title: Immunomodulatory effects of Pteridium aquilinum on natural killer cell activity and select aspects of the cellular immune response of mice.
abstract: Pteridium aquilinum (bracken fern) is one of the most common plants. Epidemiological studies have revealed a higher risk of certain types of cancers (i.e., esophageal, gastric) in people who consume bracken fern directly (as crosiers or rhizomes) or indirectly through the consumption of milk from livestock that fed on the plant. In animals, evidence exists regarding the associations between chronic bracken fern intoxication, papilloma virus infection, and the development of carcinomas. While it is possible that some carcinogens in bracken fern could be responsible for these cancers in both humans and animals, it is equally plausible that the observed increases in cancers could be related to induction of an overall immunosuppression by the plant/its various constituents. Under the latter scenario, normal tumor surveillance responses against nascent (non-bracken-induced) cancers or responses against viral infections (specifically those linked to induction of cancers) might be adversely impacted by continuous dietary exposure to this plant. Therefore, the overall objective of this study was to evaluate the immunomodulatory effects of bracken fern following daily ingestion of its extract by a murine host over a period of 14 (or up to 30) days. In C57BL/6 mice administered (by gavage) the extract, histological analyses revealed a significant reduction in splenic white pulp area. Among a variety of immune response parameters/functions assessed in these hosts and isolated cells, both delayed-type hypersensitivity (DTH) analysis and evaluation of IFNgamma production by NK cells during T(H)1 priming were also reduced. Lastly, the innate response in these hosts-assessed by analysis of NK cell cytotoxic functionality-was also diminished. The results here clearly showed the immunosuppressive effects of P. aquilinum and that many of the functions that were modulated could contribute to the increased risk of cancer formation in exposed hosts.
authors: Department of Pathology, Faculty of Veterinary Medicine and Animal Sciences, University of Sao Paulo, Brazil.
authors: Andréia Oliveira
authors: AO
authors: Latorre
authors: Maria Stella
authors: MS
authors: Furlan
authors: Mônica
authors: M
authors: Sakai
authors: Heidge
authors: H
authors: Fukumasu
authors: Isis Machado
authors: IM
authors: Hueza
authors: Mitsue
authors: M
authors: Haraguchi
authors: Silvana Lima
authors: SL
authors: Górniak
mesh_terms: D000818:Animals; D003602:Cytotoxicity, Immunologic; D004198:Disease Susceptibility; D007121:Immunocompetence; D007155:Immunologic Factors / Q000008:administration & dosage / Q000009:adverse effects; D007157:Immunologic Surveillance; D007165:Immunosuppression Therapy; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010936:Plant Extracts / Q000008:administration & dosage / Q000009:adverse effects; D032498:Pteridium / Q000009:adverse effects / Q000276:immunology*; D013154:Spleen / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology
chemical_list: D007155:Immunologic Factors; D010936:Plant Extracts; D007371:Interferon-gamma