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Experimental cutaneous leishmaniasis. II. A possible role for prostaglandins in exacerbation of disease in Leishmania major-infected BALB/c mice.
- Source :
-
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 1987 Feb 01; Vol. 138 (3), pp. 902-7. - Publication Year :
- 1987
-
Abstract
- Leishmania major infection in genetically susceptible BALB/c mice is associated with the development of chronic primary lesions as well as multiple metastatic lesions. Spleen cells from these mice were shown to have depressed in vitro responses to concanavalin A (Con A) that coincided with the development of indomethacin-sensitive suppressor cells. Depressed responses to Con A were noted as early as 1 wk after parasite inoculation and correlated with the increased production of prostaglandin E2 (PGE2) by spleen cells from infected mice. Mice induced by prior irradiation (550 rad) to heal infection did not develop indomethacin-reversible depression in responsiveness to Con A. Although macrophages appear to be the major source of PGE2 production, in vitro studies indicate that infection per se is not a sufficient stimulus to initiate prostaglandin (PG) synthesis, suggesting the involvement of other cell types. Mice treated in vivo with indomethacin exhibited significantly fewer metastatic lesions than control mice, suggesting that PG may play a role in the exacerbation of cutaneous disease in these animals.
- Subjects :
- Animals
Arachidonic Acid
Arachidonic Acids metabolism
Concanavalin A pharmacology
Dinoprostone
Female
Immune Tolerance
Indomethacin pharmacology
Leishmaniasis immunology
Lymphocyte Activation
Macrophages metabolism
Macrophages parasitology
Mice
Mice, Inbred BALB C
Prostaglandins E biosynthesis
Spleen immunology
Spleen metabolism
T-Lymphocytes immunology
Leishmaniasis metabolism
Prostaglandins physiology
Subjects
Details
- Language :
- English
- ISSN :
- 0022-1767
- Volume :
- 138
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Journal of immunology (Baltimore, Md. : 1950)
- Publication Type :
- Academic Journal
- Accession number :
- 3100619