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Prophylactic treatment with fms-like tyrosine kinase-3 ligand after burn injury enhances global immune responses to infection.
J Immunol. 2008 Mar 01; 180(5):3038-48.JI

Abstract

Severely burned patients are susceptible to infections with opportunistic organisms due to altered immune responses and frequent wound contamination. Immunomodulation to enhance systemic and local responses to wound infections may be protective after burn injury. We previously demonstrated that pretreatments with fms-like tyrosine kinase-3 (Flt3) ligand (Flt3L), a dendritic cell growth factor, increase the resistance of mice to a subsequent burn injury and wound infection by a dendritic cell-dependent mechanism. This study was designed to test the hypothesis that Flt3L administration after burn injury decreases susceptibility to wound infections by enhancing global immune cell activation. Mice were treated with Flt3L after burn injury and examined for survival, wound and systemic bacterial clearance, and immune cell activation after wound inoculation with Pseudomonas aeruginosa. To gain insight into the local effects of Flt3L at the burn wound, localization of Langerhans cells was examined. Mice treated with Flt3L had significantly greater numbers of CD25-expressing T cells and CD69-expressing T and B cells, neutrophils, and macrophages after, but not before, infection. Overall leukocyte apoptosis in response to infection was decreased with Flt3L treatment. Survival and local and systemic bacterial clearance were enhanced by Flt3L. Langerhans cells appeared in the dermis of skin bordering the burn wound, and further increased in response to wound infection. Flt3L augmented the appearance of Langerhans cells in response to both injury and infection. These data suggest that dendritic cell enhancement by Flt3L treatments after burn injury protects against opportunistic infections through promotion of local and systemic immune responses to infection.

Authors+Show Affiliations

Department of Anesthesiology, University of Texas Medical Branch, Galveston, TX 77555-0591, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18292526

Citation

Bohannon, Julia, et al. "Prophylactic Treatment With Fms-like Tyrosine Kinase-3 Ligand After Burn Injury Enhances Global Immune Responses to Infection." Journal of Immunology (Baltimore, Md. : 1950), vol. 180, no. 5, 2008, pp. 3038-48.
Bohannon J, Cui W, Cox R, et al. Prophylactic treatment with fms-like tyrosine kinase-3 ligand after burn injury enhances global immune responses to infection. J Immunol. 2008;180(5):3038-48.
Bohannon, J., Cui, W., Cox, R., Przkora, R., Sherwood, E., & Toliver-Kinsky, T. (2008). Prophylactic treatment with fms-like tyrosine kinase-3 ligand after burn injury enhances global immune responses to infection. Journal of Immunology (Baltimore, Md. : 1950), 180(5), 3038-48.
Bohannon J, et al. Prophylactic Treatment With Fms-like Tyrosine Kinase-3 Ligand After Burn Injury Enhances Global Immune Responses to Infection. J Immunol. 2008 Mar 1;180(5):3038-48. PubMed PMID: 18292526.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prophylactic treatment with fms-like tyrosine kinase-3 ligand after burn injury enhances global immune responses to infection. AU - Bohannon,Julia, AU - Cui,Weihua, AU - Cox,Robert, AU - Przkora,Rene, AU - Sherwood,Edward, AU - Toliver-Kinsky,Tracy, PY - 2008/2/23/pubmed PY - 2008/8/14/medline PY - 2008/2/23/entrez SP - 3038 EP - 48 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J. Immunol. VL - 180 IS - 5 N2 - Severely burned patients are susceptible to infections with opportunistic organisms due to altered immune responses and frequent wound contamination. Immunomodulation to enhance systemic and local responses to wound infections may be protective after burn injury. We previously demonstrated that pretreatments with fms-like tyrosine kinase-3 (Flt3) ligand (Flt3L), a dendritic cell growth factor, increase the resistance of mice to a subsequent burn injury and wound infection by a dendritic cell-dependent mechanism. This study was designed to test the hypothesis that Flt3L administration after burn injury decreases susceptibility to wound infections by enhancing global immune cell activation. Mice were treated with Flt3L after burn injury and examined for survival, wound and systemic bacterial clearance, and immune cell activation after wound inoculation with Pseudomonas aeruginosa. To gain insight into the local effects of Flt3L at the burn wound, localization of Langerhans cells was examined. Mice treated with Flt3L had significantly greater numbers of CD25-expressing T cells and CD69-expressing T and B cells, neutrophils, and macrophages after, but not before, infection. Overall leukocyte apoptosis in response to infection was decreased with Flt3L treatment. Survival and local and systemic bacterial clearance were enhanced by Flt3L. Langerhans cells appeared in the dermis of skin bordering the burn wound, and further increased in response to wound infection. Flt3L augmented the appearance of Langerhans cells in response to both injury and infection. These data suggest that dendritic cell enhancement by Flt3L treatments after burn injury protects against opportunistic infections through promotion of local and systemic immune responses to infection. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/18292526/Prophylactic_treatment_with_fms_like_tyrosine_kinase_3_ligand_after_burn_injury_enhances_global_immune_responses_to_infection_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=18292526 DB - PRIME DP - Unbound Medicine ER -