EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

Indomethacin treatment slows disease progression and enhances a Th1 response in susceptible BALB/c mice infected with Leishmania major



Indomethacin treatment slows disease progression and enhances a Th1 response in susceptible BALB/c mice infected with Leishmania major



Parasite Immunology 21(5): 273-277



Prostaglandins of the E series inhibit the development of Th1 responses. When infected with Leishmania major, BALB/c mice fail to develop a Th1 response, but instead mount a Th2 response and die of the disease. Therefore, we treated L. major-infected BALB/c mice with indomethacin, which inhibits prostaglandin production. Indomethacin lessened disease severity (parasite burden and pathology), and promoted a Th1 response, but the mice still succumbed to infection. The explanation for these observations may be two-fold: (1) the beneficial effects of indomethacin were predominantly observed later in infection (beyond two weeks), a time at which indomethacin was unable to sufficiently block the development of a Th2 response; (2) indomethacin was unable to induce a Th1 response in BALB/c mice that was of the same magnitude as the Th1 response observed in C57BL/6 mice infected with L. major.

(PDF emailed within 0-6 h: $19.90)

Accession: 003172474

Download citation: RISBibTeXText

PMID: 10320625

DOI: 10.1046/j.1365-3024.1999.00211.x



Related references

Flt3 ligand induces skin dendritic cells and is protective against disease progression in susceptible BALB/C mice infected with Leishmania major. Journal of Investigative Dermatology 112(4): 524, April, 1999

IL-1alpha promotes Th1-differentiation and inhibits disease progression in Leishmania major-susceptible BALB/c mice. Journal of Investigative Dermatology 121(5): 1234, November, 2003

In vitro indomethacin administration upregulates interleukin-12 production and polarizes the immune response towards a Th1 type in susceptible BALB/c mice infected with Leishmania mexicana. Parasite Immunology 23(11): 599-606, 2001

Interleukin 1alpha promotes Th1 differentiation and inhibits disease progression in Leishmania major-susceptible BALB/c mice. Journal of Experimental Medicine 198(2): 191-199, 2003

Interleukin-6 deficiency influences cytokine expression in susceptible BALB mice infected with Leishmania major but does not alter the outcome of disease. Infection and Immunity 69(8): 5189-5192, 2001

Protective effect of isoprinosine in genetically susceptible BALB/c mice infected with Leishmania major. Immunology 74(1): 25-30, 1991

Pre-exposure with low-dose UVA suppresses lesion development and enhances Th1 response in BALB/c mice infected with Leishmania (Leishmania) amazonensis. Journal of Dermatological Science 26(3): 217-232, 2001

Coexistence of antigen-specific TH1 and TH2 cells in genetically susceptible BALB/c mice infected with Leishmania major. Immunobiology 179(4-5): 412-421, 1989

Treatment with cathepsin L inhibitor potentiates Th2-type immune response in Leishmania major-infected BALB/c mice. International Immunology 13(8): 975-982, 2001

Effect of T-lymphocyte suppression on the parasite burden in Leishmania major-infected, genetically susceptible BALB/c mice. Infection and Immunity 54(3): 909-912, 1986

Recombinant murine IL-12 alters immunoreactive iNOS in lesions of Leishmania major-infected susceptible Balb/c mice. FASEB Journal 11(3): A333, 1997

Leishmania major H-line attenuated under pressure of gentamicin, induces a Th1 response which protects susceptible BALB/c mice against infection with virulent L. major. Parasitology 136(11): 1243-1250, 2009