title: Interleukin-13 and -4 induce death of activated microglia.
abstract: When the brain suffers injury, microglia migrate to the damaged sites and become activated. These activated microglia are not detected several days later and the mechanisms underlying their disappearance are not well characterized. In this study, we demonstrate that interleukin (IL)-13, an anti-inflammatory cytokine, selectively induces cell death of activated microglia in vitro. Cell death was detected 4 days after the coaddition of IL-13 with any one of the microglial activators, lipopolysaccharide (LPS), ganglioside, or thrombin. This cell death occurred in a time-dependent manner. LPS, ganglioside, thrombin, or IL-13 alone did not induce cell death. Among anti-inflammatory cytokines, IL-4 mimicked the effect of IL-13, while TGF-beta did not. Cells treated with IL-13 plus LPS, or IL-13 plus ganglioside, showed the characteristics of apoptosis when analyzed by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Electron micrographs also showed microglia engulfing neighboring dead cells. We propose that IL-13 and IL-4 induce death of activated microglia, and that this process is important for prevention of chronic inflammation that can cause tissue damage.
authors: Department of Pharmacology, Ajou University School of Medicine, Suwon, Korea.
authors: Myung-Soon
authors: MS
authors: Yang
authors: Eun Jung
authors: EJ
authors: Park
authors: Seonghyang
authors: S
authors: Sohn
authors: Hyuk Jae
authors: HJ
authors: Kwon
authors: Won-Ho
authors: WH
authors: Shin
authors: Han Kyung
authors: HK
authors: Pyo
authors: Byungkwan
authors: B
authors: Jin
authors: Kyeong Sook
authors: KS
authors: Choi
authors: Ilo
authors: I
authors: Jou
authors: Eun-Hye
authors: EH
authors: Joe
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001930:Brain Injuries / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D016923:Cell Death / Q000187:drug effects / Q000276:immunology*; D048429:Cell Size / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D004660:Encephalitis / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D004996:Ethidium / Q000031:analogs & derivatives*; D005452:Fluoresceins; D005456:Fluorescent Dyes; D005732:Gangliosides / Q000494:pharmacology; D005911:Gliosis / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D020287:In Situ Nick-End Labeling; D007364:Intercalating Agents; D018793:Interleukin-13 / Q000378:metabolism* / Q000494:pharmacology; D015847:Interleukin-4 / Q000378:metabolism* / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D017628:Microglia / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D008854:Microscopy, Electron; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000378:metabolism / Q000494:pharmacology
chemical_list: D005452:Fluoresceins; D005456:Fluorescent Dyes; D005732:Gangliosides; D007364:Intercalating Agents; D018793:Interleukin-13; D008070:Lipopolysaccharides; D016212:Transforming Growth Factor beta; C085925:calcein AM; D015847:Interleukin-4; C018533:ethidium homodimer; D004996:Ethidium