Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• New perspectives on the origins of bronchopulmonary dysplasia

  Bronchopulmonary dysplasia (BPD) remains one of the most consequential chronic lung disorders of preterm birth. New insights into the pathogenesis of BPD are shifting attention from a single oxygen-injury model toward interacting prenatal inflammation, placental dysfunction, impaired alveolar development, altered pulmonary vascular growth and postnatal care. At APSR 2022, this evidence provides a sharper framework for prevention, phenotyping and long-term respiratory follow-up. Learn more about 上肢リーチ動作における肩甲帯の役割.

  Organised in association with APSR and KATRD, the congress brings together clinicians and investigators working across respiratory medicine, neonatal intensive care and developmental biology. For Australian delegates, the questions are immediate: how do these mechanisms appear in units from Melbourne and Perth to regional centres, and which findings can be translated into routine care?

  Reframing bronchopulmonary dysplasia

  Older descriptions of BPD concentrated on severe oxygen dependency and radiographic changes in very preterm infants. Contemporary definitions include less invasive oxygen or respiratory support delivered around 36 weeks’ postmenstrual age, reflecting the smaller and physiologically different infants now surviving. The result is a more heterogeneous population, with outcomes shaped by developmental stage as much as by the duration of oxygen exposure.

  Phenotypes based on parenchymal injury, airway obstruction and pulmonary hypertension may be more useful than a single label. They also improve the interpretation of research because infants with similar oxygen requirements can have different inflammatory profiles, imaging findings and trajectories. This distinction matters when evaluating preventive interventions or planning follow-up.

  Prenatal inflammation and placental injury

  Placental malperfusion, pre-eclampsia and fetal growth restriction can prime the developing lung before birth. Reduced vascular supply alters pulmonary vascular development, while fetal stress and disturbed nutrient delivery affect surfactant production and alveolar maturation. Experimental models further suggest that antenatal exposures can change the balance between airway growth and immune responses long before neonatal intensive care begins.

  Chorioamnionitis and ascending infection can expose the fetus to inflammatory cytokines that disrupt normal bronchopulmonary development. The effects may depend on timing, duration and fetal response, making it difficult to isolate inflammation itself from the associated changes in oxygen delivery or mechanical forces. Sex-related differences in immune maturation and vulnerability may also contribute to the unequal severity of BPD among preterm infants.

  Oxygen, ventilation and lung injury

  Postnatal injury begins with the immature lung’s limited capacity to sustain gas exchange. Positive-pressure ventilation recruits poorly aerated regions, stretches developing tissue and may cause inflammatory injury even when oxygen concentrations appear acceptable. Excess oxygen can add oxidative stress, while abrupt transitions between support modes affect aeration and haemodynamic stability.

  Current research is separating the effects of hyperoxia, barotrauma and volutrauma more carefully. Lung-volume recruitment strategies, avoiding unnecessary intubation and refining oxygen targets may reduce some forms of injury, but the safest approach remains individualised. Regional differences in access to expertise, equipment and neonatal retrieval also influence how consistently these strategies can be applied.

  In Australian neonatal units, nasal continuous positive airway pressure is often affectionately called a “coffee break”. This familiar term reflects its ubiquity, yet its effects extend beyond keeping a “prem” comfortable: prolonged support can alter chest mechanics, feeding tolerance and family experience. Education should therefore include the physiological purpose of the device as well as its practical limitations.

  Airway and pulmonary vascular remodeling

  Persistent structural lung disease in BPD involves more than simplified alveoli. Abnormal airway development, increased smooth-muscle mass, reduced vascular branching and impaired alveolar-capillary alignment can coexist. These changes explain why some infants remain oxygen-dependent despite improved chest imaging and why pulmonary hypertension may emerge or persist long after initial respiratory support has been reduced.

  Early airway injury can create a self-reinforcing cycle of stretch, inflammation and altered airflow. At the same time, disordered angiogenic signalling restricts the pulmonary microvascular bed, raising cardiac workload and reducing the lung’s ability to grow efficiently. Preterm infants can also develop postural and motor limitations; an analysis of shoulder girdle biomechanics during upper-limb reaching provides context for rehabilitation, although it does not establish a specific causal link to BPD.

  Infection, immunity and the microbiome

  The neonatal airway microbiome develops through a combination of birth, feeding, antibiotics, nursery exposures and household environments. In preterm infants, delayed maturation and repeated respiratory infections may sustain immune activation that interferes with normal alveolar and vascular development. Associations involving Ureaplasma, Mycoplasma and other organisms are complex because detection does not always establish the direction of causation.

  Antibiotic exposure may remove protective organisms while allowing potential pathogens to expand, and mechanical ventilation provides opportunities for persistent microbial stimulation. This line of research is moving towards functional profiles of host response rather than simple microbial counts. Such approaches may identify infants whose inflammation is driven by infection, nutritional immaturity or an intrinsic regulatory defect.

  Biomarkers and precision phenotyping

  Single-cell RNA sequencing, spatial transcriptomics, proteomics and metabolomics are revealing distinct developmental cell states that cannot be recognised through conventional clinical measures. Lung ultrasound and magnetic resonance imaging can add information about regional aeration and structure, while blood and airway biomarkers may indicate ongoing inflammation. Combining these data could separate infants most likely to respond to a specific therapy from those who require supportive care alone.

  A practical phenotype remains more achievable than a universal cure. Infants can be grouped by early growth, oxygen and ventilation burden, infection history, airway dysfunction and pulmonary vascular status. Follow-up must also address less common complications of severe lung disease. The congress resource on outpatient pneumothorax management illustrates the value of clear safety-netting, escalation pathways and coordinated review for respiratory events managed outside hospital.

  Priorities for Australian neonatal practice

  Implementation varies across Australia’s tertiary neonatal intensive care units, regional hospitals and smaller maternity services. Retrieval teams, videoconferencing and shared respiratory protocols can support consistent decision-making across distance, but transfers are not always timely or appropriate for every infant. Research networks should include regional units so that evidence reflects the full range of neonatal respiratory care rather than only major metropolitan centres.

  Wider systemic inequities also shape respiratory risk and outcomes. Aboriginal and Torres Strait Islander babies experience higher rates of preterm birth and avoidable differences in neonatal health, reflecting unequal access to preconception care, housing, nutrition and culturally safe services. Long-term follow-up should be available through public services, Medicare-subsidised specialist care and telehealth where local expertise is limited, with active participation of families and Aboriginal health organisations in pathway design.

  APSR 2022 can support a coordinated Australian effort to connect laboratory findings with bedside care. The immediate next step is for each participating neonatal unit to begin a prospective BPD registry linking delivery-room respiratory support, oxygen exposure, respiratory status at 36 weeks’ postmenstrual age and respiratory outcomes at one year of age.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)