The monocyte locomotion inhibitory factor inhibits the expression of inflammation‐induced cytokines following experimental contusion in rat tibia

Rojas‐Dotor, Sara; Araujo-Monsalvo, Víctor Manuel; Sánchez‐Rojas, Marco Julio; Domínguez-Hernández, Víctor Manuel

doi:10.1111/sji.12702

Cited by 7 publications

(3 citation statements)

References 28 publications

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“…Activity of MLIF manifests clinically as less invasive intestinal amoebiasis (produced by less virulent strains) [27] , and it is not secreted by commensal E. dispar [28] . Protective effects of MLIF have been demonstrated in rats, where it reduced cellular inflammatory infiltrate and significantly reduced inflammatory cytokines levels in contused tibia [29] . It also protects mice against cerebral malaria [30] .…”

Section: Entamoeba Histolyticamentioning

confidence: 97%

Nuclear factor-kappa B signaling pathways and parasitic infections: An overview

Alhusseiny

El-Beshbishi

2021

Parasitologists United Journal

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Induced transcriptional changes are controlled by NF-κB signaling. Notably, NF-κB was first identified in active B cells by its binding affinity to immunoglobulin κ light-chain gene transcriptional enhancer [2] . Besides, NF-κB serves as dominant modulator of immunoinflammatory responses. Members of NF-κB are usually found in the cytoplasm in a dormant state. Following stimulation of the innate immune receptors, NF-κB becomes activated for nuclear translocation and activation of gene transcription [3] . Its signaling activity is essential for utmost transcription of many inflammatory mediators, chemokines, and cytokines in immune cells. Suppressing the activity of NF-κB signaling can be advantageous in controlling several disease inflammatory processes, including parasitic infections that manipulate NF-κB in different ways. However, constant NF-κB inhibition can be associated with intense adverse effects. Therefore, interpretation of the full dynamics of the pathological consequences of NF-κB activation in different diseases is fundamental [4,5] . Signaling pathwaysFamily members of NF-κB include inducible transcription factors that control an enormous array of genes concerned with inflammation and immunity [6] . There are five structurally related members; NF-κB1 (p50), NF-κB2 (p52), RelA (p65), RelB, and c-Rel, that control target genes transcription by binding to κB enhancer (a peculiar DNA element), as homo-or hetero-dimers [7] . Normally, inhibitory proteins are responsible for cytoplasmic sequestration of NF-κB proteins. These include inhibitor of nuclear factorkappa B (IκB) family members in addition to related proteins, such as inhibitor of NF-κB-α (IκBα) as the most significant inhibitor. It is worth mentioning that IκBα degradation is induced by inhibitor of nuclear factor-kappa B kinase (IKK) complex through sitespecific phosphorylation. It is observed that IKK contains two catalytic subunits: inhibitor of NF-κB kinase-α (IKKα) and inhibitor of NF-κB kinase-β (IKKβ); besides inhibitor of NF-κB kinase-γ (IKKγ), which is a regulatory subunit known as NF-κB essential modulator (NEMO) [8] .Two main pathways activate NF-κB signaling; the classical (canonical) and alternative (non-canonical or atypical) pathways (Figure 1). The first is associated

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Section: Entamoeba Histolyticamentioning

