Toll-like receptor agonists regulate β-defensin 2 release in hair follicle

Selleri, Silvia; Arnaboldi, Francesca; Palazzo, Marco; Gariboldi, Silvia; Zanobbio, Laura; Opizzi, E.; Shirai, Yuri F.; Balsari, Andrea; Rumio, Cristiano

doi:10.1111/j.1365-2133.2007.07899.x

Cited by 22 publications

(20 citation statements)

References 17 publications

(32 reference statements)

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“…Accordingly, the release of hBD-2 after treatment with MALP-2, heat-inactivated Legionella, or infection with L. pneumophila and attenuation of hBD-2 release upon silencing of TLR2 demonstrates that TLR2 mediates hBD-2 induction by L. pneumophila in human alveolar epithelial cells. Our results are in line with recently published studies showing that in various tissue cells, including airway epithelial cells, hBD-2 expression occurs in a TLR2-dependent manner (19,30,36,38). Furthermore, our study reveals that induction of hBD-2 by Legionella is dependent on the expression of flagellin.…”

Section: Discussionsupporting

confidence: 82%

“…TLR5-mediated hBD-2 release could also be observed in intestinal epithelial cell infection with enteropathogenic Escherichia coli and in hair follicle cells stimulated with flagellin. In the same study, ODN also failed to induce hBD-2 expression such as we could observe in our study using pulmonary epithelial cells (30). Together, it was shown that Legionella-induced hBD-2 expression depends on activation of TLR2 and -5 in pulmonary epithelial cells.…”

Section: Discussionsupporting

confidence: 49%

“…hBD-2 was the first inducible human antimicrobial peptide discovered and was originally isolated from lesional psoriatic skin (10). hBD-2 is inducible by bacterial factors or proinflammatory mediators in epithelial cells and macrophages (9,10,18,22,25,30,(37)(38)(39)(40).…”

mentioning

confidence: 99%

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Induction of human β-defensin-2 in pulmonary epithelial cells byLegionella pneumophila: involvement of TLR2 and TLR5, p38 MAPK, JNK, NF-κB, and AP-1

Scharf

Hippenstiel

Flieger

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium is an effective barrier for inhaled microorganisms and actively participates in the initiation of innate host defense. Induction of antimicrobial peptide human β-defensin-2 (hBD-2) by various stimuli in epithelial cells has been reported. However, the mechanisms by which bacterial infections enhance hBD-2 expression remain poorly understood. In this study, we investigated the effect of the pulmonary pathogen L. pneumophila on induction of hBD-2 in human pulmonary epithelial cells. Infection with L. pneumophila markedly increased hBD-2 production, and the response was attenuated in Toll-like receptor (TLR) 2 and TLR5 transient knockdown cells. Furthermore, pretreatment with SB-202190 (an inhibitor of p38 MAPK) and JNK II (an inhibitor of c-Jun NH2-terminal kinase), but not U0126 (an inhibitor of ERK), reduced L. pneumophila-induced hBD-2 release in A549 cells. L. pneumophila-induced hBD-2 liberation was mediated via recruitment of NF-κB and AP-1 to the hBD-2 gene promoter. Additionally, we showed that exo- and endogenous hBD-2 elicited a strong antimicrobial effect towards L. pneumophila. Together, these results suggest that L. pneumophila induces hBD-2 release in A549 cells, and the induction seems to be mediated through TLR2 and TLR5 as well as activation of p38 MAPK, JNK, NF-κB, and AP-1.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 49%

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Induction of human β-defensin-2 in pulmonary epithelial cells byLegionella pneumophila: involvement of TLR2 and TLR5, p38 MAPK, JNK, NF-κB, and AP-1

Scharf

Hippenstiel

Flieger

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Thus, it remains to be elucidated if HBD production is dependent on TLR2, TLR4 or TLR6 or even if the three receptors are activated in response to cell wall components of T. rubrum, since it has been reported that BDEF-2 (a murine homolog of HBD-2) is TLR2-and TLR4-dependent [31].…”

