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Biomedical subjects

Peck Y Ong

Publications and source records attributed to Peck Y Ong.

9 recordsLinked to original sources
PubMed2006

Immune dysregulation in atopic dermatitis.

Atopic dermatitis is a chronic inflammatory skin disease that causes significant morbidity in affected individuals. It is characterized by dysregulated immune responses that consist of an increased systemic Th2 response and a combination of Th2 and Th1 responses in the skin lesions. In this article, we review factors that contribute to these abnormal responses, including key effector cells of the immune system, chemokines, defective skin barrier, genetic predisposition, and environmental triggers. Understanding these pathomechanisms may improve our current therapies for atopic dermatitis.

Allergens↗
PubMed2006

Pectin anaphylaxis and possible association with cashew allergy.

BACKGROUND: Inhalation of pectin has been identified as a cause of occupational asthma. However, allergic reactions to orally ingested pectin have not been reported. OBJECTIVES: To describe a child with pectin-induced food anaphylaxis and to discuss its possible relationship to cashew allergy. METHODS: A 3 1/2-year-old boy developed anaphylaxis once after eating cashews and later after eating a pectin-containing fruit "smoothie." He also has a history of generalized pruritus after eating grapefruit. Skin tests or radioallergosorbent tests (RASTs) were performed to pectin and other suspected food allergens. RESULTS: The child had a positive skin prick test reaction to pectin and a high RAST reaction to cashew and pistachio. He had a low-level positive RAST reaction to grapefruit. Results of allergy tests for the other potential food allergens were negative. The pectin in the smoothie was confirmed to be of citrus origin. Review of previous case reports of pectin-induced occupational asthma revealed several patients with allergies to and cross-reactivity with cashew. CONCLUSIONS: Ingestion, not only inhalation, of pectin can cause hypersensitivity reactions. Cashew, and possibly pistachio, allergy may be associated with pectin allergy, and the possibility of pectin allergy should be considered in cashew- or pistachio-allergic patients who have unexplained allergic reactions.

Anacardium↗
PubMed2006

Is/are pattern recognition receptor(s) for Staphylococcus aureus defective in atopic dermatitis?

It is known that Staphylococcus aureus induces the expression of human beta-defensin-2 (hBD-2), a well-characterized antimicrobial peptide, in keratinocytes. However, in spite of heavy colonization of atopic dermatitis (AD) skin lesions by S. aureus, these lesions have consistently been shown to contain low expression of hBD-2. The current article discusses various possible mechanisms for the low expression of hBD-2 in AD and raises the question whether the innate recognition of S. aureus by keratinocytes in AD is intact.

Dermatitis, Atopic↗
PubMed2003

Cytokine milieu of atopic dermatitis, as compared to psoriasis, skin prevents induction of innate immune response genes.

Atopic dermatitis (AD) and psoriasis are the two most common chronic skin diseases. However patients with AD, but not psoriasis, suffer from frequent skin infections. To understand the molecular basis for this phenomenon, skin biopsies from AD and psoriasis patients were analyzed using GeneChip microarrays. The expression of innate immune response genes, human beta defensin (HBD)-2, IL-8, and inducible NO synthetase (iNOS) was found to be decreased in AD, as compared with psoriasis, skin (HBD-2, p = 0.00021; IL-8, p = 0.044; iNOS, p = 0.016). Decreased expression of the novel antimicrobial peptide, HBD-3, was demonstrated at the mRNA level by real-time PCR (p = 0.0002) and at the protein level by immunohistochemistry (p = 0.0005). By real-time PCR, our data confirmed that AD, as compared with psoriasis, is associated with elevated skin production of Th2 cytokines and low levels of proinflammatory cytokines such as TNF-alpha, IFN-gamma, and IL-1beta. Because HBD-2, IL-8, and iNOS are known to be inhibited by Th2 cytokines, we examined the effects of IL-4 and IL-13 on HBD-3 expression in keratinocyte culture in vitro. We found that IL-13 and IL-4 inhibited TNF-alpha- and IFN-gamma-induced HBD-3 production. These studies indicate that decreased expression of a constellation of antimicrobial genes occurs as the result of local up-regulation of Th2 cytokines and the lack of elevated amounts of TNF-alpha and IFN-gamma under inflammatory conditions in AD skin. These observations could explain the increased susceptibility of AD skin to microorganisms, and suggest a new fundamental rule that may explain the mechanism for frequent infection in other Th2 cytokine-mediated diseases.

