title: Effects of thymol and carvacrol on T-helper cell subset cytokines and their main transcription factors in ovalbumin-immunized mice.
abstract: Thymol and carvacrol, two main components of thyme, have several valuable effects on the immune system. This study aims to evaluate the effects of these components on T-helper (TH) cell responses and their subsets in mice immunized with ovalbumin. The effects of these components on: a specific in vivo immune response were evaluated by assessing changes in delayed-type hypersensitivity (DTH); ex vivo splenocyte proliferative responses were evaluated using a BrdU assay gene expression of cytokines and key transcription factors involved in T-cells subset differentiation among the mouse splenocytes were assessed using real-time polymerase chain reaction (PCR); and splenocyte cytokine formation (ex vivo) and levels of the cytokines in mouse sera were measured by ELISA. Mice treated with thymol or carvacrol had reduced DTH responses (26% and 50%, respectively) compared with control mice. Thymol and carvacrol each diminished splenocyte proliferation to nearly 65-72% of control levels (p < 0.01). These agents also led to decreased TH1 [interleukin (IL)-2, interferon (IFN)-γ)], TH2 (IL-4) and TH17 (IL-17A) levels in the splenocyte cultures and in the sera of mice but increased levels of IL-10 and transforming growth factor (TGF)-β. Treated immunized mice showed significantly reduced T-box 21 (T-bet) expression from 3.8 [± 0.3]-fold in untreated ovalbumin-immunized mice to 0.9 [± 0.4]-(thymol) and 0.8 [± 0.2]-fold (carvacrol) (p < 0.01). GATA binding protein 3 (GATA-3) expression declined from 3.4 [± 0.4]- to 0.5 [± 0.3]-fold (thymol) and 0.6 [± 0.4]-fold (carvacrol), whereas RORγc decreased from 13.4 [± 1.6]- to 1.5 [± 0.6]-fold (thymol) and 0.8 [± 0.4]-fold (carvacrol) (p < 0.001). As carvacrol and thymol each suppressed the antigen-specific immune response by reducing TH cell-related cytokines\specific transcription factors, this indicated their potential to modulate destructive immune responses attributed to T-cells over-activation.
authors.affiliation: a Autoimmune Disease Research Center, Shiraz University of Medical Sciences , Shiraz , Iran ;
authors.forename: Nasser
authors.initials: N
authors.lastname: Gholijani
authors.affiliation: b Department of Immunology and Medicinal and Natural Products Chemistry Research Center , Shiraz University of Medical Sciences , Shiraz , Iran.
authors.forename: Zahra
authors.initials: Z
authors.lastname: Amirghofran
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D049109:Cell Proliferation; D002478:Cells, Cultured; D000081007:Cymenes; D016207:Cytokines / Q000378:metabolism; D050990:GATA3 Transcription Factor / Q000235:genetics / Q000378:metabolism; D006968:Hypersensitivity, Delayed / Q000188:drug therapy* / Q000276:immunology; D007114:Immunization; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D039821:Monoterpenes / Q000627:therapeutic use*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000378:metabolism; D010047:Ovalbumin / Q000276:immunology; D020825:T-Box Domain Proteins / Q000235:genetics / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects* / Q000276:immunology; D013943:Thymol / Q000627:therapeutic use*; D046930:Thymus Plant / Q000276:immunology*; D015533:Transcriptional Activation; D000098815:T-bet Transcription Factor
chemical_list: D000941:Antigens; D000081007:Cymenes; D016207:Cytokines; D050990:GATA3 Transcription Factor; D039821:Monoterpenes; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D013943:Thymol; D010047:Ovalbumin; C073316:carvacrol
keywords: Carvacrol; T-helper cells; immunization; immunomodulation; ovalbumin; thymol