Elevated levels of interleukin-1β (IL-1β) and interleukin-8 (IL-8/CXCL8) are linked to bronchopulmonary dysplasia (BPD) in premature infants. These inflammatory markers play a key role in the development of this chronic lung disease.

Area of Science:

  • Neonatal immunology
  • Pulmonology
  • Inflammatory diseases

Background:

  • Bronchopulmonary dysplasia (BPD) is a significant chronic lung disease in extremely premature newborns.
  • Both prenatal and postnatal factors, alongside innate immune system activation, contribute to BPD etiology.
  • Interleukin-1β (IL-1β) and IL-8 (CXCL8) are key bioactive mediators in the inflammatory response.

Purpose of the Study:

  • To review the role of the innate immune system in BPD development.
  • To synthesize evidence on IL-1β and IL-8 (CXCL8) in BPD from human and animal studies.
  • To explore the interaction between IL-1β and IL-8 (CXCL8) in chronic lung disease pathogenesis.

Main Methods:

  • A comprehensive literature search was performed across major biomedical databases (PubMed, Scopus, Web of Science, Ovid MEDLINE).
  • Studies published between 1993 and November 2025 were included.
  • Evidence from human and animal studies was synthesized narratively.

Main Results:

  • The review details the innate immune system's mechanisms in initiating inflammation in BPD.
  • Evidence from human and animal models links IL-1β and IL-8 (CXCL8) to BPD.
  • The interplay between IL-1β and IL-8 (CXCL8) in chronic lung disease development is described.

Conclusions:

  • Human and animal studies indicate a strong association between elevated IL-1β and IL-8 (CXCL8) levels and BPD.
  • These cytokines are implicated as significant contributors to the pathogenesis of BPD in premature infants.

Keywords:
chemokineschronic lung diseasecytokinesinflammationpremature infant

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