Bacteria and endotoxin enhance basophil histamine release and potentiation is abolished by carbohydrates

Abstract

Histamine release caused by anti-IgE, specific antigens and calcium ionophore A23187 was examined in leukocyte suspensions from healthy individuals and patients allergic to house dust mite and birch pollen. Staphylococcus aureus and LPS from Salmonella typhimurium were found to cause a synergistic enhancement of the release. The potentiation of mediator release by the bacteria and the endotoxin depends on a binding to the basophilocyte, followed by a non-transient event, since the potentiating effect persists after preincubation of the cells with the LPS followed by washout and leaving the cells for 30 min at 37 degrees C before stimulation with anti-IgE. The potentiation was abolished or reduced by galactose (10(-7) and 10(-6) M) and N-acetylglucosamine (10(-6) and 10(-5) M), acting by a binding to the basophil cell membrane, demonstrated by the persistence of effect after preincubation and washout of unbound sugar.

Toll-Like Receptor (TLR)2 and TLR4 in Human Peripheral Blood Granulocytes: A Critical Role for Monocytes in Leukocyte Lipopolysaccharide Responses

“…Only a few studies have examined the responses of basophils to LPS, most of which have shown that in mixed cell suspensions LPS primes or enhances basophil histamine release (20,28). However, one study showed that purified basophils did not make IL-8 mRNA when stimulated with LPS, but did make IL-8 mRNA in response to control stimuli (43).…”

“…Eosinophils have been recently reported to be LPS responsive and to express CD14 protein and TLR2 and TLR4 mRNAs (26), but a contradictory report found them to be CD14 negative and their apparent LPS responsiveness to be dependent upon the presence of monocytes (27). Basophils have been shown to be LPS responsive, but again in cell suspensions not fully depleted of CD14 ϩ monocytes (28,29), and their patterns of TLR expression are wholly unknown. Therefore, we set out to investigate whether patterns of TLR mRNA and protein expression on these cell types correlated with patterns with LPS responsiveness in standard gradient-purified preparations and after further purification by negative selection to remove contaminating monocytes.…”

Staphylococcus aureus superantigens and airway disease

“…Mechanistic studies have shown that S. aureus can induce the release of histamine from leukocytes of both house-dust mite (Dermatophagoides pteronyssinus)-and birch-pollen-allergic individuals [40,41], and additionally potentiate D. pteronyssinus-induced release of histamine in asthmatics sensitized to D. pteronyssinus [42]. It appears that the expression of TCR-Vbeta8(+) T cells obtained in bronchoalveolar lavage (BAL) of patients with poorly controlled asthma is also significantly increased, compared with cells in BAL of patients with well-controlled asthma and normal control subjects, suggesting that the staphylococcal superantigens are a potential trigger of T-cell activation in poorly controlled asthma [43•].…”

Prevalence of Serum IgE Antibodies to the <i>Staphylococcus aureus </i>Enterotoxins (SAE, SEB, SEC, SED, TSST-1) in Patients with Persistent Allergic Rhinitis

“…Different groups have shown that S. aureus increased the release of histamine from basophils of both house dust mite (HDM)- and birch pollen-allergic patients [20, 21]and potentiated Dermatophagoides pteronyssinus- induced histamine release in patients with asthma due to HDM [22]. Recently, Bachert et al [23]demonstrated that in about 50% of the polyp homogenates, specific IgE to SEA and/or SEB were present and linked to a polyclonal IgE synthesis towards inhalant allergens.…”