Differential expression of human beta-defensin 2 in keratinized and non-keratinized oral epithelial lesions; immunohistochemistry and in situ hybridization

Abiko, Yoshihiro; Suraweera, Anura; Nishimura, Michiko; Arakawa, Toshiya; Teratani, Takuma; Mizoguchi, Itaru; Kaku, Tohru

doi:10.1007/s004280000303

Cited by 40 publications

(37 citation statements)

References 11 publications

(21 reference statements)

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“…Also, most HBD-2 heavily stained cells showed enlarged cell size characteristic of more differentiated keratinocytes. This observation correlates correlates to the reports by Liu et al [10] in dermal tissue and by Abiko et al [33] in oral mucosal tissue that HBD-2 mainly expressed in upper layers of more differentiated epithelial cells.…”

Section: Immunohistochemical Analysis Of Hbd-2 Expression In Sin18-hbsupporting

confidence: 92%

“…Bacteria and cytokines IL-1 and TNFα upregulate HBD-2 expression in lung and skin epithelial cells [10,28] and induction of HBDs by these stimuli is differentially regulated involving multiple mechanisms [29]. Expression of HBDs in oral tissues has also been extensively studied [23,[30][31][32][33][34][35][36][37][38][39][40]. In gingival epithelium, variable expression levels of HBD-1, -2 or -3 are found in either healthy or diseased gingival tissues [41,42] Previously, we transduced a number of non-HBD-2-expressing cell lines to produce HBD-2 with the notion that these cells may become part of the innate defense mechanisms against infection [6,49].…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

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Capacity of human β-defensin expression in gene-transduced and cytokine-induced cells

Yin¹,

Dang²,

Zhang³

et al. 2006

Biochemical and Biophysical Research Communications

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The purpose of this study was to determine the capacity of cells transduced with human β-defensins (HBDs) to express antimicrobial peptides, since sufficient expression level is required for effective antimicrobial activity. Retroviral vector pBabeNeo and lentiviral vector SIN18cPPTRhMLV (SIN18) carrying HBDs were utilized to transduce non-HBD-expressing cells such as fibroblasts or HBD-producing oral epithelial cells. We found that HBD-3 gene transfer to fibroblasts was possible not via retrovirus but by direct vector transfection. SIN18 had high transduction efficiencies (80.9-99.9%) and transduced cells expressed higher amounts of HBD-2 than those by pBabe-Neo. Primary human gingival epithelial cells (HGECs) expressed greater amounts of HBD-2 than primary fibroblasts after lentiviral transduction. Additionally, HBD-2 secretion from transduced HGECs cells was further increased when stimulated with IL-1 or TNFα. Our data indicate that while HBD-2 expression is limited in primary fibroblasts, its expression in HGECs may be maximized by gene transduction plus cytokine induction. KeywordsHBD-2; HBD-3; Lentiviral vectors; Retroviral vectors; IL-1; TNFα; Gingival epithelial cells Natural antimicrobial peptides have been considered as an alternative option for infection control due to the increasing resistance of microbes to conventional antibiotics. Because some potent antimicrobial peptides are encoded by single genes, the possibility of artificially delivering these genes into tissues/organs to augment innate immunity against infection or creating transgenic animals to produce antimicrobial peptides has been explored [1][2][3][4][5]. Subsequently, the term antimicrobial gene therapy has emerged [6] and engineered skin NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript models have been used to test the concept of antimicrobial gene therapy both in vitro and in vivo [7,8]. Human β-defensins (HBDs or DEFB) and cathelicidin LL37 are being actively used as study models for their potent ability to kill a broad spectrum of bacteria and fungi [6,7,[9][10][11][12][13], as well as to inhibit viral infections [14,15]. HBDs are expressed mostly in epithelia [11,12,[16][17][18][19][20][21][22][23][24]. Besides the cloned, sequenced, and well-characterized HBD-1, -2, -3, and -4, there appears to be at least 28 more HBDs existing based on the genomic surveys using computational search strategy [25][26][27]. Fourteen HBDs or DEFB gene transcripts (DEFB-1, -4, and DEFB-103 to -114) were investigated using reverse transcriptionpolymerase chain reaction (RT-PCR) to detect their expression in gingival keratinocytes and a selected few have been classified as constitutive or inducible [27].HBDs are considered to play an important role in epithelial defense mechanism and the regulation of their expression in diseased conditions is being actively investigated. Bacteria and cytokines IL-1 and TNFα upregulate HBD-2 expression in lung and skin epithelial cells [10,28] and induction of HBDs by these stimuli is...