Section: Il-1bmentioning

confidence: 99%

Trichophyton rubrum manipulates the innate immune functions of human keratinocytes

et al. 2011

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Evasion or subversion of host immune responses have been shown for a variety of microorganisms, and this might be the case for Trichophyton rubrum, the most common pathogenic fungus causing chronic dermatophytosis in humans. Keratinocytes, the main epidermal cells, have important roles as a first defense against microbial challenges in local immune reactions. Epidermal keratinocytes express several Toll-like receptors and produce host defense peptides, cytokines and chemokines in response to various stimuli. We analyzed the expression of Toll-Like receptor TLR2, TLR4, TLR6, and Human Beta Defensin (HBD)-1, HBD-2, Interleukin IL-1b and IL-8 production, when exposing primary keratinocyte cultures to T. rubrum. We observed changes in size and granularity of keratinocytes stimulated with either whole conidia or conidial homogenates compared to other treatments. Intact conidia decreased keratinocytes’ TLR2 and TLR6 expression without affecting that of TLR4, while conidial homogenates increased the expression of these three receptors. Interestingly, whole conidia decreased HBD-1 and HBD-2 production, whereas conidial homogenate increased it. No changes were observed in IL-1b and IL-8 production after stimulation with conidia or conidial homogenate. CONCLUSIONS. Our results suggest that: 1) Keratinocytes can recognize and respond to cell wall components of T. rubrum; 2) Viable intact conidia inhibit TLR-2 and TLR6 expression and decrease HBD-1 and HBD-2 production; 3) Conidial homogenate from T. rubrum increases the expression of TLR2, TLR4 and TLR6 and induces HBD-1 and HBD-2 production; 4) Therefore, innate immune functions of keratinocytes as the first level of local skin immunity are apparently manipulated by T. rubrum, likely to ensure its establishment, persistence and survival.

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“…KCs are able to sense various exogenous harmful pathogens and endogenous cellular damages through pattern recognition receptors (PRRs), which exist both on the cellular membranes and in the cytosol, to mediate immune responses. First, KCs express various Toll-like receptors (TLRs): TLR1, TLR2, TLR4, TLR5, and TLR6 on cell surfaces, and TLR3, TLR7, and TLR9 in endosomes [5,6,7,8,9]. Pathogen-associated molecular patterns (PAMPs) of microbial origin, such as lipopolysaccharide (LPS), peptidoglycan, agellin, and nucleic acids are sensed by some of these TLRs.…”

Section: Epidermismentioning

confidence: 99%

Novel insights into the role of immune cells in skin and inducible skin-associated lymphoid tissue (iSALT)

Ono¹,

Kabashima²

2015

Allergo J

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Summarye skin is equipped with serial barriers that provide rapid and e cient protection against external intruders. Beneath the epidermal physical barriers of the stratum corneum and the tight junctions, the integrated immune systems in both the epidermis and the dermis act in a coordinated manner to protect the host.is "immunological" barrier is composed of various cells, including skin-resident cells, such as keratinocytes, dendritic cells, tissue-resident macrophages, resident memory T cells, mast cells, and innate lymphoid cells. Additionally, in ltrating memory T cells, monocytes, neutrophils, basophils, and eosinophils are recruited in support of the host immunity.In addition to discussing the role of each of these cellular populations, we describe the concept of skin associated lymphoid tissue (SALT), which reminds us that the skin is an important component of the lymphatic system. We further describe the newly discovered phenomenon of multiple cell gathering under skin in ammation, which can be referred to as inducible SALT (iSALT). iSALT contributes to our understanding of SALT by highlighting the importance of direct cell-cell interaction in skin immunity.Cite this as Ono S, Kabashima K. Novel insights into the role of immune cells in skin and inducible skin-associated lymphoid tissue (iSALT). Allergo J Int 2015;24:170-9

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Toll-like receptor agonists regulate β-defensin 2 release in hair follicle

Abstract: Our data show that the hair follicle is equipped with TLR2, TLR4 and TLR5, and that these receptors are able to respond to microbial stimuli inducing the production of DEFB2 by epithelial cells. This immune response might be important in preserving the skin from microorganism infections.

Cited by 22 publications

References 17 publications

Induction of human β-defensin-2 in pulmonary epithelial cells byLegionella pneumophila: involvement of TLR2 and TLR5, p38 MAPK, JNK, NF-κB, and AP-1

Induction of human β-defensin-2 in pulmonary epithelial cells byLegionella pneumophila: involvement of TLR2 and TLR5, p38 MAPK, JNK, NF-κB, and AP-1

Trichophyton rubrum manipulates the innate immune functions of human keratinocytes

Novel insights into the role of immune cells in skin and inducible skin-associated lymphoid tissue (iSALT)

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