Virus, bacteria and lipopolysaccharide increase basophil cell response to histamine releasing stimulators and calcium

Abstract

Histamine release from human basophil leukocytes from allergic patients or controls was induced by specific antigens, anti-IgE or calcium ionophore A23187. Influenza A virus, S. aureus and lipopolysaccharide from S. typhimurium increased the maximum release of histamine and caused a shift to the left of the dose-response curves showing increased cell sensitivity and lowering of the threshold to these stimuli. The mechanism of action was elucidated by examining the mediator release as a function of increasing extracellular concentration of calcium. In these experiments the dose-response curves were changed by the microorganisms and lipopolysaccharide as before. This indicates that the microorganisms and lipopolysaccharide change the basophil cell response to IgE-dependent and non-immunological stimuli by causing a change in the subcellular handling of calcium.

Potential allergens stimulate the release of mediators of the allergic response from cells of mast cell lineage in the absence of sensitization with antigen‐specific IgE

“…Histamine release in response to lectins, bacteria, viruses, and LPS is well documented [5,. No apparent variation in the reactivity of IgE from different individuals to specific lectins has been observed, although it has been suggested that lectin-induced histamine release is an IgEdependent reaction [39].…”

Mechanisms of virus‐induced asthma exacerbations: state‐of‐the‐art. A GA2LEN and InterAirways document

“…In vitro incubation of basophils with viruses does not in itself cause release of mediators; however, some viruses (e.g. RSV, adenovirus and influenza) have been shown to enhance anti-immunoglobulin (Ig)E-mediated histamine release (66). These effects were shown to occur ex vivo with basophils from asthmatic volunteers during the acute phase compared with the convalescent phase of symptomatic colds, the increase in histamine and leukotriene release occurring in response to cross-linking of VLA 4 (67).…”

Modulation of gastric hemorrhage and ulceration by oxidative stress and histamine release in Salmonella typhimurium-infected rats

“…Mast cells are one of the important resources of histamine release. In the infective disease, bacterial products may also act as basophil histamine liberators through immunological (IgE-mediated) and nonimmunological reaction, in particular via the lectin-sugar pathway (Clementsen, 1991). Pharmacologically, histamine produces vasodilatation and increase in permeability of blood vessel walls that may contribute to gastric hemorrhage (Hung, 2001).…”