The HFE genotype and a formulated diet controlling for iron status attenuate experimental cerebral malaria in mice

Leitner, Dominique F.; Stoute, José A.; Landmesser, Mary E.; Neely, Elizabeth B.; Connor, James R.

doi:10.1016/j.ijpara.2015.07.003

Cited by 7 publications

(11 citation statements)

References 75 publications

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“…For example, Sema4A regulates proper retina formation [29], correct guidance of hippocampal neurons [30], angiogenesis [18,31], and adaptive immune response [12,13,14,16,19]. On the other hand, the Sema4A pathways are dysregulated in different diseases such as retinal degenerative diseases (retinitis pigmentosa type 35 and cone-rod dystrophy type 10) [29], allergy [10,14,19,22,23], infectious [14,32] and autoimmune diseases [14,26,28], and certain types of cancer [16,33]. The individual impact of each Sema4A-receptor pair in disease pathogenesis and/or progression needs to be dissected separately for the whole picture of Sema4A impact to be envisioned.…”

Section: Introductionmentioning

confidence: 99%

Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation: A Promoter or a Suppressor?

Iyer

Chapoval

2018

IJMS

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Neuroimmune semaphorin 4A (Sema4A), a member of semaphorin family of transmembrane and secreted proteins, is an important regulator of neuronal and immune functions. In the nervous system, Sema4A primarily regulates the functional activity of neurons serving as an axon guidance molecule. In the immune system, Sema4A regulates immune cell activation and function, instructing a fine tuning of the immune response. Recent studies have shown a dysregulation of Sema4A expression in several types of cancer such as hepatocellular carcinoma, colorectal, and breast cancers. Cancers have been associated with abnormal angiogenesis. The function of Sema4A in angiogenesis and cancer is not defined. Recent studies have demonstrated Sema4A expression and function in endothelial cells. However, the results of these studies are controversial as they report either pro- or anti-angiogenic Sema4A effects depending on the experimental settings. In this mini-review, we discuss these findings as well as our data on Sema4A regulation of inflammation and angiogenesis, which both are important pathologic processes underlining tumorigenesis and tumor metastasis. Understanding the role of Sema4A in those processes may guide the development of improved therapeutic treatments for cancer.

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Section: Introductionmentioning

confidence: 99%

Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation: A Promoter or a Suppressor?

Iyer

Chapoval

2018

IJMS

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“…104 In addition, in a mouse model with an HFE H63D mutation, increased survival over wild-type mice was observed following an infection with Plasmodium falciparum , a parasite that causes cerebral malaria. 105 Besides being critical for micro-organismal growth, intramacrophage iron levels influence the inflammatory state of macrophages. While reduced iron levels attenuate the inflammatory response of macrophages to Salmonella infection or LPS-stimulation, 106 increased iron levels trigger a phenotypic switch of macrophages towards a pro-inflammatory state.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiological consequences and benefits of HFE mutations: 20 years of research

Hollerer

Bachmann²,

Muckenthaler

2017

Haematologica

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Mutations in the HFE (hemochromatosis) gene cause hereditary hemochromatosis, an iron overload disorder that is hallmarked by excessive accumulation of iron in parenchymal organs. The HFE mutation p.Cys282Tyr is pathologically most relevant and occurs in the Caucasian population with a carrier frequency of up to 1 in 8 in specific European regions. Despite this high prevalence, the mutation causes a clinically relevant phenotype only in a minority of cases. In this review, we summarize historical facts and recent research findings about hereditary hemochromatosis, and outline the pathological consequences of the associated gene defects. In addition, we discuss potential advantages of HFE mutations in asymptomatic carriers.

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“…Nine common genes were found shared between WGCNA and Limma (Figure 3C and Table 1). Within the nine genes, five genes (MBP, SAMSN1, PSMF1, SLC39A8, and EIF3B) were previously found to be involved in malaria, 10–14 and the remaining four genes (SMPDL3A, FABP5, SPSB3, and SHARPIN) were identified for the first time in the current study. SAMSN1, SLC39A8, SMPDL3A, and FABP5 were positively correlated with malaria phenotype/severity and showed an upregulation in the CM group compared with healthy controls, while MBP, SPSB3, PSMF1, SHARPIN, EIF3B were negatively correlated with malaria severity and downregulated in the DEG (Figure 3C and Table ).…”

Section: Resultsmentioning

confidence: 56%

Genomic analysis of host gene responses to cerebral Plasmodium falciparum malaria

Han

Zhang

et al. 2021

Immunity Inflam & Disease

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Introduction A vaccine for malaria is urgently required but no vaccine has yet shown satisfactory protective efficacy especially for Plasmodium falciparum. P. falciparum infection can progress to cerebral malaria (CM), a neurological syndrome with exceedingly high mortality. Designing effective P. falciparum vaccines require more understanding of the protective immune response while the host immune response to CM and the mechanisms are still elusive. Here, we aim to identify host gene responses to CM and host gene networks associated with CM pathogenesis. Methods An innovative genomic analysis strategy, the weighted gene coexpression network analysis (WGCNA) combined with differential gene expression analysis, was used in this study. Data for analysis contain 93 whole blood samples, derived from two previous public transcriptome datasets. Results This approach led to the identification of numerous differentially expressed human transcripts and dozens of coexpression gene modules. We further identified nine key genes, including MBP, SAMSN1, PSMF1, SLC39A8, EIF3B, SMPDL3A, FABP5, SPSB3, and SHARPIN, of which the last four genes were first identified to be related to CM in the present study. Conclusion The results provided a comprehensive characterization of host gene expression profiles in CM and offered some new insight into malaria vaccine design. These identified key genes could be potential targets or immune modulators for novel therapeutic interventions of CM.

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The HFE genotype and a formulated diet controlling for iron status attenuate experimental cerebral malaria in mice

Cited by 7 publications

References 75 publications

Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation: A Promoter or a Suppressor?

Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation: A Promoter or a Suppressor?

Pathophysiological consequences and benefits of HFE mutations: 20 years of research

Genomic analysis of host gene responses to cerebral Plasmodium falciparum malaria

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