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Published on: March 17, 2014
Lung development and immune status under chronic LPS exposure in rat pups with and without CD26/DPP4 deficiency
Andreas Schmiedl1,2, Inga Wagener3, Meike Jungen3
1Functional and Applied Anatomy, Hannover Medical School, Carl-Neuberg Str. 1, 30625, Hannover, Germany. Schmiedl.Andreas@mh-hannover.de.
Insights
Daily low-dose LPS exposure in newborn rats delayed lung development and altered immune cell composition, with effects persisting longer in CD26-deficient pups. This highlights CD26
Area of Science:
- Pulmonary immunology
- Developmental biology
- Inflammation research
Background:
- Dipeptidyl-peptidase IV (CD26) is involved in lung inflammation.
- CD26 expression in lungs during development is crucial.
- LPS exposure can impact lung development and immune status.
Purpose of the Study:
- To investigate CD26-dependent retardation in lung development caused by LPS.
- To determine if LPS alters immune status in a CD26-dependent manner.
- To assess the impact of early-life LPS exposure on lung maturation.
Main Methods:
- Newborn rats (with and without CD26 deficiency) were exposed to LPS.
- Stereological methods assessed lung morphology and alveolarization.
- Fluorescence activated cell sorting (FACS) analyzed pulmonary leukocyte content.
Main Results:
- LPS exposure significantly retarded alveolarization in both CD26-sufficient and deficient rats.
- Immune status alterations included increased B lymphocytes and decreased CD4+CD25+ T cells.
- CD26 deficiency exacerbated LPS-induced delays in lung development and immune cell changes.
Conclusions:
- Early postnatal LPS exposure delays lung septa formation.
- CD26 plays a role in modulating the pulmonary immune response to LPS.
- These findings suggest CD26 influences lung development resilience to inflammatory insults.
Abstract:
Dipeptidyl-peptidase IV (CD26), a multifactorial integral type II protein, is expressed in the lungs during development and is involved in inflammation processes. We tested whether daily LPS administration influences the CD26-dependent retardation in morphological lung development and induces alterations in the immune status. Newborn Fischer rats with and without CD26 deficiency were nebulized with 1 µg LPS/2 ml NaCl for 10 min from days postpartum (dpp) 3 to 9. We used stereological methods and fluorescence activated cell sorting (FACS) to determine morphological lung maturation and alterations in the pulmonary leukocyte content on dpp 7, 10, and 14. Daily LPS application did not change the lung volume but resulted in a significant retardation of alveolarization in both substrains proved by significantly lower values of septal surface and volume as well as higher mean free distances in airspaces. Looking at the immune status after LPS exposure compared to controls, a significantly higher percentage of B lymphocytes and decrease of CD4+CD25+ T cells were found in both subtypes, on dpp7 a significantly higher percentage of CD4 T+ cells in CD26+ pups, and a significantly higher percentage of monocytes in CD26- pups. The percentage of T cells was significantly higher in the CD26-deficient group on each dpp. Thus, daily postnatal exposition to low doses of LPS for 1 week resulted in a delay in formation of secondary septa, which remained up to dpp 14 in CD26- pups. The retardation was accompanied by moderate parenchymal inflammation and CD26-dependent changes in the pulmonary immune cell composition.
