Expression of Tim-1 and Tim-3 in Plasmodium berghei ANKA infection

Huang, Bo; Liu, Man; Huang, Shiguang; Wu, Bin; Guo, Hong; Su, Xin-zhuan; Lü, Fangli

doi:10.1007/s00436-013-3442-z

Cited by 13 publications

(7 citation statements)

References 36 publications

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“…The data in the present study showed that approximately 30% of the KM mice with Pb ANKA infection developed to ECM. Our data is consistent with our early report (Huang et al, 2013b), but is contrast to the other report that 100% of Pb ANKA-infected KM mice succumbed to ECM (Ding et al, 2016). It remains an open question that the obvious different incidence of ECM was observed in the same lethal murine malaria model of KM mice infected with Pb ANKA.…”

Section: Discussionsupporting

confidence: 93%

“…This mouse strain was derived from Swiss mice from the Indian Haffkine Institute in 1944 with the characteristics of high disease resistance, good adaptive capacity, high breeding coefficient and good survival rate (Shang et al, 2009). KM mice with Pb ANKA infection have been widely employed to study malaria pathogenesis, and showed high mortality, hyperparasitemia, and pathological lesion in brain, liver or lung tissue) (Huang et al, 2013b; Ding et al, 2016). All mice were housed in pathogen-free environment and received a commercial basal diet and sterile drinking water ad libitum .…”

Section: Methodsmentioning

confidence: 99%

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Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model

Huang

Chen

et al. 2019

Front. Cell. Infect. Microbiol.

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Malaria, a mosquito-borne infectious disease, is a severe health problem worldwide. As reported, some anti-malarial drugs with anti-parasitic properties also block mast cells (MCs) activities. It is hypothesized that MCs activity may be correlated with the pathogenesis of malaria. Thus, the role of MCs on malarial pathogenesis and the involved physiological action and pathways need to be further investigated. This study aimed to investigate the effect of MCs activation on malaria disease severity using KunMing mice with Plasmodium berghei ANKA (PbANKA) infection treated with MCs degranulator (compound 48/80, C48/80) or MCs stabilizer (disodium cromoglycate, DSCG). PbANKA infection caused a dramatic increase in MCs density and level of MCs degranulation in cervical lymph node (CLN) and skin. Compared with infected control, C48/80 treatment had shortened survival time, increased parasitemia, exacerbated liver inflammation and CLN hyperplasia, accompanied with increase in vascular leakage and leukocyte number. The infected mice with C48/80 treatment also elevated the release of CCL2, CXCL1, and MMP-9 from MCs in CLN and skin, and TNF-α, IFN-γ, CCR2, and CXCR2 mRNA expression in CLN and liver. In contrast, the infected mice treated with DSCG showed longer survival time, lower parasitemia, improved liver inflammation and CLN hyperplasia, followed by a decline of vascular leakage and leukocyte number. Decreased MCs-derived CCL2, CXCL1, and MMP-9 from CLN and skin, mRNA expression in CLN and liver (TNF-α, IFN-γ, CCR2, and CXCR2) were also observed in infected mice with DSCG treatment. Our data indicated that MCs activation may facilitate the pathogenesis of PbANKA infection.

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Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model

Huang

Chen

et al. 2019

Front. Cell. Infect. Microbiol.

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“…Previous work from our laboratory has shown that KM mice may be a good alternative animal model for the study of lethal murine malaria (Huang et al 2013). In this study, we successfully constituted a PbANKA-induced ALI in KM mice, dyspnea, or respiratory insufficiency occurred between 18 to 22 days p.i.…”

Section: Discussionmentioning

confidence: 99%

Upregulated Tim-3/galectin-9 expressions in acute lung injury in a murine malarial model

Liu¹,

Xiao²,

Huang³

et al. 2015

Parasitol Res

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Malaria is the most relevant parasitic disease worldwide, and severe malaria is characterized by cerebral edema, acute lung injury (ALI), and multiple organ dysfunctions; however, the mechanisms of lung damage need to be better clarified. In this study, we used Kunming outbred mice infected with Plasmodium berghei ANKA (PbANKA) to elucidate the profiles of T cell immunoglobulin and mucin domain-3 (Tim-3) and its ligand galecin-9 (Gal-9) in the development of ALI. Mice were injected intraperitoneally with 10(6) PbANKA-infected red blood cells. The lungs and mediastinal lymph nodes (MLNs) were harvested at days 5, 10, 15, and 20 post infections (p.i.). The grade of lung injury was histopathologically evaluated. Tim-3- and Gal-9-positive cells in the lungs and MLNs were stained by immunohistochemistry, and the messenger RNA (mRNA) expressions of Tim-3, Gal-9, and related cytokines were assessed using quantitative real-time polymerase chain reaction (qRT-PCR). Bronchoalveolar lavage fluid (BALF) analyses were performed from days 18 to 20 p.i. The results showed that the pathological severities in the lungs were increased with times and the total protein level in the BALFs was significantly elevated in PbANKA-infected mice. The numbers of Gal-9(+) and Tim-3(+) cells in the lungs were significantly increased, and the mRNA levels of both Gal-9 and Tim-3 in the lungs and MLNs were over-expressed in PbANKA-infected mice. In conclusion, our data suggested that Tim-3/Gal-9 may play a role in PbANKA-induced ALI.

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“…The secretion of pro-inflammatory cytokines by these T cells was inversely associated with parasitemia and expression of TIM3 (73). Similarly, TIM3 expression is also significantly increased in mice infected with P. berghei (84, 85). Experimental models have shown upregulation of TIM3 during malaria leads to lymphocyte exhaustion which can be reversed with blockade of TIM3, resulting in the accelerated clearance of parasites and relief from the symptoms of P. berghi –mediated ECM (84).…”

Section: Introductionmentioning

confidence: 93%

The Contribution of Co-signaling Pathways to Anti-malarial T Cell Immunity

et al. 2018

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Plasmodium spp., the causative agent of malaria, caused 212 million infections in 2016 with 445,000 deaths, mostly in children. Adults acquire enough immunity to prevent clinical symptoms but never develop sterile immunity. The only vaccine for malaria, RTS,S, shows promising protection of a limited duration against clinical malaria in infants but no significant protection against severe disease. There is now abundant evidence that T cell functions are inhibited during malaria, which may explain why vaccine are not efficacious. Studies have now clearly shown that T cell immunity against malaria is subdued by multiple the immune regulatory receptors, in particular, by programmed cell-death-1 (PD-1). Given there is an urgent need for an efficacious malarial treatment, compounded with growing drug resistance, a better understanding of malarial immunity is essential. This review will examine molecular signals that affect T cell-mediated immunity against malaria.

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Expression of Tim-1 and Tim-3 in Plasmodium berghei ANKA infection

Cited by 13 publications

References 36 publications

Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model

Activation of Mast Cells Promote Plasmodium berghei ANKA Infection in Murine Model

Upregulated Tim-3/galectin-9 expressions in acute lung injury in a murine malarial model

The Contribution of Co-signaling Pathways to Anti-malarial T Cell Immunity

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