Vitamin D Deficiency Does Not Result in a Breach of Host Defense in Murine Models of Pneumonia.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Lehr, Claus M
MetadataShow full item record
AbstractVitamin D (VitD) has a role in the regulation of calcium and phosphate metabolism and in addition impacts the activity of the immune system. VitD deficiency might be linked to increased susceptibility to respiratory tract infection. The aim of the present study was to characterize the impact of VitD deficiency on the susceptibility to bacterial infection in murine models. C57BL/6N mice were fed a diet with or without VitD for 10 weeks. The VitD-deficient or -sufficient mice were infected with Pseudomonas aeruginosa or Streptococcus pneumoniae The colonization and inflammatory response in the lung were analyzed at defined time points. The serum 25-hydroxy-VitD concentration was significantly lower in mice on the VitD-deficient diet. In infection experiments with Pseudomonas aeruginosa or Streptococcus pneumoniae, no differences could be observed in the numbers of viable bacteria or in differential cell counts in the bronchoalveolar lavage fluids. Measurements of inflammatory cytokines (KC and interleukin-1β [IL-1β]) did not show significant differences between the groups. In conclusion, VitD-deficient animals did not show significantly increased susceptibility to infection or an altered course of infection. The immune systems of humans and mice likely respond differently to VitD. Murine models are likely not appropriate for drawing conclusions on the role of VitD in human pulmonary host defense.
AffiliationHIPS, Helmholtz-Institut für pharmazeutische Forschung Saarland, Universitätscampus 8.1, 66123 Saarbrücken, Germany.
The following license files are associated with this item:
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 3.0 United States
- Chitinase 3-Like 1 (Chil1) Regulates Survival and Macrophage-Mediated Interleukin-1β and Tumor Necrosis Factor Alpha during Pseudomonas aeruginosa Pneumonia.
- Authors: Marion CR, Wang J, Sharma L, Losier A, Lui W, Andrews N, Elias JA, Kazmierczak BI, Roy CR, Dela Cruz CS
- Issue date: 2016 Jul
- The alternative activation pathway and complement component C3 are critical for a protective immune response against Pseudomonas aeruginosa in a murine model of pneumonia.
- Authors: Mueller-Ortiz SL, Drouin SM, Wetsel RA
- Issue date: 2004 May
- Cigarette smoke-promoted acquisition of bacterial pathogens in the upper respiratory tract leads to enhanced inflammation in mice.
- Authors: Voss M, Wonnenberg B, Honecker A, Kamyschnikow A, Herr C, Bischoff M, Tschernig T, Bals R, Beisswenger C
- Issue date: 2015 Mar 20
- Regulatory T cell activity is partly inhibited in a mouse model of chronic Pseudomonas aeruginosa lung infection.
- Authors: Ding FM, Zhu SL, Shen C, Ji XL, Zhou X
- Issue date: 2015 Feb
- Streptococcus pneumoniae and Pseudomonas aeruginosa pneumonia induce distinct host responses.
- Authors: McConnell KW, McDunn JE, Clark AT, Dunne WM, Dixon DJ, Turnbull IR, Dipasco PJ, Osberghaus WF, Sherman B, Martin JR, Walter MJ, Cobb JP, Buchman TG, Hotchkiss RS, Coopersmith CM
- Issue date: 2010 Jan