Intrinsic asthma and bacterial histamine release

Norn, S.; Skov, Per Stahl; Kock, Chr; Andersen, Peter Riis; Pedersen, Michael; Tønnesen, Philip; Pedersen, Preben Ulrich; Møller, Niels; Hertz, J. B.; Høiby, Niels

doi:10.1007/bf01965116

Cited by 14 publications

(3 citation statements)

References 4 publications

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“…It has previously been shown that bacteria can induce histamine release from human basophil leukocytes in vitro in both normal individuals and patients with intrinsic asthma (10,18,19), and a similar release was observed in human lung mast cells (2). In this study we examined the effect of influenza A virus on histamine release caused by S. aureus.…”

Section: Discussionmentioning

confidence: 88%

Influenza A virus enhances Staphylococcus aureus‐induced basophil histamine release in normal individuals and patients with intrinsic asthma

Clemensten

Bindslev‐Jensen

Jarløv

et al. 1989

Allergy

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Influenza A virus was found to enhance Staphylococcus aureus-induced histamine release in human leukocyte suspensions, but did not per se release histamine. This potentiating effect was found to be similar in cells from normal individuals and from patients with intrinsic asthma. The enhancement of mediator release could be due to viral neuraminidase on the surface of the virus, since a similar potentiating effect was caused by a purified neuraminidase preparation obtained from Vibrio cholerae, and the effect of virus as well as of the purified neuraminidase was completely abolished by a potent neuraminidase inhibitor. The potentiating effect of virus on bacteria-induced mediator release might be of importance for the conversion from latent to manifest asthma in upper respiratory tract infections.

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Section: Discussionmentioning

confidence: 88%

Influenza A virus enhances Staphylococcus aureus‐induced basophil histamine release in normal individuals and patients with intrinsic asthma

Clemensten

Bindslev‐Jensen

Jarløv

et al. 1989

Allergy

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“…It seems that at least two different mechanisms are involved in this bacterial histamine release: an immunoglobulin E (IgE)-dependent mechanism, in which removal of IgE from the basophils abolished or reduced the bacteria-induced histamine release, and a nonimmunological mechanism, in which this was not the case (6). We found that bacterial ultrasonicates of several strains from the normal flora of the upper respiratory tract caused release of histamine from basophil leukocytes in both intrinsic asthma patients and normal individuals (8,13). This release might be a pathogenic mechanism in intrinsic asthma and in bacterial infections.…”

mentioning

confidence: 87%

Staphylococcus aureus peptidoglycan induces histamine release from basophil human leukocytes in vitro

Espersen¹,

Jarløv²,

Bindslev‐Jensen³

et al. 1984

Infect Immun

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Whole killed cells, cell walls, and peptidoglycans of Staphylococcus aureus were found to release histamine from human leukocytes and isolated rat mast cells in vitro. The histamine-releasing capability increased in the order of whole bacteria, cell walls, and peptidoglycans. Peptidoglycan was found to release histamine by a nonimmunological mechanism, as demonstrated by release in cells deprived of surface immunoglobulins, whereas whole bacteria and cell walls seemed to operate both by immunological and nonimmunological mechanisms. Histamine release was not a specific property of S. aureus; a wide range of whole bacterial species had this activity. We suggest that peptidoglycan may be a common factor responsible for histamine release by different bacteria.

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“…through interaction with the specific receptors on the surface of mast cells, induce a slow release of chemical mediators [58]. In addition, components of bacterial cell walls may directly interact with the surface of mast cells and basophils, to initiate mediator secretion by a non-immunological mechanism [59]. Thus, it is possible that within the airways selective bacteria may incite mast cell mediator release with the inflammatory consequences that this may produce.…”

Section: Non-specific Mechanismsmentioning

confidence: 99%