Endogenous Antimicrobial Peptides and Skin Infections in Atopic Dermatitis

Ong, Peck Y.; Ohtake, Takaaki; Brandt, Corinne; Strickland, Ian; Boguniewicz, Mark; Ganz, Tomas; Gallo, Richard L.; Leung, Donald Y.M.

doi:10.1056/nejmoa021481

Cited by 1,786 publications

(1,655 citation statements)

References 25 publications

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“…IL-22 also stimulates keratinocytes to secrete antimicrobial peptides [47,48,49••]. This is clinically relevant, because the overexpression of antimicrobial peptides in psoriatic plaques is believed to the main reason lesional skin rarely becomes infected by viruses or bacteria [50]. In addition, IL-22 causes keratinocytes to produce matrix metalloproteinase 1, which is involved in tissue remodeling [49••].…”

Section: Th17 Effector Cytokines: Il-17a Il-22 and Il-21mentioning

confidence: 99%

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

Fitch¹,

Harper²,

Skorcheva³

et al. 2007

Curr Rheumatol Rep

350

260

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T helper (Th) 17 cells, a novel T-cell subset, have been implicated in the pathogenesis of psoriasis and other autoimmune inflammatory diseases. Interleukin (IL)-23 stimulates survival and proliferation of Th17 cells, and thus serves as a key master cytokine regulator for these diseases. In psoriasis, IL-23 is overproduced by dendritic cells and keratinocytes, and this cytokine stimulates Th17 cells within dermis to make IL-17A and IL-22. IL-22, in particular, drives keratinocyte hyperproliferation in psoriasis. Future targeting of these key cytokines is likely to lead to dramatic clinical improvement in patients with psoriasis. This review focuses on the numerous recent studies on the roles of IL-23 and Th17 cells in the pathogenesis of psoriasis.

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Section: Th17 Effector Cytokines: Il-17a Il-22 and Il-21mentioning

confidence: 99%

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

Fitch¹,

Harper²,

Skorcheva³

et al. 2007

Curr Rheumatol Rep

350

260

View full text Add to dashboard Cite

show abstract

“…Primer and probe sequences for cathelicidin were designed as previously described. 3 Primer and probe sequences used to assay HSV-2 gene transcripts were: Forward, 5 -CGC TCT CGT AAA TGC TTC CCT -3 , Reverse, 5 -TCT ACC CAC AAC AGA CCC ACG -3 . This region of the genome encodes the glycoprotein D (gD) of HSV-2.…”

Section: Real-time Rt-pcrmentioning

confidence: 99%

“…It has been postulated that this may explain susceptibility of these individuals to recurrent bacterial skin infections. 3,4 Eczema herpeticum (ADEH) is a disseminated herpes simplex virus (HSV)-1 or -2 infection that occurs in a subset of patients with AD. 5,6 Left un-treated, ADEH may be fatal due to systemic viremia.…”

Section: Introductionmentioning

confidence: 99%

Cathelicidin deficiency predisposes to eczema herpeticum

Howell

Wollenberg

Gallo³

et al. 2006

Journal of Allergy and Clinical Immunology

240

157

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“…LL37 is highly detectable in granulocytes during wound repair, in inflammatory skin disorders such as psoriasis, and nickel allergy epidermis [93]. hBD2 is found in chronic wounds of the skin [4,117]. The interaction of S. aureus with its host in vivo is supported by the presence of high concentrations of HNP1-3 and hBD2 in the nasal cavity of S. aureus carriers [118].…”

Section: Interaction Of Anti-microbial Peptides With S Aureusmentioning

confidence: 99%

“…The anti-microbial peptides kill micro-organisms directly and some act as chemokines. Crohn's disease [1][2][3], atopic dermatitis [3,4], Kostmann's disease [5], and cystic fibrosis [6,7] are linked to microbial infections due to decreased expression of anti-microbial peptides in these patients. By contrast, the anti-microbial peptides are highly expressed in the lesions of psoriasis, resulting in fewer microbial infections [3,8,9].…”

Section: Introductionmentioning

confidence: 99%

Innate defences against methicillin‐resistant Staphylococcus aureus (MRSA) infection

Komatsuzawa

Ouhara

Yamada

et al. 2005

The Journal of Pathology

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The innate immune system is the primary defence against bacterial infection. Among the factors involved in innate defence, anti-microbial peptides produced by humans have recently attracted attention due to their relevance to some diseases and also to the development of new chemotherapeutic agents. Staphylococcus aureus is one of the major human pathogens, causing a variety of infections from suppurative disease to food poisoning. Methicillin-resistant S. aureus (MRSA) is a clinical problem and with the recent emergence of a vancomycin-resistant strain, this will pose serious problems in the near future. In investigating the molecular biology of S. aureus infections to develop new chemotherapeutic agents against MRSA infections, knowledge of the interaction of innate anti-microbial peptides with S. aureus is important. In vitro and in vivo experiments demonstrate that exposure of S. aureus to host cells can induce the anti-microbial peptides β-defensin-2 (hBD2), hBD3, and LL37/CAP18. The induction level of these peptides differs among strains, as does the susceptibility of the strains, with MRSA strains exhibiting lower susceptibility. In summary, the susceptibility of S. aureus strains, including MRSA strains, to components of the innate immune system varies, with the MRSA strains showing more resistance to both innate immune factors and chemotherapeutic agents.

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Endogenous Antimicrobial Peptides and Skin Infections in Atopic Dermatitis

Abstract: A deficiency in the expression of antimicrobial peptides may account for the susceptibility of patients with atopic dermatitis to skin infection with S. aureus.

Cited by 1,786 publications

References 25 publications

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

Cathelicidin deficiency predisposes to eczema herpeticum

Innate defences against methicillin‐resistant Staphylococcus aureus (MRSA) infection

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