LBP and CD14 Secreted in Tears by the Lacrimal Glands Modulate the LPS Response of Corneal Epithelial Cells

Blais, David R.; Vascotto, Sandy G.; Griffith, May; Altosaar, Illimar

doi:10.1167/iovs.05-0543

Cited by 64 publications

(54 citation statements)

References 48 publications

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“…TLR3 and TLR5, which are activated by double-stranded RNA and bacterial flagellin, respectively, are also present and functional in human corneal epithelial cells (16,22,38) Although TLR9 has not been described in human corneal epithelial cells, TLR9 activation in the mouse cornea induces keratitis (15) and TLR9 short interfering RNA reduces the severity of Pseudomonas aeruginosa keratitis (12). In contrast, there are conflicting reports of the role of TLR4 in the cornea; two reports indicate it is nonfunctional due to either an intracellular location or the absence of costimulatory molecules (1,35), whereas another report shows that TLR4 is functional (31). The underlying difference for this discrepancy is not clear, but LPS can induce keratitis in murine and rabbit models of epithelial abrasion (15,18,28).…”

Section: Vol 74 2006 Tlr2 and Myd88 In S Aureus Keratitis 5329mentioning

confidence: 99%

Staphylococcus aureus -Induced Corneal Inflammation Is Dependent on Toll-Like Receptor 2 and Myeloid Differentiation Factor 88

Sun¹,

Hise

Kalsow³

et al. 2006

Infect Immun

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Toll-like receptors (TLRs) expressed by the corneal epithelium represent a first line of host defense to microbial keratitis. The current study examined the role of TLR2, TLR4, and TLR9 and the common adaptor molecule myeloid differentiation factor 88 (MyD88) in a Staphylococcus aureus model of corneal inflammation. The corneal epithelia of C57BL/6, TLR2 ؊/؊ , TLR4 ؊/؊ , TLR9 ؊/؊ , and MyD88 ؊/؊ mice were abraded using a trephine and epithelial brush and were exposed to heat-or UV-inactivated S. aureus clinical strain 8325-4 and other clinical isolates. Corneal thickness and haze were measured by in vivo confocal microscopy, neutrophil recruitment to the corneal stroma was quantified by immunohistochemistry, and cytokine production was measured by enzyme-linked immunosorbent assay. The exposure of corneal epithelium to S. aureus induced neutrophil recruitment to the corneal stroma and increased corneal thickness and haze in control C57BL/6 mice but not in TLR2 ؊/؊ or MyD88 ؊/؊ mice. The responses of TLR4 ؊/؊ and TLR9 ؊/؊ mice were similar to those of C57BL/6 mice. S. aureus-induced cytokine production by corneal epithelial cells and neutrophils was also significantly reduced in TLR2 ؊/؊ mice compared with that in C57BL/6 mice. These findings indicate that S. aureus-induced corneal inflammation is mediated by TLR2 and MyD88 in resident epithelial cells and infiltrating neutrophils.

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Section: Vol 74 2006 Tlr2 and Myd88 In S Aureus Keratitis 5329mentioning

confidence: 99%

Staphylococcus aureus -Induced Corneal Inflammation Is Dependent on Toll-Like Receptor 2 and Myeloid Differentiation Factor 88

Sun¹,

Hise

Kalsow³

et al. 2006

Infect Immun

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“…In the present study, we went to determine whether age affects the expression profile of miRNAs in mouse peritoneal macrophages stimulated with or without lipopolysaccharide (LPS), one of the most powerful bacterial virulence factors in terms of proinflammatory properties (Blais et al, 2005). We found that seven miRNAs (miR-101b, miR-223, miR-142-3P, miR-M1-8, miR-146a, miR-26b, and miR-191) were up-regulated in the LPS-stimulated macrophages of young mice but not in aged group.…”

Section: Introductionmentioning

confidence: 99%

Dysregulated expression of miR‐146a contributes to age‐related dysfunction of macrophages

Jiang¹,

Xiang²,

Wang

et al. 2011

Aging Cell

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SummaryAge-associated immune dysfunction, characterized by increased systemic levels of cytokines, manifests as an increased susceptibility to infections. Thus, understanding these negative regulators of the immune response has paved the way to delineating signaling pathways that impact immune senescence. In the present study, we found that miR-146a, which negatively regulated the expression of IL-1b and IL-6, was highly expressed in aged mice. However, there was a lack of response to the stimulation of lipopolysaccharide (LPS) and proinflammatory cytokines in macrophages of aged mice. As a result, the negative feedback regulation loop with miR-146a involving down-regulation of inflammation factors was interrupted in aged mice. Aberrant NF-jB binding to the miR-146a promoter was demonstrated to be associated with the abnormal expression of miR-146a in aged mice. The DNA methyltransferase inhibitor (5-aza-2-deoxycytidine) and the histone deacetylase inhibitor [trichostatin A (TSA)] both significantly up-regulated miR-146a transcriptional activation by altering the DNA-binding activity of NF-jB in macrophages isolated from aged mice, which suggests that DNA methylation and histone acetylation are involved in the suppression of age-dependent miR-146a expression. Additionally, high levels of histone deacetylase (HDACs) expressions contributed to the inhibition of miR-146a expression in LPS-stimulated macrophages from aged mice in vitro. While the suppression of HDACs activities by TSA could improve LPS-induced inflammatory responses owing to up-regulation of miR-146a expression in macrophages from aged mice. These data indicate that the dysregulated expression of miR-146a results in the age-associated dysfunction of macrophages, and miR-146a may be a good target for the treatment of age-related inflammatory diseases.

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“…sTLRs in blood plasma are speculated to be derived from monocytes or macrophages, because sTLR-2 and -4 have been shown to be secreted into the culture supernatant by freshly isolated human monocytes or a mouse macrophage cell line [21,25]. sTLRs are detected in various exocrine glands, such as the parotid gland, lacrimal gland and gland of the uterine cervix using immunohistochemistry or RT-PCR methods [5,14,24]. However, the entire spectrum of sTLRs secretion sites in the animal alimentary tract has never been clarified.…”

mentioning

confidence: 99%

Immunohistochemical Detection of Toll-Like Receptor-2, -4 and -9 in Exocrine Glands Associated with Rat Alimentary Tract

Mantani

Yokoo

Kamezaki

et al. 2012

The Journal of Veterinary Medical Science

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LBP and CD14 Secreted in Tears by the Lacrimal Glands Modulate the LPS Response of Corneal Epithelial Cells

Cited by 64 publications

References 48 publications

Staphylococcus aureus -Induced Corneal Inflammation Is Dependent on Toll-Like Receptor 2 and Myeloid Differentiation Factor 88

Staphylococcus aureus -Induced Corneal Inflammation Is Dependent on Toll-Like Receptor 2 and Myeloid Differentiation Factor 88

Dysregulated expression of miR‐146a contributes to age‐related dysfunction of macrophages

Immunohistochemical Detection of Toll-Like Receptor-2, -4 and -9 in Exocrine Glands Associated with Rat Alimentary Tract

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