confidence: 97%

Nuclear factor-kappa B signaling pathways and parasitic infections: An overview

Alhusseiny

El-Beshbishi

2021

Parasitologists United Journal

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“…It was first identified as an anti-inflammatory peptide that inhibited the migration of monocytes (Kretschmer et al, 2001;Barrientos-Salcedo et al, 2009; Silva-Garcia and Rico-Rosillo, 2011) and the expression of interleukin (IL)-1β, IL-5, IL-6, and interferon (IFN)-γ and increased the expression of IL-10 in macrophages (Utrera- Barillas et al, 2003;Rojas-Dotor et al, 2006;Silva-Garcia et al, 2008). Subsequent studies showed that MLIF participated in other biological effects, such as expression of immunomodulatory genes (Silva-Garcia et al, 2008;Rojas-Dotor et al, 2018), cell proliferation, extracellular matrix formation, angiogenesis, and axon guidance. In a previous study, we discovered that MLIF exerts a protective effect on the vascular system by acting on eukaryotic elongation factor1A1 (eEF1A1) to upregulate the expression of vascular endothelial nitric oxide synthase (eNOS) and reduce the level of ICAM-1 and VCAM-1 (Zhang et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Anti-Inflammatory Dipeptide, a Metabolite from Ambioba Secretion, Protects Cerebral Ischemia Injury by Blocking Apoptosis Via p-JNK/Bax Pathway

et al. 2021

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MQ (l-methionyl-l-glutamic acid), anti-inflammatory dipeptide, is one of the metabolites of monocyte locomotion inhibitory factor, a thermostable pentapeptide secreted by Entamoeba histolytica. Monocyte locomotion inhibitory factor injection has been approved as an investigational drug for the potential neural protection in acute ischemic stroke. This study further investigated the neuroprotective effect of MQ in ischemic brain damage. Ischemia-reperfusion injury of the brain was induced in the rat model by middle cerebral artery occlusion. 2,3,5-triphenyltetrazolium chloride staining assay was used to measure cerebral infarction areas in rats. Laser Doppler measurement instrument was used to detect blood flow changes in the rat model. Nissl staining and NeuN staining were utilized to observe the numbers and structures of neuron cells, and the pathological changes in the brain tissues were examined by hematoxylin–eosin staining. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) staining was used to assess cell apoptosis. The changes in oxidative stress indexes, superoxide dismutase and malondialdehyde (MDA), were measured in serum. Methyl thiazolyl tetrazolium was used to measure the survival rates of PC12 cells. Flow cytometry assessed the apoptosis rates and the levels of reactive oxygen species. Real-time PCR was used to evaluate the mRNA expression levels, and Western blotting was used to analyze the changes in protein levels of p-JNK, Bax, cleaved Caspase3. We revealed that MQ improved neurobehavior, decreased cerebral infarction areas, altered blood flow volume, and the morphology of the cortex and hippocampus. On the other hand, it decreased the apoptosis of cortical neurons and the levels of MDA, and increased the levels of superoxide dismutase. In vitro studies demonstrated that MQ enhanced the cell survival rates and decreased the levels of reactive oxygen species. Compared to the oxygen-glucose deprivation/reperfusion group, the protein and mRNA expressions of p-JNK, Bax, cleaved Caspase3 was decreased significantly. These findings suggested that MQ exerts a neuroprotective effect in cerebral ischemia by blocking apoptosis via the p-JNK/Bax pathway.

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“…It is with great pleasure that we present the ECI2018 issue of the journal. It contains two discussion forum articles on the concept of immune tolerance, two reviews and four regular articles, which together reflect the scope and the international profile of the Journal. I hope that you will enjoy these papers and that you will continue to follow us and, above all, submit your future papers to the Scandinavian Journal of Immunology .…”

mentioning

confidence: 99%

Dear readers of the Scandinavian Journal of Immunology and ECI 2018 attendees

Höglund¹

2018

Scand J Immunol

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The monocyte locomotion inhibitory factor inhibits the expression of inflammation‐induced cytokines following experimental contusion in rat tibia

Cited by 7 publications

References 28 publications

Nuclear factor-kappa B signaling pathways and parasitic infections: An overview

Nuclear factor-kappa B signaling pathways and parasitic infections: An overview

Anti-Inflammatory Dipeptide, a Metabolite from Ambioba Secretion, Protects Cerebral Ischemia Injury by Blocking Apoptosis Via p-JNK/Bax Pathway

Dear readers of the Scandinavian Journal of Immunology and ECI 2018 attendees

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