Tumour Necrosis Factor‐alpha (<scp>TNF</scp>‐α) and its soluble receptor type 1 (<scp>sTNFR</scp> I) in human active and healed leishmaniases

Rostami, Mahmoud Nateghi; Jasbi, E; Khamesipour, Ali

doi:10.1111/pim.12305

Cited by 19 publications

(24 citation statements)

References 28 publications

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“…Collectively, it seems that IL‐17a has a dual permissive and protective role during the Leishmania infection. In fact, regulated levels of IL‐17a yield protective immunity against leishmaniasis, whereas extreme levels of this pro‐inflammatory cytokine associate with persistent tissue damage .…”

Section: Discussionsupporting

confidence: 93%

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Comparison of pro‐inflammatory cytokines of non‐healing and healing cutaneous leishmaniasis

et al. 2017

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Cutaneous leishmaniasis (CL) heals spontaneously within several weeks or months, but, in rare cases, CL-active lesions last for many years. In this study, we assessed cell-mediated immunity in non-healing CL through the measurement of three pro-inflammatory cytokines: Interferon-γ (IFN-γ), IL-17a and CXCL-11. For this, 32 patients afflicted with healing or non-healing CL were recruited in this study. Peripheral blood mononuclear cells (PBMCs) of every patient were treated with three antigens: purified protein derivative (PPD), soluble Leishmania antigen (SLA) and phytohaemagglutinin (PHA). Cytokine quantification was performed using enzyme-linked immunosorbent assay (ELISA) method. Results of our study showed that neither cytokine produced in the presence of a PPD stimulator (as an irrelevant antigen) significantly differed between the healing and non-healing groups (P-value ≥0.05 for all of them). However, IFN-γ, CXCL-11 and IL-17a levels produced in the presence of PHA or SLA were significantly higher within the healing than in the non-healing group (P-value <0.01 for all of them). It seems that appropriate levels of IFN-γ, as well as IL-17a and CXCL-11, contribute to the control of Leishmania infection.

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Section: Discussionsupporting

confidence: 93%

“…Leishmanicidal activity of IFN‐ γ is, however, supported by IL‐17a cytokine produced by TH17 cells. These cells protect mucosal and skin tissue of Leishmania ‐infected mice through neutrophil and monocyte recruitment .…”

Section: Introductionmentioning

confidence: 93%

Comparison of pro‐inflammatory cytokines of non‐healing and healing cutaneous leishmaniasis

et al. 2017

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“…Duthie and coworkers [50] have shown that both IL-10 and IL-17 cytokines are elevated in the serum of active VL patients, reverting to baseline levels with standard antimonial treatments. AHR activation has also been shown to inhibit inflammation through upregulation of IL-22 [52], another cytokine that has been shown to be significantly higher in Leishmania antigen stimulated peripheral blood mononuclear cells from active VL cases compared to treated cases [53]. AHR activation during VL may underpin the complex regulation of pro- and anti-inflammatory responses during disease pathogenesis and during response to therapy.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Blood Signatures for Active and Amphotericin B Treated Visceral Leishmaniasis in India

Blackwell

Fakiola

Singh

et al. 2019

Preprint

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31Amphotericin B provides improved therapy for visceral leishmaniasis (VL) caused by 32 Leishmania donovani, with single dose liposomal-encapsulated Ambisome providing the best 33 cure rates. The VL elimination program aims to reduce the incidence rate in the Indian 34 subcontinent to <1/10,000 population/year. Ability to predict which asymptomatic 35 individuals (e.g. anti-leishmanial IgG and/or Leishmania-specific modified Quantiferon 36 positive) will progress to clinical VL would help in monitoring disease outbreaks. Here we 37 examined whole blood transcriptional profiles associated with asymptomatic infection, active 38 disease, and in treated cases. Two independent microarray experiments were performed, with 39 analysis focussed primarily on differentially expressed genes (DEGs) concordant across both 40 experiments. No DEGs were identified for IgG or Quantiferon positive asymptomatic groups 41 compared to negative healthy endemic controls. We therefore concentrated on comparing 42 concordant DEGs from active cases with all healthy controls, and in examining differences in 43 the transcriptome following different regimens of drug treatment. In these comparisons 6 44 major themes emerged: (i) expression of genes and enrichment of gene sets associated with 45 erythrocyte function in active cases; (ii) strong evidence for enrichment of gene sets involved 46 in cell cycle in comparing active cases with healthy controls; (iii) identification of IFNG 47 encoding interferon- as the major hub gene in concordant gene expression patterns across 48 experiments comparing active cases with healthy controls or with treated cases; (iv) 49 enrichment for interleukin signalling (IL-1/3/4/6/7/8) and a prominent role for CXCL10/9/11 50 and chemokine signalling pathways in comparing active cases with treated cases; (v) the 51 novel identification of Aryl Hydrocarbon Receptor signalling as a significant canonical 52 pathway when comparing active cases with healthy controls or with treated cases; and (vi) 53 global expression profiling support for more effective cure at day 30 post-treatment with a 3 54 single dose of liposomal encapsulated amphotericin B compared to multi-dose non-liposomal 55 amphotericin B treatment over 30 days. (296 words; 300 words allowed) 56 57 Author Summary 58 Visceral leishmaniasis (VL), also known as kala-azar, is a potentially fatal disease caused by 59 intracellular parasites of the Leishmania donovani species complex. VL is a serious public 60 health problem in rural India, causing high morbidity and mortality, as well as major costs to 61 local and national health budgets. Amphotericin B provides improved therapy for VL with 62 single dose liposomal-encapsulated Ambisome, now affordable through WHO-negotiated 63price reductions, providing the best cure rates. The VL elimination program aims to reduce 64 the incidence rate in the Indian subcontinent to <1/10,000 population/year. By assessing 65 immune responses to parasites in people infected with L. donovani, but with different clinical 66 s...

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“…Europe (KAYE and SCOTT, 2011;NATEGHI ROSTAMI et al, 2016). Though, more than 90% of potentially fatal infections occur in just six regions: Brazil, Ethiopia, Sudan, South Sudan, India and Bangladesh (PIGOTT et al, 2014).…”

Section: Leishmaniases: Life Cycle Clinical Manifestations and Chemomentioning

confidence: 99%

“…Europe (KAYE and SCOTT, 2011;NATEGHI ROSTAMI et al, 2016). The intracellular localization of leishmaniases parasites hinders access of the chemotherapy to the site of action.…”

Section: Introductionmentioning

confidence: 99%

Buparvaquone nanostructured lipid carrier development: physicochemical and <i>in vitro</i> leishmanicidal performances

Monteiro¹

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Tumour Necrosis Factor‐alpha (TNF‐α) and its soluble receptor type 1 (sTNFR I) in human active and healed leishmaniases

Cited by 19 publications

References 28 publications

Comparison of pro‐inflammatory cytokines of non‐healing and healing cutaneous leishmaniasis

Comparison of pro‐inflammatory cytokines of non‐healing and healing cutaneous leishmaniasis

Transcriptional Blood Signatures for Active and Amphotericin B Treated Visceral Leishmaniasis in India

Buparvaquone nanostructured lipid carrier development: physicochemical and <i>in vitro</i> leishmanicidal performances

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