Interleukin-27 Regulates Adaptative Immune Responses Associated With Control of Parasite Replication in Canine Leishmaniasis.

Interleukin 27 (IL-27) is a cytokine that regulates susceptibility to Leishmania infantum infection in humans and experimental models. This cytokine has not yet been described in canine leishmaniasis (CanL). Therefore, we investigated whether IL-27 has a regulatory role in CanL.

Leishmania infantum infection modulates messenger RNA, microRNA and long non-coding RNA expression in human neutrophils in vitro.

In the Americas, L. infantum (syn. chagasi) is the main cause of human visceral leishmaniasis.

MicroRNA-194 regulates parasitic load and IL-1β-dependent nitric oxide production in the peripheral blood mononuclear cells of dogs with leishmaniasis.

Domestic dogs are the primary urban reservoirs of Leishmania infantum, the causative agent of visceral leishmaniasis. In Canine Leishmaniasis (CanL), modulation of the host's immune response may be associated with the expression of small non-coding RNAs called microRNA (miR). miR-194 expression increases in peripheral blood mononuclear cells (PBMCs) of dogs with leishmaniasis with a positive correlation with the parasite load and in silico analysis demonstrated that the TRAF6 gene is the target of miR-194 in PBMCs from diseased dogs.

MiR-150 regulates the Leishmania infantum parasitic load and granzyme B levels in peripheral blood mononuclear cells of dogs with canine visceral leishmaniosis.

Leishmania infantum causes visceral leishmaniosis, a neglected tropical disease that can modulate the host immune response by altering the expression of small non-coding RNAs called microRNAs (miRNAs). Some miRNAs are differentially expressed in peripheral blood mononuclear cells (PBMCs) of dogs with canine visceral leishmaniosis (CanL), like the down-regulated miR-150. Even though miR-150 is negatively correlated with L.

MicroRNA-21 and microRNA-148a affects PTEN, NO and ROS in canine leishmaniasis.

Canine Visceral leishmaniasis (CanL) poses a severe public health threat in several countries. Disease progression depends on the degree of immune response suppression. MicroRNAs (miRs) modulate mRNA translation into proteins and regulate various cellular functions and pathways associated with immune responses.

miR-148a regulation interferes in inflammatory cytokine and parasitic load in canine leishmaniasis.

Canine leishmaniasis (CanL) is a severe public health threat. Infected animals mediate transmission of the Leishmania protozoan to humans via the sandfly's bite during a blood meal. CanL progression depends on the degree of suppression of the immune response, possibly associated with microRNAs (miR), which can modulate mRNA translation into proteins and (consequently) regulate cell function.

miRNA-21 regulates CD69 and IL-10 expression in canine leishmaniasis.

Visceral leishmaniasis in humans is a chronic and fatal disease if left untreated. Canine leishmaniasis (CanL) is a severe public health problem because infected animals are powerful transmitters of the parasite to humans via phlebotomine vectors. Therefore, dogs are an essential target for control measures.

Vitamins A and D and Zinc Affect the Leshmanicidal Activity of Canine Spleen Leukocytes.

Canine leishmaniasis (CanL) is a chronic disease caused by , and the limitations of the current treatments have encouraged new alternatives, such as the use of immunomodulatory nutrients. The objective of this study was to determine the serum levels of vitamin A (retinol), vitamin D (25(OH)VD), and zinc (Zn) in dogs with CanL and the effect of in vitro supplementation with the respective active forms ATRA, 1,25(OH)VD, and SZn on spleen leukocyte cultures. Serum retinol, 25(OH)VD, and Zn were determined by HPLC, ELISA, and ICP-MS, respectively.

Blocking IL-10 signaling with soluble IL-10 receptor restores in vitro specific lymphoproliferative response in dogs with leishmaniasis caused by Leishmania infantum.

rIL-10 plays a major role in restricting exaggerated inflammatory and immune responses, thus preventing tissue damage. However, the restriction of inflammatory and immune responses by IL-10 can also favor the development and/or persistence of chronic infections or neoplasms. Dogs that succumb to canine leishmaniasis (CanL) caused by L.

