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Wound Healing in a Model of Systemic Lupus Erythematosus may be Delayed by a Lack of Interleukin‐2
Author(s) -
Doersch Karen Melissa,
NewellRogers M Karen
Publication year - 2016
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.30.1_supplement.922.6
Subject(s) - medicine , immunology , cytokine , cytotoxic t cell , interleukin , wound healing , systemic lupus erythematosus , interleukin 2 , cd8 , immune system , biology , biochemistry , disease , in vitro
Objective The purpose of this study is to examine the mechanism of delayed wound closure in a mouse model of Systemic Lupus Erythematosus (SLE). Background SLE is a common and devastating autoimmune disease with symptoms that include skin changes and poor wound healing. SLE patients are frequently deficient in Interleukin‐2. Quercetin is known to alter the apoptosis‐verses‐proliferation balance and also to decrease Interleukin‐2 production by immune cells. This study uses quercetin to perturb wound healing in a mouse model of SLE and seeks to examine the Interleukin‐2‐dependent mechanism by which wounds in SLE patients fail to heal appropriately. Hypothesis Decreased Interleukin‐2 delays and perturbs wound healing in SLE. Methods Fas‐deficient (LPR), and Fas‐Ligand mutant (GLD) mice served as the SLE model. These mice were wounded with an 8 mm biopsy punch, treated daily with intraperitoneal injections of quercetin and compared to wild‐type quercetin‐treated mice. Wounds were measured with calipers and lymphocyte frequencies and Interleukin‐2 receptor expression were measured by flow cytometry. Results Quercetin administration to LPR and GLD mice delayed wound healing compared with wild‐type mice. At day 10 post‐wounding, LPR and GLD mice had decreased percentages of both T‐helper and cytotoxic T lymphocytes in the draining lymph nodes of the wounds compared to wild‐type. This decrease in T‐cells may prevent adequate cytokine production at the wound site. Furthermore, CD4‐CD8‐ lymphocytes accumulate in LPR and GLD mice and express high levels of Interleukin‐2 receptor that can remove Interleukin‐2 from the wound environment. These cells appear to modulate the impaired wound closure. Conclusions Quercetin impairs wound healing in SLE‐model mice, possibly in an Interleukin‐2 dependent manner. This study describes a novel model for understanding delayed wound healing in SLE and identifies Interleukin‐2 as a treatment target for wound healing in patients with SLE. Support or Funding Information Scott and White Foundation, Texas A&M Health Science Center College of Medicine