Developmental changes in interleukin-10 expression in the neonatal rat

D. V. Dallas, S. E. Keeney, K. H. Palkowetz, H. E. Rudloff, D. Tarrant, F. C. Schmalstieg

Research output: Contribution to journalArticle

Abstract

A developmental delay in the ability of mononuclear blood cells from human neonates to produce IL-10 in response to stimulation with lipopolysaccharide (LPS) has been documented (Chheda, S., et.al., Pediatr. Res. 40:475, 1996). This delay is potentially important in the pathogenesis of bronchopulmonary dysplasia. In this study, we examined whether the delay extended to the neonatal rat and determined the longitudinal ability of liver and lung to produce IL-10 in response to LPS stimulation. IL-10 protein expression by mononuclear blood cells of Sprague Dawley neonatal rats at 3 days of age induced by incubation with LPS (1 μg/ml) for 24 h was 179 ± 324 pg/ml/106 mononuclear cells (mean ± S.D.) in comparison to 12 week old female rats who produced 1,031 ± 338 pg/ml/106 mononuclear cells (mean ± S.D.) (p < 0.005) as measured by a double monoclonal antibody ELISA assay. Barely detectable amounts of IL-10 (< 50 pg/mg lung tissue) were present in unstimulated neonatal lungs. Constitutive mRNA for IL-10 production in the lung increased only marginally through the first 13 days of life. In contrast, substantial amounts of mRNA for IL-10 were present constitutively in the liver, 1,666 ± 1,558 copies/μg/RNA (mean ± S.D.). This increased substantially with LPS administration in both lung and liver and peaked at approximately 5 days of age in lung, 796 ± 115 copies/μg/RNA (mean ± S.D.) and 7 days of age in liver, 10,200 ± 7,731 copies/μg/RNA (mean ± S.D.). These results indicate that neonatal rats can produce IL-10 in response to LPS in lung and liver. The etiology of increased production of mRNA for IL-10 between 5 and 7 days of age in response to LPS is unknown. However, an increased number of animals died during this time after LPS administration. This suggests the possibility that the animals are most susceptible to LPS-induced inflammatory response during this time period. In conclusion, blood cells and lungs have limited ability to produce IL-10 in response to small amounts of LPS during the first 14 days of life. In contrast, the liver produces substantial amounts of IL-10 and is able to respond briskly to LPS stimulation. These data will be useful in rat models of lung injury.

Original languageEnglish (US)
JournalJournal of Investigative Medicine
Volume47
Issue number2
StatePublished - 1999

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Interleukin-10
Lipopolysaccharides
Rats
Liver
Lung
Blood Cells
Blood
Cells
RNA
Messenger RNA
Animals
Bronchopulmonary Dysplasia
Lung Injury
Sprague Dawley Rats
Assays
Enzyme-Linked Immunosorbent Assay
Monoclonal Antibodies
Tissue

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Dallas, D. V., Keeney, S. E., Palkowetz, K. H., Rudloff, H. E., Tarrant, D., & Schmalstieg, F. C. (1999). Developmental changes in interleukin-10 expression in the neonatal rat. Journal of Investigative Medicine, 47(2).

Developmental changes in interleukin-10 expression in the neonatal rat. / Dallas, D. V.; Keeney, S. E.; Palkowetz, K. H.; Rudloff, H. E.; Tarrant, D.; Schmalstieg, F. C.

In: Journal of Investigative Medicine, Vol. 47, No. 2, 1999.

Research output: Contribution to journalArticle

Dallas, DV, Keeney, SE, Palkowetz, KH, Rudloff, HE, Tarrant, D & Schmalstieg, FC 1999, 'Developmental changes in interleukin-10 expression in the neonatal rat', Journal of Investigative Medicine, vol. 47, no. 2.
Dallas DV, Keeney SE, Palkowetz KH, Rudloff HE, Tarrant D, Schmalstieg FC. Developmental changes in interleukin-10 expression in the neonatal rat. Journal of Investigative Medicine. 1999;47(2).
Dallas, D. V. ; Keeney, S. E. ; Palkowetz, K. H. ; Rudloff, H. E. ; Tarrant, D. ; Schmalstieg, F. C. / Developmental changes in interleukin-10 expression in the neonatal rat. In: Journal of Investigative Medicine. 1999 ; Vol. 47, No. 2.
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abstract = "A developmental delay in the ability of mononuclear blood cells from human neonates to produce IL-10 in response to stimulation with lipopolysaccharide (LPS) has been documented (Chheda, S., et.al., Pediatr. Res. 40:475, 1996). This delay is potentially important in the pathogenesis of bronchopulmonary dysplasia. In this study, we examined whether the delay extended to the neonatal rat and determined the longitudinal ability of liver and lung to produce IL-10 in response to LPS stimulation. IL-10 protein expression by mononuclear blood cells of Sprague Dawley neonatal rats at 3 days of age induced by incubation with LPS (1 μg/ml) for 24 h was 179 ± 324 pg/ml/106 mononuclear cells (mean ± S.D.) in comparison to 12 week old female rats who produced 1,031 ± 338 pg/ml/106 mononuclear cells (mean ± S.D.) (p < 0.005) as measured by a double monoclonal antibody ELISA assay. Barely detectable amounts of IL-10 (< 50 pg/mg lung tissue) were present in unstimulated neonatal lungs. Constitutive mRNA for IL-10 production in the lung increased only marginally through the first 13 days of life. In contrast, substantial amounts of mRNA for IL-10 were present constitutively in the liver, 1,666 ± 1,558 copies/μg/RNA (mean ± S.D.). This increased substantially with LPS administration in both lung and liver and peaked at approximately 5 days of age in lung, 796 ± 115 copies/μg/RNA (mean ± S.D.) and 7 days of age in liver, 10,200 ± 7,731 copies/μg/RNA (mean ± S.D.). These results indicate that neonatal rats can produce IL-10 in response to LPS in lung and liver. The etiology of increased production of mRNA for IL-10 between 5 and 7 days of age in response to LPS is unknown. However, an increased number of animals died during this time after LPS administration. This suggests the possibility that the animals are most susceptible to LPS-induced inflammatory response during this time period. In conclusion, blood cells and lungs have limited ability to produce IL-10 in response to small amounts of LPS during the first 14 days of life. In contrast, the liver produces substantial amounts of IL-10 and is able to respond briskly to LPS stimulation. These data will be useful in rat models of lung injury.",
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AU - Dallas, D. V.

AU - Keeney, S. E.

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AU - Tarrant, D.

AU - Schmalstieg, F. C.

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