Adult↗
PubMed2003

Unresponsive wheezing to asthma therapy in a 32-year-old female.

Repeat failure of any patient to respond to asthma therapy, particularly corticosteroids, should alert physicians to carry out further pulmonary evaluation. This will prevent unnecessary side effects of asthma therapy and provide prompt treatment for other diseases that may require urgent attention.

Adult↗
PubMed2002

Endogenous antimicrobial peptides and skin infections in atopic dermatitis.

BACKGROUND: The innate immune system of human skin contains antimicrobial peptides known as cathelicidins (LL-37) and beta-defensins. In normal skin these peptides are negligible, but they accumulate in skin affected by inflammatory diseases such as psoriasis. We compared the levels of expression of LL-37 and human beta-defensin 2 (HBD-2) in inflamed skin from patients with atopic dermatitis and from those with psoriasis. METHODS: The expression of LL-37 and HBD-2 protein in skin-biopsy specimens from patients with psoriasis, patients with atopic dermatitis, and normal subjects was determined by immunohistochemical analysis. The amount of antimicrobial peptides in extracts of skin samples was also analyzed by immunodot blot analysis (for LL-37) and Western blot analysis (for HBD-2). Quantitative, real-time reverse-transcriptase-polymerase-chain-reaction (RT-PCR) assays were used to confirm the relative expression of HBD-2 and LL-37 messenger RNA (mRNA) in the skin-biopsy specimens. These peptides were also tested for antimicrobial activity against Staphylococcus aureus with the use of a colony-forming assay. RESULTS: Immunohistochemical analysis confirmed the presence of abundant LL-37 and HBD-2 in the superficial epidermis of all patients with psoriasis. In comparison, immunostaining for these peptides was significantly decreased in acute and chronic lesions from patients with atopic dermatitis (P=0.006 and P=0.03, respectively). These results were confirmed by immunodot blot and Western blot analyses. Real-time RT-PCR showed significantly lower expression of HBD-2 mRNA and LL-37 mRNA in atopic lesions than in psoriatic lesions (P=0.009 and P=0.02, respectively). The combination of LL-37 and HBD-2 showed synergistic antimicrobial activity by effectively killing S. aureus. CONCLUSIONS: A deficiency in the expression of antimicrobial peptides may account for the susceptibility of patients with atopic dermatitis to skin infection with S. aureus.

Adult↗
PubMed2002

Decreased IL-15 may contribute to elevated IgE and acute inflammation in atopic dermatitis.

PBMC and acute skin lesions of patients with atopic dermatitis (AD) are characterized by increased IL-4 and IL-13, but decreased IFN-gamma production. This bias toward an increased Th2 cytokine profile may contribute to the elevated IgE levels and acute skin inflammation seen in AD. In this study, we examined the levels of IL-15, a Th1-like cytokine, in the PBMC and the skin lesions of AD patients. IL-15 secretion by Staphylococcal enterotoxin B-treated PBMC of AD patients was significantly lower than that of normals and psoriasis patients (p < 0.001). Membrane-bound IL-15 expression as measured by mean fluorescence intensity and percentage of IL-15-positive cells in Staphylococcal enterotoxin B-treated monocytes of AD patients (644 +/- 49% and 12.7 +/- 0.6%, respectively) were significantly lower than that of normals (869 +/- 56% and 15.8 +/- 1.2%, respectively) and psoriasis patients (1488 +/- 217% and 22.7 +/- 0.8%, respectively; p < 0.0007 and p < 0.0001, respectively). The membrane-bound IL-15 expression was also significantly lower in the control monocytes of AD patients compared with that in normals and psoriasis patients. There was no significant difference in the absolute number or percentage of monocytes between the study subjects. However, psoriasis skin lesions were found to have significantly more IL-15 mRNA-expressing cells (22.4 +/- 1.7) compared with that in acute AD (7.5 +/- 1.7) and chronic AD (13.7 +/- 1.7) skin lesions (p < 0.05). IL-15 enhanced IFN-gamma production by the PBMC of AD patients (p < 0.01), but not by that of normal individuals or psoriasis patients. In addition, IL-15 was found to suppress IgE synthesis (p < 0.01) by the PBMC of AD patients. These data support the concept that reduced IL-15 expression may contribute to the pathogenesis of AD.

Acute Disease↗