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Region Hovedstaden - en del af Københavns Universitetshospital
E-pub ahead of print

Early IL-2 treatment of mice with Pseudomonas aeruginosa pneumonia induced PMN-dominating response and reduced lung pathology

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BACKGROUND: IL-2 is a pro-inflammatory and a Th1 inducing cytokine, which is important for activation of the cell-mediated immunity. IL-2 in serum and sputum has been observed to be reduced in cystic fibrosis (CF) patients. The present IL-2 treatment study of Pseudomonas aeruginosa (PA) lung infected mice was performed in order to evaluate the effect of IL-2 supplement.

METHODS: One hundred-and-twenty female BALB/c mice were divided into three groups: 1) IL-2 treatment/infection (TIG), 2) non-treatment/infection (NTIG), and 3) IL-2 treatment/non-infection (TNIG). The mice were challenged intra-tracheally with PA (PAO579) embedded in seaweed alginate to resemble the biofilm mode of growth. At day 0 and 1, the treatment groups received IL-2 s.c. Mice were killed on day 1 or 2, and cytokine production, lung pathology, and quantitative lung bacteriology was estimated.

RESULTS: IL-2 treatment of infected mice reduced the number of mice with signs of macroscopic lung pathology at day 2 (p<0.05). The reduced macroscopic pathology was paralleled by a reduced IL-1b and TNF-a. In contrast, an increased PMN response at day 2 was observed in the IL-2 treated mice (p<0.01). This was preceded by a significantly higher degree of microscopic inflammation at day 1 (p<0.02). The IL-12 levels decreased in both groups of infected mice at day 2 (p<0.01), however significantly more in the IL-2 treated mice (p<0.02). In accordance, but surprisingly, IFN-g was significantly reduced in the IL-2 treated PA infected group at day 2 (p<0.05).

CONCLUSION: The present results indicate that early IL-2 treatment prolongs the PMN response but also reduces proinflammatory IL-1b and TNF-a and macroscopic signs of pathology.

OriginalsprogEngelsk
TidsskriftAPMIS - Journal of Pathology, Microbiology and Immunology
ISSN0903-4641
DOI
StatusE-pub ahead of print - 13 aug. 2020

ID: 60681122