Staphylococcal IgE Antibodies, Hyperimmunoglobulinemia E and<i>Staphylococcus aureus</i>Infections

Schopfer, K; Baerlocher, K; Price, Patricia; Krech, U; Quie, P. G.; Douglas, Steven D.

doi:10.1056/nejm197904123001506

Cited by 150 publications

(52 citation statements)

References 23 publications

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“…Two cases in man have been described with similar findings; the chemotactic deficit was transient [ 141. A current proposal suggests that recurrent, atypical staphylococcal infections in man may not be due to primary cell defects of neutrophil chemotaxis, but rather the result of an abnormal immunologic response to Staphylococcus aureus by the production of immunoglobulin E antistaphylococcal antibodies [23].…”

Section: Discussionmentioning

confidence: 99%

A Transient Deficit in Neutrophilic Chemotaxis in a Dog with Recurrent Staphylococcal Pyoderma

1982

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Abstract. A transient neutrophilic chemotactic deficit was confirmed in a 3X-year-old castrated male dog with recurrent staphylococcal pyoderma accompanied by a persistent eosinophilia and intermittent basophilia. Neutrophilic chemotaxis was quantitatively assessed over the next seven months, and the disappearance of the chemotactic deficit correlated with complete clinical remission of the skin lesions. Aberrations of the complement system were not discovered, and the dog's serum showed increased chemoattractiveness for control neutrophi1 preparations.

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Section: Discussionmentioning

confidence: 99%

A Transient Deficit in Neutrophilic Chemotaxis in a Dog with Recurrent Staphylococcal Pyoderma

1982

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“…Patients with the hyperimmunoglobulin E (HIE) and recurrent infection syndrome produce high levels of IgE antibody directed against the cell wall of S. aureus (17)(18)(19). Although recurrent superficial staphylococcal pustulosis can be a significant problem in AD, the invasive S. aureus infections, e.g., recurrent pneumonias, seen in HIE syndrome, do not occur (20).…”

Section: Introductionmentioning

confidence: 99%

“…None ofthese patients, however, had a history of deep-seated S. aureus skin infections. Four control groups were studied: first, 15 (17)(18)(19)(20) was based on a history ofrecurrent sinusitis, pneumonia, deep-seated skin and pulmonary abscesses predominantly caused by S. aureus, chronic eczematoid dermatitis, and marked elevation of serum IgE (median IgE = 22,000, range: 5500-34,000 IU/ml) with an increased proportion of IgE directed to S. aureus strain Wood 46 (protein A-deficient). Informed consent was obtained from all subjects before performing these studies.…”

Section: Introductionmentioning

confidence: 99%

Presence of IgE antibodies to staphylococcal exotoxins on the skin of patients with atopic dermatitis. Evidence for a new group of allergens.

Leung¹,

Harbeck²,

Bina³

et al. 1993

J. Clin. Invest.

482

323

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In the current study, we investigated whether Staphylococcus aureus grown from affected skin of atopic dermatitis (AD) patients secreted identifiable toxins that could act as allergens to induce IgE-mediated basophil histamine release. The secreted toxins of S. aureus grown from AD patients were identified by ELISA using antibodies specific for staphylococcal enterotoxin (SE) exfoliative toxin (ET), or toxic shock syndrome toxin (TSST-1). S. aureus isolates from 24 of 42 AD patients secreted identifiable toxins with SEA, SEB, and TSST accounting for 92% of the isolates. 32 of 56 AD sera (57%) tested contained significant levels of IgE primarily to SEA, SEB, and/ or TSST. In contrast, although SEA, SEB, or TSST secreting S. aureus could be recovered from the skin of psoriasis patients, their sera did not contain IgE antitoxins.Freshly isolated basophils from 10 AD patients released 5-59% of total histamine in response to SEA, SEB, or TSST-1 but only with toxins to which patients had specific IgE. Basophils from eight other AD patients and six normal controls who had no IgE antitoxin failed to demonstrate toxin-induced basophil histamine release. Stripped basophils sensitized with three AD sera containing IgE to toxin released 1541% of total basophil histamine only when exposed to the relevant toxin, but not to other toxins. Sensitization of basophils with AD sera lacking IgE antitoxin did not result in release of histamine to any of the toxins tested.These data indicate that a subset of patients with AD mount an IgE response to SEs that can be grown from their skin. These toxins may exacerbate AD by activating mast cells, basophils, and/or other Fce-receptor bearing cells armed with the relevant IgE antitoxin. (J. Clin. Invest. 1993Invest. . 92:1374Invest. -1380

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“…The increase of IgE has been suggested to be caused by decreased activity ofThl cells that produce interferon-y and interleukin (IL)-2, combined with hyperactivity of Th2 cells that generate IL-4, IL-5, and IL-13, i.e., an imbalance between Thl and Th2 activity. In patients with this syndrome, a specific IgE antibody to S. aureus has been detected in the serum (8), and the high incidence of S. aureus infection has been suggested to be related to a defective immune response (9). Methylprednisolone and interferon-y are reported to inhibit FceR2 (CD 23) expression at the mRNAand protein levels Skinrash IgE (U/ml) 9,000-6,000-3,000-0 visceral abscesses with or without septicemia (1 1, 12).…”

Section: Discussionmentioning

confidence: 99%

Hyperimmunoglobulin E Syndrome Associated with Nephrotic Syndrome.

Tanji¹,

Yorioka

Kanahara

et al. 1999

Intern. Med.

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A 21-year-old man was admitted to Kure National Hospital with nephrotic syndrome in September 1996. He had suffered from an intractable pruritic skin rash and recurrent subcutaneous abscesses caused by the hyperimmunoglobulin E syndrome since the age of 18 months. Renal biopsy gave a diagnosis of membranoproliferative glomerulonephritis. Steroid therapy decreased urinary protein loss and hypoproteinemia, and his pruritic skin rash was improved. Patients with hyperimmunoglobulin E syndrome have a defective immune response, especially to Staphylococcus aureus infection. Continuous antigen stimulation mayhave caused this patient's renal histological damage as in immunecomplex glomerulonephritis. (Internal Medicine 38: 491-494, 1999)

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Staphylococcal IgE Antibodies, Hyperimmunoglobulinemia E andStaphylococcus aureusInfections

Cited by 150 publications

References 23 publications

A Transient Deficit in Neutrophilic Chemotaxis in a Dog with Recurrent Staphylococcal Pyoderma

A Transient Deficit in Neutrophilic Chemotaxis in a Dog with Recurrent Staphylococcal Pyoderma

Presence of IgE antibodies to staphylococcal exotoxins on the skin of patients with atopic dermatitis. Evidence for a new group of allergens.

Hyperimmunoglobulin E Syndrome Associated with Nephrotic Syndrome.

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