Prevention of ultraviolet radiation-induced suppression of contact and delayed hypersensitivity by Aloe barbadensis gel extract

J Invest Dermatol. 1994 Feb;102(2):197-204. doi: 10.1111/1523-1747.ep12371762.

Abstract

We investigated the ability of Aloe barbadensis gel extract to prevent suppression of contact hypersensitivity (CHS) and delayed-type hypersensitivity (DTH) responses in mice by ultraviolet (UV) irradiation. Local immune suppression was induced in C3H mice by exposure to four daily doses of 400 J/m2 UV-B (280-320 nm) radiation from FS40 sunlamps, followed by sensitization with 0.5% fluorescein isothiocyanate (FITC) through the irradiated skin. Topical application of 0.167-1.67% Aloe gel after each irradiation significantly reduced this suppression. Aloe treatment partially preserved the number and morphology of Langerhans and Thy-1+ dendritic epidermal cells in skin, compared to those in the skin of mice given only UVR or UVR plus the vehicle. Experiments using a single (2 kJ/m2) dose of UVR followed by Aloe treatment showed that the effect of Aloe was not due to screening of the UVR. Systemic suppression of DTH to Candida albicans or CHS to FITC was induced in C3H mice exposed to 5 or 10 kJ/m2 UV-B radiation, respectively, on shaved dorsal skin and sensitized 3 d later with a subcutaneous injection of formalin-fixed Candida or FITC painted on unirradiated, ventral skin. Treatment of the UV-irradiated skin with Aloe immediately after irradiation prevented suppression of both DTH to Candida and CHS to FITC. Aloe treatment did not prevent the formation of cyclobutyl pyrimidine dimers in the DNA of UV-irradiated skin or accelerate the repair of these lesions. These studies demonstrate that topical application of Aloe barbadensis gel extract to the skin of UV-irradiated mice ameliorates UV-induced immune suppression by a mechanism that does not involve DNA damage or repair.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenosine Triphosphatases / analysis
  • Adenosine Triphosphatases / metabolism
  • Administration, Topical
  • Aloe*
  • Animals
  • Antigens, Surface / analysis
  • Antigens, Surface / metabolism
  • Candida albicans / physiology
  • DNA / genetics
  • DNA Damage
  • Dendritic Cells / chemistry
  • Dendritic Cells / metabolism
  • Dendritic Cells / pathology
  • Dermatitis, Contact / drug therapy*
  • Dermatitis, Contact / etiology*
  • Dermatitis, Contact / prevention & control*
  • Dose-Response Relationship, Radiation
  • Female
  • Fluorescein-5-isothiocyanate
  • Gels
  • Histocompatibility Antigens Class II / analysis
  • Histocompatibility Antigens Class II / metabolism
  • Hypersensitivity, Delayed / drug therapy*
  • Hypersensitivity, Delayed / etiology*
  • Hypersensitivity, Delayed / prevention & control*
  • Immunosuppression
  • Langerhans Cells / chemistry
  • Langerhans Cells / metabolism
  • Langerhans Cells / pathology
  • Membrane Glycoproteins / analysis
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred C3H
  • Plant Extracts
  • Plants, Medicinal*
  • Radiation Injuries, Experimental / drug therapy*
  • Radiation Injuries, Experimental / prevention & control*
  • Skin / drug effects
  • Skin / pathology
  • Skin / radiation effects
  • Sunscreening Agents / standards
  • Thy-1 Antigens
  • Time Factors
  • Ultraviolet Rays / adverse effects*

Substances

  • Antigens, Surface
  • Gels
  • Histocompatibility Antigens Class II
  • Membrane Glycoproteins
  • Plant Extracts
  • Sunscreening Agents
  • Thy-1 Antigens
  • DNA
  • Adenosine Triphosphatases
  • Fluorescein-5-isothiocyanate