MyD88 in Mycobacterium tuberculosis infection

Cervantes, Jorge

doi:10.1007/s00430-017-0495-0

Cited by 32 publications

(19 citation statements)

References 93 publications

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“…The TB of CNS is probably the most severe type of tuberculosis and in most cases leads to death. Invasion of the CNS by M. tuberculosis is associated with formation of myddosome (see below), disruption of BBB due to cytoskeletal rearrangement in cerebral microvessel endothelial cells (Jain et al, 2006; Cervantes, 2017) and matrix metalloproteinase-mediated degradation of BBB (Green and Friedland, 2007). Tumor necrosis factor (TNF) is a proinflammatory cytokine, which is involved in priming the host immune system against M. tuberculosis infection by activating the innate immunity and maintaining the granulomas structure.…”

Section: Association Of Infectious Diseases With Neuroinflammationmentioning

confidence: 99%

Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

Tohidpour

Моргун

Boitsova

et al. 2017

Front. Cell. Infect. Microbiol.

127

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Neuroinflammation is a complex inflammatory process in the central nervous system, which is sought to play an important defensive role against various pathogens, toxins or factors that induce neurodegeneration. The onset of neurodegenerative diseases and various microbial infections are counted as stimuli that can challenge the host immune system and trigger the development of neuroinflammation. The homeostatic nature of neuroinflammation is essential to maintain the neuroplasticity. Neuroinflammation is regulated by the activity of neuronal, glial, and endothelial cells within the neurovascular unit, which serves as a “platform” for the coordinated action of pro- and anti-inflammatory mechanisms. Production of inflammatory mediators (cytokines, chemokines, reactive oxygen species) by brain resident cells or cells migrating from the peripheral blood, results in the impairment of blood-brain barrier integrity, thereby further affecting the course of local inflammation. In this review, we analyzed the most recent data on the central nervous system inflammation and focused on major mechanisms of neurovascular unit dysfunction caused by neuroinflammation and infections.

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Section: Association Of Infectious Diseases With Neuroinflammationmentioning

confidence: 99%

Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

Tohidpour

Моргун

Boitsova

et al. 2017

Front. Cell. Infect. Microbiol.

127

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“…The Bayesian network analyses refined these relationships while suggesting that TLR2 and TLR4 SNPs may sometimes act combined to increase odds of TST conversion. Both TLR2 and TLR4 are expressed on cell surface and share common intracellular signaling adaptors [33]. Our findings are intriguing and deserve additional investigations to validate the results and narrow down potential interdependency between TLR2 and TLR4 in the immune response against Mtb.…”

Section: Discussionmentioning

confidence: 58%

Polymorphisms in TLR4 and TNFA and Risk of Mycobacterium tuberculosis Infection and Development of Active Disease in Contacts of Tuberculosis Cases in Brazil: A Prospective Cohort Study

Angulo

Arriaga

Silva

et al. 2018

Clinical Infectious Diseases

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Background The role of genetic polymorphisms in latent tuberculosis (TB) infection and progression to active TB is not fully understood. Methods We tested the single-nucleotide polymorphisms (SNPs) rs5743708 (TLR2), rs4986791 (TLR4), rs361525 (TNFA), rs2430561 (IFNG) rs1143627 (IL1B) as risk factors for tuberculin skin test (TST) conversion or development of active TB in contacts of active TB cases. Contacts of microbiologically confirmed pulmonary TB cases were initially screened for longitudinal evaluation up to 24 months, with clinical examination and serial TST, between 1998 and 2004 at a referral center in Brazil. Data and biospecimens were collected from 526 individuals who were contacts of 177 active TB index cases. TST conversion was defined as induration ≥5 mm after a negative TST result (0 mm) at baseline or month 4 visit. Independent associations were tested using logistic regression models. Results Among the 526 contacts, 60 had TST conversion and 44 developed active TB during follow-up. Multivariable regression analysis demonstrated that male sex (odds ratio [OR]: 2.3, 95% confidence interval [CI]: 1.1–4.6), as well as SNPs in TLR4 genes (OR: 62.8, 95% CI: 7.5–525.3) and TNFA (OR: 4.2, 95% CI: 1.9–9.5) were independently associated with TST conversion. Moreover, a positive TST at baseline (OR: 4.7, 95% CI: 2.3–9.7) and SNPs in TLR4 (OR: 6.5, 95% CI: 1.1–36.7) and TNFA (OR: 12.4, 95% CI:5.1–30.1) were independently associated with incident TB. Conclusions SNPs in TLR4 and TNFA predicted both TST conversion and active TB among contacts of TB cases in Brazil.

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“…In addition, MyD88 can activate IκB kinase polymerase chain reaction, and further degrade IκBα. Next NF-κBp65, which has been freed from IκBα, transfers from the cytoplasm to the nucleus ( 20 ). In turn, NF-κBp65 binds to the specific downstream target gene sequence, thus regulating the transcription of associated-target genes.…”

Section: Discussionmentioning

confidence: 99%

An analysis of the expression and function of myeloid differentiation factor 88 in human osteosarcoma

Yang

Jiang

2018

Oncol Lett

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The aim of the present study was to investigate the expression and function of myeloid differentiation factor 88 (MyD88) in osteosarcoma. Immunohistochemical staining was used to detect MyD88 protein in osteosarcoma tissues and matched normal bone tissues. The association between MyD88 expression and the clinical characteristics of patients with osteosarcoma was analyzed. Furthermore, survival analysis of patients with osteosarcoma was performed to study the association between MyD88 expression and patient prognosis. Finally, the effect of the MyD88 inhibitor, ST2825, on the proliferation and apoptosis of the human osteosarcoma cell line U2OS was examined. Additionally, cell proliferation, invasion and apoptosis were examined using an MTT assay, Transwell assay and Annexin V-fluorescein isothiocyanate staining kit, respectively. The expression of proteins associated with the NF-κB signaling pathway was analyzed by western blotting. The positive expression rate of MyD88 in osteosarcoma and normal bone tissues was 71.4 and 6.1%, respectively. Statistical analysis demonstrated that MyD88 was not associated with gender, age, histological type or tumor location, but that it was associated with Enneking stage and tumor metastasis (P<0.05). According to the survival analysis, patients with osteosarcoma in the high MyD88 expression group displayed a reduced overall survival rate (P<0.05). Furthermore, inhibition of MyD88 by ST2825 in U2OS cells resulted in a marked decrease in cellular proliferation and migration, and an increase in the rate of apoptosis (P<0.05). Notably, ST2825 significantly decreased cyclin D1, matrix metallopeptidase-9 and nucleus p65 expression, but increased cleaved-caspase 3 expression in ST2825-treated U2OS cells (P<0.05). The results of the present study indicated that MyD88 expression is associated with the progression of osteosarcoma and may be a potential therapeutic target for the treatment of osteosarcoma.

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MyD88 in Mycobacterium tuberculosis infection

Cited by 32 publications

References 93 publications

Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

Polymorphisms in TLR4 and TNFA and Risk of Mycobacterium tuberculosis Infection and Development of Active Disease in Contacts of Tuberculosis Cases in Brazil: A Prospective Cohort Study

An analysis of the expression and function of myeloid differentiation factor 88 in human osteosarcoma

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