Open AccessA role for prostaglandins in the suppression of cutaneous cellular immunity and tumour development in benzo(a)pyrene‐ but not dimethylbenz(a)anthracene‐treated mice
Author(s) -
ANDREWS F. J.,
HALLIDAY G. M.,
MULLER H. K.
Publication year - 1991
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1991.tb05674.x
Subject(s) - dmba , 7,12 dimethylbenz[a]anthracene , benzo(a)pyrene , carcinogen , immune system , carcinogenesis , prostaglandin , immunology , prostaglandin e , prostaglandin e2 , immunity , cellular immunity , chemistry , endocrinology , ratón , anthracene , pharmacology , medicine , cancer , biochemistry , organic chemistry
SUMMARY Prostaglandins have been implicated in the immune suppression associated with the development of some tumours. Application of the prostaglandin synthetase inhibitor indomethacin, to murinc skin prior to treatment with the chemical carcinogens benzo(a)pyrene (BP) or 7 , 12 dimethylbenz(a)anthracene (DMBA), restored contact sensitivity responses to 2 ,4‐dinitrofluorobenzene in BP‐ but not DM BA‐treated mice. However, indomethacin failed to restore antibody responses in either group of mice. Prolonged treatment with BP or DMBA led to cutaneous tumour formation. Indomethacin was found to delay the onset and reduce the size of tumours in BP‐ but not DM BA‐treated mice. It is proposed that prostaglandin‐induced suppression of cellular cutaneous immunity may play a role in BP‐ but not DMBA‐induced cutaneous carcinogenesis.