title: Rapamycin enhances IFN-γ and IL-4 production in co-culture of gδ T and dendritic cells from mice with lipopolysaccharide-induced acute lung injury.
abstract: This study aimed to study the role of rapamycin (RAPA) in modulating the interaction between gδ T cells and dendritic cells (DCs) in a lipopolysaccharide (LPS)-induced acute lung injury mouse model. Mice were injected with LPS to establish the acute lung injury model or LPS + RAPA to assess the role of RAPA in modulating cell interactions. Mice were injected with PBS or RAPA alone as controls. gδ T cells and DCs were isolated from all mice and assessed by flow cytometry and fluorescence microscopy. The isolated gδ T cells and DCs were cultured independently or co-cultured to study their interactions. Enzyme-linked immunosorbent assay was performed to assess the expression of the cytokines, namely, interferon (IFN)-γ, interleukin (IL)-4, tumor necrosis factor (TNF)-α and IL-12 in the individually cultured or co-cultured gδ T cells and DCs, and reverse transcription-polymerase chain reaction (RT-PCR) was employed to investigate the levels of relevant mRNAs. Our study found that co-culture of gδ T cells and DCs from mice treated with LPS + RAPA have reduced expression of IFN-γ and IL-4 (but not TNF-α and IL-12) compared to mice treated with LPS only. These results were confirmed by RT-PCR, where the levels of IFN-γ and IL-4 mRNA were also reduced. This study may provide useful information in understanding the interaction between gδ T cells and DCs in the LPS-induced lung injury model in mice.
authors.affiliation: Department of Gerontology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
authors.forename: X L
authors.initials: XL
authors.lastname: Chen
authors.affiliation: Nanlou Respiratory Diseases Department, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China.
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.affiliation: Nanlou Respiratory Diseases Department, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China.
authors.forename: G G
authors.initials: GG
authors.lastname: Xu
authors.affiliation: Nanlou Respiratory Diseases Department, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China.
authors.forename: H X
authors.initials: HX
authors.lastname: Li
authors.affiliation: Nanlou Respiratory Diseases Department, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China.|Department of Respiratory Medicine, Beijing Tsinghua Changgung Hospital, Medical Center, Tsinghua University, Beijing, China.
authors.forename: J
authors.initials: J
authors.lastname: Guo
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000276:immunology*; D000818:Animals; D018920:Coculture Techniques; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology*; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism*; D018664:Interleukin-12 / Q000235:genetics / Q000378:metabolism; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity; D051379:Mice; D008810:Mice, Inbred C57BL; D011971:Receptors, Immunologic / Q000235:genetics / Q000378:metabolism; D020123:Sirolimus / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D007166:Immunosuppressive Agents; D008070:Lipopolysaccharides; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma; D020123:Sirolimus