Regulatory effect of PGE on microbicidal activity and inflammatory cytokines in canine leishmaniasis.

Canine leishmaniasis (CanL) is caused by the intracellular parasite Leishmania infantum. Prostaglandin E2 (PGE ) exerts potent regulatory effects on the immune system in experimental model Leishmania infection, but this influence has not yet been studied in CanL. In this study, PGE and PGE receptor levels and the regulatory effect of PGE on arginase activity, NO , IL-10, IL-17, IFN-γ, TNF-α and parasite load were evaluated in cultures of splenic leucocytes obtained from dogs with CanL in the presence of agonists and inhibitors.

Combined in vitro IL-12 and IL-15 stimulation promotes cellular immune response in dogs with visceral leishmaniasis.

Domestic dogs are the main reservoir of Leishmania infantum, a causative agent of visceral leishmaniasis (VL). The number of human disease cases is associated with the rate of canine infection. Currently available drugs are not efficient at treating canine leishmaniasis (CanL) and months after the treatment most dogs show disease relapse, therefore the development of new drugs or new therapeutic strategies should be sought.

Induction of miR 21 impairs the anti-Leishmania response through inhibition of IL-12 in canine splenic leukocytes.

Visceral Leishmaniasis is a chronic zoonosis and, if left untreated, can be fatal. Infected dogs have decreased cellular immunity (Th1) and develop a potent humoral response (Th2), which is not effective for elimination of the protozoan. Immune response can be modulated by microRNAs (miRNAs), however, characterization of miRNAs and their possible regulatory role in the spleen of infected dogs have not been done.

PD-1 regulates leishmanicidal activity and IL-17 in dogs with leishmaniasis.

Leishmaniasis is an immunosuppressive disease caused by protozoa of the genus Leishmania, for which dogs are the domestic reservoir. The programmed cell death-1 molecule (PD-1) is highly expressed in leukocyte cells of dogs with leishmaniasis, and it promotes T lymphocyte exhaustion and suppression of cytokine secretion. Because PD-1 has a suppressive function regarding cell immunity, we evaluated the effect of PD-1 blocking antibodies on NO, ROS and interleukin 17 (IL-17) production and on parasite load in spleen leukocyte cultures from dogs with leishmaniasis.

Plasmonic rK28 ELISA improves the diagnosis of canine Leishmania infection.

In this study, we evaluated the performance of a new enzyme-linked immunosorbent assay (ELISA) variant known as indirect "plasmonic ELISA" (pELISA) for the detection of Leishmania spp. infection. Serum samples from 170 dogs from an area where canine leishmaniosis (CanL) is endemic and from 26 healthy dogs from a nonendemic area were tested by indirect pELISA, and the results were compared to those of an indirect ELISA (both with recombinant antigen rK28) and those of an immunochromatographic test (dual-path platform, TR-DPP®) using real-time PCR on blood samples or conjunctival swabs as the gold standard.

Development of plasmonic ELISA for the detection of anti-Leishmania sp. IgG antibodies.

Recently, a novel Enzyme-Linked Immunosorbent Assay (ELISA) strategy has emerged, known as "plasmonic ELISA" (pELISA), which enables the detection of disease biomarkers at low concentrations with the naked eye. For the first time, this research has developed a signal-generation mechanism for the detection of anti-Leishmania sp. IgG antibodies with the naked eye using pELISA.

Eosinophilic inflammation in lymph nodes of dogs with visceral leishmaniasis.

Eosinophils are traditionally associated with the immune response against helminth parasites. However, several studies have demonstrated that these cells have a role regarding protective immunity in leishmaniasis. Here, we examined the relationship between the presence of eosinophils and parasite load in biopsy samples from dogs, obtained through fine needle puncture and aspiration of lymph nodes.