Regulation of human β-defensin-2 by Mycobacterium bovis bacillus Calmette-Guérin (BCG): Involvement of PKC, JNK, and PI3K in human lung epithelial cell line (A549)

Méndez-Samperio, Patricia; Miranda, Elena; Trejo, Artemisa

doi:10.1016/j.peptides.2008.05.019

Cited by 19 publications

(24 citation statements)

References 39 publications

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“…Several MAPKs are linked to the expression of hBD-2 by various stimuli (16,22,39,40). In a previous study (23), and in data presented here, we observed that L. pneumophila causes a marked increase in the level of phosphorylated ERK, p38 MAPK, and JNK in A549 cells notably.…”

Section: Discussionsupporting

confidence: 73%

“…The family of MAPKs has been shown to mediate hBD-2 expression induced by various inflammatory stimuli (16,18,22,39,40). Therefore, we determined the effect of L. pneumophila on the activation of ERK, p38 MAPK, and JNK in A549 cells.…”

Section: Role Of Mapks On L Pneumophila-induced Hbd-2 Releasementioning

confidence: 99%

“…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).…”

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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: 73%

Section: Role Of Mapks On L Pneumophila-induced Hbd-2 Releasementioning

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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show abstract

“…AB308318). It has been known that in addition to the NF-B pathway, the mitogen-activated protein kinase (MAPK) signal transduction pathway is involved in HDP regulation [23]. Therefore, the involvement of this pathway in chCATH-B1 regulation should be investigated in the future.…”

Section: Discussionmentioning

confidence: 99%

Bacterial toxin-inducible gene expression of cathelicidin-B1 in the chicken bursal lymphoma-derived cell line DT40: Functional characterization of cathelicidin-B1

et al. 2014

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“…Because the MAPK pathway occupies a central position in a wide range of cellular responses, including HDP secretion [1,2,8], and because IL-1 family members activate this pathway [3,4], we investigated MAPK activation as a mechanism by which IL-36s might stimulate keratinocytes. We observed enhanced phosphorylation of the MAPKs ERK, p38 and JNK after a 5-60 min-exposure to IL-36s ( Fig.…”

Section: To the Editormentioning

confidence: 99%

Interleukin-36 cytokines enhance the production of host defense peptides psoriasin and LL-37 by human keratinocytes through activation of MAPKs and NF-κB

Niyonsaba

Ushio

Akiyama

et al. 2012

Journal of Dermatological Science

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Regulation of human β-defensin-2 by Mycobacterium bovis bacillus Calmette-Guérin (BCG): Involvement of PKC, JNK, and PI3K in human lung epithelial cell line (A549)

Cited by 19 publications

References 39 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

Bacterial toxin-inducible gene expression of cathelicidin-B1 in the chicken bursal lymphoma-derived cell line DT40: Functional characterization of cathelicidin-B1

Interleukin-36 cytokines enhance the production of host defense peptides psoriasin and LL-37 by human keratinocytes through activation of MAPKs and NF-κB

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