title: Inhibitory effect of lidocaine on T cells from patients with allergic asthma.
abstract: BACKGROUND
  Nebulized lidocaine enables dosages of oral corticosteroids to be tapered in the treatment of severe asthma.
  
  
  OBJECTIVE
  We sought to investigate the effect of lidocaine on T cells from patients with allergic asthma.
  
  
  METHODS
  PBMCs and CD4(+) T cells were isolated from 6 patients with asthma and house dust mite allergy. PBMCs were cultured with lidocaine for up to 7 days and then stained with propidium iodide to evaluate the involvement of apoptosis. In addition, the viability of CD4(+) T cells when cultured with lidocaine was investigated. Effects of lidocaine on proliferative response, mRNA expression, and protein production of IL-5 and IFN-gamma by PBMCs were investigated after stimulation with Dermatophagoides farinae, purified protein derivative, and phorbol 12-myristate 13-acetate plus calcium ionophore. The effects of lidocaine on the proliferative response of steroid-insensitive PBMCs from 6 nonallergic donors induced by preculture with IL-2 and IL-4 were also investigated.
  
  
  RESULTS
  No significant increase in the staining of PBMCs with propidium iodide was observed in the presence of 100 micromol/L lidocaine. The viability of CD4(+) T cells was not significantly affected by culture with lidocaine at this concentration. However, lidocaine inhibited, in a dose-dependent manner, the proliferative response and mRNA expression and protein production of IL-5 and IFN-gamma of PBMCs stimulated with D farinae, purified protein derivatives, or phorbol 12-myristate 13-acetate plus calcium ionophore. Preincubation of PBMCs with IL-2 and IL-4 significantly decreased the inhibitory effects of both corticosteroids and lidocaine compared with that after preincubation with medium alone.
  
  
  CONCLUSIONS
  Lidocaine has immunoregulatory effects on T cells. Therefore, lidocaine might be studied as an anti-inflammatory agent in the treatment of severe steroid-dependent asthma.
authors.affiliation: First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: Akihiko
authors.initials: A
authors.lastname: Tanaka
authors.forename: Kenji
authors.initials: K
authors.lastname: Minoguchi
authors.forename: Naruhito
authors.initials: N
authors.lastname: Oda
authors.forename: Takuya
authors.initials: T
authors.lastname: Yokoe
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Matsuo
authors.forename: Shinji
authors.initials: S
authors.lastname: Okada
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Tasaki
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Adachi
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001249:Asthma / Q000188:drug therapy / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000502:physiology; D016207:Cytokines / Q000096:biosynthesis; D003907:Dexamethasone / Q000494:pharmacology; D004391:Dust; D006801:Humans; D006967:Hypersensitivity / Q000188:drug therapy / Q000209:etiology / Q000276:immunology*; D008012:Lidocaine / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008925:Mites
chemical_list: D000485:Allergens; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D004391:Dust; D003907:Dexamethasone; D008012:Lidocaine