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Published on: October 31, 2025
Postnatal morphological lung development of wild type and CD26/DPP4 deficient rat pups in dependency of LPS exposure
Inga Wagener1, Meike Jungen1, Stephan von Hörsten2
1Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany.
Insights
CD26 deficiency worsens lung development delays caused by LPS exposure in newborn rats. While CD26-positive rats recover by day 10, CD26-deficient rats show slower recovery, indicating CD26
Area of Science:
- Developmental biology
- Immunology
- Pulmonology
Background:
- Rodent lungs are immature at birth.
- CD26/DPP4 (CD26) is a protein involved in development and inflammation.
- LPS exposure simulates perinatal infection and delays lung development.
Purpose of the Study:
- To investigate if CD26 deficiency affects LPS-induced delays in rat lung development.
Main Methods:
- Newborn CD26-positive and CD26-deficient rats were exposed to LPS on postnatal days 3 and 5.
- Stereological methods were used to assess lung morphology.
- Lung development was analyzed at 7, 10, 14, and 21 days postpartum.
Main Results:
- LPS caused mild inflammation and delayed lung development in both groups.
- CD26-deficient rats showed more pronounced delays in alveolar development until day 14.
- CD26-positive rats exhibited recovery from LPS-induced delays by day 10.
Conclusions:
- CD26 absence exacerbates LPS-induced delays in morphological lung development.
- Morphological recovery is slower in CD26-deficient lungs after LPS exposure.
Background:
Rodents are born with morphological immature lungs and an intact surfactant system. CD26/DPP4 is a multifactorial transmembrane integral type II protein, which is involved in physiological and pathophysiological processes and is already expressed during development. CD26/DPP4, called CD26 in the following, is able to enhance or dampen differently triggered inflammation. LPS exposure often used to simulate perinatal infection delays lung development.
Objective:
A perinatal LPS rat model was used to test the hypothesis that CD26 deficiency modulates LPS-induced retardation in morphological lung development.
Methods:
New born Fischer CD26 positive (CD26+) and deficient (CD26-) rats were exposed to LPS on postnatal day (day post partum, dpp) 3 and 5. Morphological parameters of lung development were determined stereologically. Lung development was analysed in 7, 10 14 and 21day old rats.
Results:
Compared to controls LPS application resulted (1) in a mild inflammation independent of the strain, (2) in significantly lower total surface and volume of alveolar septa combined with significantly higher total volume of airspaces and alveolar size on dpp 7 in both substrains. However, compared to controls in LPS treated CD26- rats significant lower values of total septal surface and volume combined with higher values of total parenchymal airspaces and alveolar size were found until the end of classical alveolarization (dpp14). In LPS treated CD26+ rat pups the retardation was abolished already on dpp 10.
Conclusion:
In absence of CD26, LPS enhances the delay of morphological lung development. Morphological recovery was slower after the end of LPS exposure in CD26 deficient lungs.