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Section: Immunohistochemical Analysis Of Hbd-2 Expression In Sin18-hbsupporting

confidence: 92%

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Capacity of human β-defensin expression in gene-transduced and cytokine-induced cells

Yin¹,

Dang²,

Zhang³

et al. 2006

Biochemical and Biophysical Research Communications

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“…Tissue sections were stained by immunohistochemical analyses for the presence of human ␣-defensins 1 to 3 using a 1:1,000 dilution of mouse MAb anti-human defensin, clone DEF-3 (Serotec, Raleigh, NC). Human ␤-defensin-2 was detected using a 1:4,000 dilution of polyclonal rabbit anti-hBD-2 antiserum (Peptide Institute, Louisville, KY), as previously described (1). Human ␤-defensins 1 to 3 were detected following the described protocol below, using the respective affinity purified antibodies.…”

Section: Methodsmentioning

confidence: 99%

Human β-Defensins Suppress Human Immunodeficiency Virus Infection: Potential Role in Mucosal Protection

Sun

Finnegan

Kish-Catalone

et al. 2005

J Virol

224

230

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␤-Defensins are small (3 to 5 kDa in size) secreted antimicrobial and antiviral proteins that are components of innate immunity. ␤-Defensins are secreted by epithelial cells, and they are expressed at high levels in several mucosae, including the mouth, where the concentration of these proteins can reach 100 g/ml. Because of these properties, we wondered whether they could be part of the defenses that lower oral transmission of human immunodeficiency virus (HIV) compared to other mucosal sites. Our data show that select ␤-defensins, especially human ␤-defensin 2 (hBD2) and hBD3, inhibit R5 and X4 HIV infection in a dose-dependent manner at doses that are compatible with or below those measured in the oral cavity. We observed that ␤-defensin treatment inhibited accumulation of early products of reverse transcription, as detected by PCR. We could not, however, detect any reproducible inhibition of env-mediated fusion, and we did not observe any modulation of HIV coreceptors following treatment with hBD1 and hBD2, in both resting and phytohemagglutinin-activated cells. Our data instead suggest that, besides a direct inactivation of HIV virions, hBD2 inhibits HIV replication in the intracellular environment. Therefore, we speculate that ␤-defensins mediate a novel antiretroviral mechanism that contributes to prevention of oral HIV transmission in the oral cavity. Immunohistochemical data on hBD2 expression in oral mucosal tissue shows that hBD2 is constitutively expressed, forming a barrier layer across the epithelium in healthy subjects, while in HIV-positive subjects levels of hBD2 expression are dramatically diminished. This may predispose HIV-positive subjects to increased incidence of oral complications associated with HIV infection.

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“…In the observations of Abiko et al the increased expression of HBD-2 and decreased expression of HBD-1 were found in highly-differentiated, keratinized lesions, while in poorly differentiated, squamous call carcinomas the expression of HBD-2 was not detected at all [33]. Malignant neoplasms are very often accompanied by the inflammatory reaction, which, according to Abiko, may additionally stimulate the HBD-2 expression in some oral neoplasms.…”

Section: Defensins and Their Role In The Maintenance Of The Oral Cavimentioning

confidence: 91%

“…In many studies it was found that the β-defensin oral expression significantly rises in the presence of bacteria species responsible for the development of periodontitis, which include: Actinomycetes actinomycetemcomitans, Porphyromonas gingivalis and Fusobacterium nucleatum [6,25,28,33] and the induction of the HBD expression occurs in several ways, most probably with MAPK (mitogen-activated protein kinases) or NF-κB (nuclear factor κB) paths [1,4,14]. In this light the results of Bissell's et al research, who did not observe any elevation in the expression of the β-defensin 1-3 in the inflamed periodontal tissue, while the HBD-3 expression was significantly higher in the healthy controls than in their study group, may be considered surprising [29].…”

Section: The Expression and The Role Of Defensins In The Oral Cavitymentioning

confidence: 99%

Defensins and their role in the maintenance of the oral cavity homeostasis – a literature review

Ślebioda¹,

Szponar²,

Kowalska³

2013

cejoi

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Differential expression of human beta-defensin 2 in keratinized and non-keratinized oral epithelial lesions; immunohistochemistry and in situ hybridization

Cited by 40 publications

References 11 publications

Capacity of human β-defensin expression in gene-transduced and cytokine-induced cells

Capacity of human β-defensin expression in gene-transduced and cytokine-induced cells

Human β-Defensins Suppress Human Immunodeficiency Virus Infection: Potential Role in Mucosal Protection

Defensins and their role in the maintenance of the oral cavity homeostasis – a literature review

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