Microbial metabolite effects on TLR to develop autoimmune diseases

Moghadam, Zeinab Mohseni; Hosseini, Hamideh Mahmoodzadeh; Amin, Mohsen; Behzadi, Elham; Fooladi, Abbas Ali Imani

doi:10.1080/15569543.2018.1469512

Cited by 1 publication

(1 citation statement)

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“…Although no evidences are available regarding a direct relationship between GTX and TLRs, a recent review discusses the possible effects of microbial metabolites on TLR expression in the context of autoimmune diseases. According to the authors, microbial toxins elicit the expression of TLRs and pro-inflammatory mediators that upregulate and activate tissue damage, leading to the aggregation of damage-associated molecular patterns that can activate immune cells and result in chronic inflammation and autoimmunity [30].…”

Section: Discussionmentioning

confidence: 99%

Gliotoxin Aggravates Experimental Autoimmune Encephalomyelitis by Triggering Neuroinflammation

Fraga-Silva

Mimura

Leite

et al. 2019

Toxins

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Gliotoxin (GTX) is the major and the most potent mycotoxin that is secreted by Aspergillus fumigatus, which is capable of injuring and killing microglial cells, astrocytes, and oligodendrocytes. During the last years, studies with patients and experimental models of multiple sclerosis (MS), which is an autoimmune disease of the central nervous system (CNS), suggested that fungal infections are among the possible initiators or aggravators of this pathology. The deleterious effect can occur through a direct interaction of the fungus with the CNS or by the toxin release from a non-neurological site. In the present work, we investigated the effect of GTX on experimental autoimmune encephalomyelitis (EAE) development. Female C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein and then intraperitoneally injected with three doses of GTX (1 mg/kg b.w., each) on days 4, 7, and 10. GTX aggravated clinical symptoms of the disease in a dose-dependent way and this outcome was concomitant with an increased neuroinflammation. CNS analyses revealed that GTX locally increased the relative expression of inflammatory genes and the cytokine production. Our results indicate that GTX administered in a non-neuronal site was able to increase neuroinflammation in EAE. Other mycotoxins could also be deleterious to many neurological diseases by similar mechanisms.

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Section: Discussionmentioning

confidence: 99%