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Effect of N‐Acetyl‐Seryl‐Aspartyl‐Lysyl‐Proline (Ac‐SDKP) on intercellular adhesion molecule 1 (ICAM‐1) and proinflammatory cytokines and chemokines in experimental autoimmune myocarditis (EAM)
Author(s) -
Nakagawa Pablo,
Rhaleb Nour-Eddine,
Chen Xiaojuan,
Liao Tang- Dong,
Smolarek Derek M.,
Yang Xiao-Ping,
Liu Yun-He,
Carretero Oscar A.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.680.20
Subject(s) - chemokine , inflammation , proinflammatory cytokine , cytokine , icam 1 , intercellular adhesion molecule 1 , immunology , infiltration (hvac) , chemistry , medicine , cell adhesion molecule , materials science , composite material
The naturally occurring tetrapeptide Ac‐SDKP improves cardiac function in EAM. We hypothesize that in EAM, Ac‐SDKP interferes with leukocyte infiltration and this is mediated by the reduction of ICAM‐1, cytokine and chemokine expression. EAM was induced in rats by porcine cardiac myosin and treated with vehicle or Ac‐SDKP (800 μg/kg/day). Cardiac inflammation was graded according to a four‐tier system. Infiltration of macrophage and T helper cells were quantified by immunohistochemistry. ICAM‐1 was detected by Western blot. Chemokines and cytokines were quantified using a proteomic cytokine array. Ac‐SDKP reduced cardiac inflammation (EAM: 2.2 ± 0.2 A.U. vs. EAM + Ac‐SDKP: 1.5 ± 0.2 **A.U.), infiltration of macrophages (257 ± 37 vs.138 ± 9 * ED‐1 cells/mm 2 ) and T helpers (148 ± 20 vs. 97 ± 17 * CD4 cells/mm 2 ), ICAM‐1 (2.918 ± 0.880 vs. 0.012 ± 0.002 ** A.U.), interleukin1α (IL‐1α )(1.6 ± 0.4 vs. 0.1 ± 0.1 **A.U.), and cytokine‐inducible neutrophil chemoattractant (CINC‐1) (1.2 ± 0.2 vs.0.2 ± 0.1 *A.U.). In conclusion, Ac‐SDKP prevents leukocyte infiltration, which may be mediated by a reduction of ICAM‐1, IL‐1α and CINC‐1 expression. Supported by NIH HL028982