Prostaglandin E2 contributes to L. braziliensis survival and therapeutic failure in cutaneous leishmaniasis
Patients with cutaneous leishmaniasis (CL) present an exacerbated inflammatory response associated with tissue damage and ulcer development. In recent years, higher rates of failure to pentavalent antimoniate therapy have been observed, yet the underlying reason remains poorly understood. We hypothe...
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| Published in: | Emerging microbes & infections Vol. 12; no. 2; p. 2261565 |
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| Abstract | Patients with cutaneous leishmaniasis (CL) present an exacerbated inflammatory response associated with tissue damage and ulcer development. In recent years, higher rates of failure to pentavalent antimoniate therapy have been observed, yet the underlying reason remains poorly understood. We hypothesize that the eicosanoid PGE2 favours the establishment of infection by
, which contributes to therapeutic failure. The aim of the present study was to investigate the influence of PGE2 on the survival of
in macrophages and rates of therapeutic failure in CL patients. PGE2, an eicosanoid derived from the metabolism of arachidonic acid by the COX-2 enzyme, plays several roles in immune response. We found that increased PGE2 decreases the microbicidal function of macrophages and is associated with disease severity and therapeutic failure. Additionally, the neutralization of COX-2 by NS398, a selective NSAID, increases the ability of macrophages to kill
and protects against the pathological inflammatory response. Our data suggest that NS398 may serve as an adjunct treatment for CL patients. |
|---|---|
| AbstractList | Patients with cutaneous leishmaniasis (CL) present an exacerbated inflammatory response associated with tissue damage and ulcer development. In recent years, higher rates of failure to pentavalent antimoniate therapy have been observed, yet the underlying reason remains poorly understood. We hypothesize that the eicosanoid PGE2 favours the establishment of infection by L. braziliensis, which contributes to therapeutic failure. The aim of the present study was to investigate the influence of PGE2 on the survival of L. braziliensis in macrophages and rates of therapeutic failure in CL patients. PGE2, an eicosanoid derived from the metabolism of arachidonic acid by the COX-2 enzyme, plays several roles in immune response. We found that increased PGE2 decreases the microbicidal function of macrophages and is associated with disease severity and therapeutic failure. Additionally, the neutralization of COX-2 by NS398, a selective NSAID, increases the ability of macrophages to kill L. braziliensis and protects against the pathological inflammatory response. Our data suggest that NS398 may serve as an adjunct treatment for CL patients. Patients with cutaneous leishmaniasis (CL) present an exacerbated inflammatory response associated with tissue damage and ulcer development. In recent years, higher rates of failure to pentavalent antimoniate therapy have been observed, yet the underlying reason remains poorly understood. We hypothesize that the eicosanoid PGE2 favours the establishment of infection by L. braziliensis , which contributes to therapeutic failure. The aim of the present study was to investigate the influence of PGE2 on the survival of L. braziliensis in macrophages and rates of therapeutic failure in CL patients. PGE2, an eicosanoid derived from the metabolism of arachidonic acid by the COX-2 enzyme, plays several roles in immune response. We found that increased PGE2 decreases the microbicidal function of macrophages and is associated with disease severity and therapeutic failure. Additionally, the neutralization of COX-2 by NS398, a selective NSAID, increases the ability of macrophages to kill L. braziliensis and protects against the pathological inflammatory response. Our data suggest that NS398 may serve as an adjunct treatment for CL patients. Patients with cutaneous leishmaniasis (CL) present an exacerbated inflammatory response associated with tissue damage and ulcer development. In recent years, higher rates of failure to pentavalent antimoniate therapy have been observed, yet the underlying reason remains poorly understood. We hypothesize that the eicosanoid PGE2 favours the establishment of infection by , which contributes to therapeutic failure. The aim of the present study was to investigate the influence of PGE2 on the survival of in macrophages and rates of therapeutic failure in CL patients. PGE2, an eicosanoid derived from the metabolism of arachidonic acid by the COX-2 enzyme, plays several roles in immune response. We found that increased PGE2 decreases the microbicidal function of macrophages and is associated with disease severity and therapeutic failure. Additionally, the neutralization of COX-2 by NS398, a selective NSAID, increases the ability of macrophages to kill and protects against the pathological inflammatory response. Our data suggest that NS398 may serve as an adjunct treatment for CL patients. |
| Author | Peixoto, Fábio C Carvalho, Edgar M Carvalho, Lucas P Arruda, Sérgio M Nascimento, Maurício T Viana, Débora L |
| Author_xml | – sequence: 1 givenname: Maurício T orcidid: 0000-0002-3791-8048 surname: Nascimento fullname: Nascimento, Maurício T organization: Programa de Pós-Graduação em Ciências da Saúde, PPgCS, Universidade Federal da Bahia, Salvador, Brazil – sequence: 2 givenname: Débora L orcidid: 0000-0003-2342-1935 surname: Viana fullname: Viana, Débora L organization: Laboratório de Pesquisas Clínicas, LAPEC, Instituto Gonçalo Moniz - Fiocruz, Salvador, Brazil – sequence: 3 givenname: Fábio C orcidid: 0000-0003-3804-8192 surname: Peixoto fullname: Peixoto, Fábio C organization: Programa de Pós-Graduação em Ciências da Saúde, PPgCS, Universidade Federal da Bahia, Salvador, Brazil – sequence: 4 givenname: Sérgio M orcidid: 0000-0002-3071-6339 surname: Arruda fullname: Arruda, Sérgio M organization: Laboratório Avançado de Saúde Pública, LASP, Instituto Gonçalo Moniz - Fiocruz, Salvador, Brazil – sequence: 5 givenname: Edgar M orcidid: 0000-0002-2697-8002 surname: Carvalho fullname: Carvalho, Edgar M organization: Instituto de Ciência e Tecnologia em Doenças Tropicais, INCT-DT, Salvador, Brazil – sequence: 6 givenname: Lucas P orcidid: 0000-0001-5033-1666 surname: Carvalho fullname: Carvalho, Lucas P organization: Instituto de Ciência e Tecnologia em Doenças Tropicais, INCT-DT, Salvador, Brazil |
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| SubjectTerms | Cutaneous leishmaniasis Cyclooxygenase 2 - genetics Cyclooxygenase 2 - therapeutic use Dinoprostone Humans inflammation L. braziliensis Leishmania braziliensis Leishmaniasis, Cutaneous - drug therapy Parasitic diseases PGE2 therapeutic failure |
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| Title | Prostaglandin E2 contributes to L. braziliensis survival and therapeutic failure in cutaneous leishmaniasis |
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