Cimetidine enhances delayed-type hypersensitivity responses and serum interleukin (IL)-2, -10, -12, and IL-17 levels after burn injury in an animal model.
Summary of "Cimetidine enhances delayed-type hypersensitivity responses and serum interleukin (IL)-2, -10, -12, and IL-17 levels after burn injury in an animal model."
The immunosuppression that occurs after burn injury causes an increase in susceptibility to infection. The aim was to investigate time-related alterations in various cytokines following thermal injury and to modulate cytokines by use of an immunomodulant, cimetidine. Male Balb/c mice were anesthetized and given a 10% total body surface area full-thickness burn by submerging in 90°C water for 9 s. Time-dependent changes in delayed type hypersensitivity (DTH) and serum levels of the cytokines IL-2, IL-10, IL-12, IL-17 and TGFβ were then assessed at various post-burn day (PBD) timepoints. Effects of 10 mg cimetidine/kg on DTH responses and cytokine levels were evaluated up to PBD 14. In comparison to healthy non-burned control mice, levels of IL-2 and IL-17 significantly decreased at PBD 3, 5, 10, and 14, those of IL-10 at PBD 1, 3, 5, and 10, and those of IL-12 at PBD 1, 3, 5, 10, and 14. Administration of cimetidine significantly augmented the levels of IL-2 (at PBD 3, 5, and 10), IL-10 (at PBD 1 and 5), IL-12 (at PBD 3, 5, 10, and 14), and IL-17 (at PBD 3 and 14) as compared to those in burned counterparts who did not receive drug. In comparison to healthy mice, biphasic alterations were observed regarding TGFβ levels; values were significant decreased and increased at PBD 3 and PBD 14, respectively. Cimetidine significantly diminished the elevated TGFβ levels at PBD 14. Cimetidine also significantly augmented DTH responses at PBD 5, 10, and 14 as compared to responses in non-drug-treated burned hosts. Taken together, the results here showed significant time-dependent changes in serum cytokines levels after burn injury and that cimetidine was able to significantly augment IL-2, IL-10, IL-12, and IL-17 levels as well as DTH responses that are normally suppressed following thermal trauma.
Department of Microbiology and Immunology, Medical School.
This article was published in the following journal.
Name: Journal of immunotoxicology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22946962
- DOI: http://dx.doi.org/10.3109/1547691X.2012.708365
Medical and Biotech [MESH] Definitions
Allergic reaction to products containing processed natural rubber latex such as rubber gloves, condoms, catheters, dental dams, balloons, and sporting equipment. Both T-cell mediated (HYPERSENSITIVITY, DELAYED) and IgE antibody-mediated (HYPERSENSITIVITY, IMMEDIATE) allergic responses are possible. Delayed hypersensitivity results from exposure to antioxidants present in the rubber; immediate hypersensitivity results from exposure to a latex protein.
Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.
Receptors, Interleukin-1 Type I
An interleukin-1 receptor subtype that is involved in signaling cellular responses to INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The binding of this receptor to its ligand causes its favorable interaction with INTERLEUKIN-1 RECEPTOR ACCESSORY PROTEIN and the formation of an activated receptor complex.
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Receptors, Interleukin-1 Type Ii
An interleukin-1 receptor subtype that competes with the INTERLEUKIN-1 RECEPTOR TYPE I for binding to INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The interleukin-1 type II receptor appears to lack signal transduction capability. Therefore it may act as a "decoy" receptor that modulates the activity of its ligands. Both membrane-bound and soluble forms of the receptor have been identified.
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