Differential expression of Toll‐like receptors in chronic hyperplastic candidosis

Ali, Ahmed; Natah, Sirajedin; Konttinen, Yrjö T.

doi:10.1111/j.1399-302x.2007.00428.x

Cited by 16 publications

(28 citation statements)

References 44 publications

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“…Increased expression of TLR2 and TLR4 has previously been observed in inflamed gingival epithelial tissues (Sugawara et al, 2006). The immunohistochemical expression of 9 classes of TLRs (TLR1 to TLR9) was demonstrated in a series of sections from chronic hyperplastic candidiasis, leukoplakia, and healthy tissue (Ali et al, 2008).…”

Section: Expression Of Prrs In Oral Epithelial Cellsmentioning

confidence: 93%

“…Most TLRs are expressed constitutively in oral epithelial cells, healthy epithelial tissue (Mahanonda and Pichyangkul, 2007;Beklen et al, 2008), and oral mucosa biopsies from patients with oral candidiasis (Ali et al, 2008). Previously, using a model of oral reconstituted human epithelium (RHE), we studied several different aspects of host-Candida interactions (Schaller et al, 1998(Schaller et al, , 1999(Schaller et al, , 2002(Schaller et al, , 2006Weindl et al, 2007;Schaller and Weindl, 2009).…”

Section: Expression Of Prrs In Oral Epithelial Cellsmentioning

confidence: 99%

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Epithelial Cells and Innate Antifungal Defense

2010

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The human pathogenic fungus Candida albicans is the predominant cause of both superficial and invasive forms of candidiasis. Clinical observations indicate that mucocutaneous Candida infections are commonly associated with defective cell-mediated immune responses. The importance of the innate immune system as a first-line defense against pathogenic challenge has long been recognized. Over the last decade, many key molecules mediating innate host defense have been identified. Central to these developments is the discovery of pattern recognition receptors such as Toll-like receptors and C-type lectin-receptors that induce innate immune responses and also modulate cellular and humoral adaptive immunity during Candida infections. Although a large amount of information is now available in systemic infections, little is known about localized infections. We address the most relevant pattern recognition receptors and their signaling mechanisms in oral epithelial cells, to gain a better understanding of their contributions to antifungal innate immunity.

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Section: Expression Of Prrs In Oral Epithelial Cellsmentioning

confidence: 93%

Section: Expression Of Prrs In Oral Epithelial Cellsmentioning

confidence: 99%

Epithelial Cells and Innate Antifungal Defense

2010

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“…Gingival tissue samples from patients with chronic periodontitis obtained during periodontal flap operations were used as positive controls for all immunohistological staining [21, 22]. …”

Section: Methodsmentioning

confidence: 99%

TLR1-10, NF-κB and p53 expression is increased in oral lichenoid disease

et al. 2017

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Toll-like receptors (TLRs) and nuclear factor-κB (NF-κB) in keratinocytes play an important role in dermatological autoimmune diseases. Tumour suppressor protein p53 regulates TLR expression. The aim of this study was to compare the expression of TLR1-TLR10, p53 and NF-κB in patients with oral lichenoid disease (OLD) with healthy mucosa. Oral mucosal biopsies from 24 patients with OLD and 26 healthy controls (HC) were analysed for the expression of TLR1-TLR10, NF-κB and p53 by immunohistochemistry. The expression of all TLRs was increased in OLD epithelia compared to HC samples and the difference was significant in TLR1, TLR3, TLR4, TLR5, TLR6 and TLR7. In the basement membrane zone, the immunoreactivity of TLR5 was significantly more intense in OLD compared to HC. In the intermediate layer, the immunoreactivity of NF-κB was significantly stronger in OLD, whereas the staining for p53 was more intense in all layers of OLD compared to HC samples. In OLD, a positive correlation between TLR2 and NF-κB in the basal layer and between TLR5, p53 and NF-κB in the intermediate layers was discovered. The expression of TLRs, p53 and NF-κB is increased in OLD, which may play a role in the pathogenesis of this chronic immune-mediated mucosal disease.

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“…462 Clinically, it ranges from mild and superficial to a severe inflammatory pustular folliculitis. 477,478 C. albicans is a human commensal inhabiting the gastrointestinal tract, oral cavity, vagina, and skin in a significant proportion of healthy individuals; therefore, the source of infection is usually endogenous. 461,463 Tinea Capitis (Scalp Ringworm) Tinea capitis can be located on the scalp, eyebrows, or eyelashes and is caused by members of the genera Microsporum and Trichophyton.…”

Section: White Piedra and Trichosporonosismentioning

confidence: 99%

“…19-60) or endothrix (arthroconidia formed within the hair shaft) (Fig. 478 The superficial infections mainly include cutaneous, oral, and genital candidosis. 464 Since the 1950s, Trichophyton tonsurans has been observed to be the most frequent cause of tinea capitis in the United States and the United Kingdom.…”

Section: White Piedra and Trichosporonosismentioning

confidence: 99%