Endogenous antimicrobial peptides and skin infections in atopic dermatitis.

By P. Ong, T. Ohtake, C. Brandt, I. Strickland, M. Boguniewicz, T. Ganz, R. Gallo, D. Leung. New England Journal of Medicine, 2002

1,941 citations recorded by the source corpus.

Subfields: Dermatology, Emergency Medical Services, Microbiology

View Paper: https://www.semanticscholar.org/paper/e6f21cfe5be3846be8e8512174f6ae80def1f1ef

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Dermatology

1. J. Segre
2. H. Kong
3. Julia Oh
4. J. Kolls
5. Y. Belkaid

In Emergency Medical Services

1. Robert E. W. Hancock

In Microbiology

1. Robert E. W. Hancock
2. S. Gellatly
3. Amy T. Y. Yeung
4. M. Zanetti
5. A. Ramamoorthy
6. K. Brown
7. M. Selsted
8. A. Ouellette

Citations in the corpus

• Cationic host defense (antimicrobial) peptides. (2006, background): “Low expression of LL-37, human b-defensin (hBD)-2 and hBD-3 in skin lesions caused by atopic dermatitis coincides with enhanced susceptibility to skin infections [27,28].”
• Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis (2012, background): “Reduced antimicrobial peptide expression in the skin of AD patients may contribute to this susceptibility (Ong et al. 2002).”
• Cytokine Milieu of Atopic Dermatitis, as Compared to Psoriasis, Skin Prevents Induction of Innate Immune Response Genes 1 (2003, background): “AD patients compared with psoriasis patients (11).”
• LL-37, the only human member of the cathelicidin family of antimicrobial peptides. (2006, background): “Downregulation in disease Atopic dermatitis [62,63] Chronic ulcer epithelium [61] Enteric infection [64] Neutrophils, acute myeloid leukemia [105,106]”
• Geography, Ethnicity or Subsistence-Specific Variations in Human Microbiome Composition and Diversity (2017, background): “Studies suggested that diseases like atopic dermatitis, psoriasis, rosacea, acne etc. are often caused not because of pathogens but due to disruption in normal skin microbiota (Ong et al., 2002; Nomura et al., 2003a,b; de Jongh et al., 2005; Gudjonsson et al., 2009).”
• The skin microbiome (2011, result): “This is in sharp contrast to psoriatic lesions, which produce abundant quantities of AMPs and are characterized by an activated innate immune respons”
• Mammalian defensins in the antimicrobial immune response (2005, background): “Conversely, expression of hBD-2 and hBD-3 and the cathelicidin LL-37 is diminished substantially in atopic dermatitis, a skin condition often accompanied by bacterial, fungal or viral infectio”
• The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide (2010, neutral): “Patients that express low levels of LL-37 are at increased risk for serious infections [12].”
• Immune surveillance in the skin: mechanisms and clinical consequences (2004, background): “Recent studies have shown that atopic epidermis, unlike psoriatic epidermis, does not produce the antibacterial peptides β-defensin and cathelicidin in response to such infectio”
• Stratum corneum defensive functions: an integrated view. (2005, background): “Moreover, whereas hBD2 and hCAP-18 levels upregulate in psoriasis, which rarely becomes secondarily infected, these peptides fail to upregulate in lesional skin of active atopic dermatitis (AD)”
• An angiogenic role for the human peptide antibiotic LL-37/hCAP-18. (2003, background): “A deficiency of LL-37/hCAP-18 in the skin of patients with atopic dermatitis may account for the increased susceptibility to skin infections (13).”