The effect of nicotine on basophil histamine release

Thompson-Cree, Margaret E. M.; Stevenson, Michael R.; Shields, Michael; Ennis, Madeleine

doi:10.1007/s00011-004-1249-1

Cited by 8 publications

(7 citation statements)

References 16 publications

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“…29 Smokers have higher rates of carriage of pneumococci 30 and higher rates of invasive pneumococcal disease. 5 Various substances in tobacco smoke (e.g., nicotine, nicotine-derived nitrosamine ketone) can influence dysfunction of numerous immune cell types, including macrophages, 6 basophils, 7 and mast cells. 8 For these reasons, respiratory infections were of particular interest, and did in fact show a slightly higher AOR of antibiotic usage (1.31) compared with infections overall (1.20) in the findings.…”

Section: Discussionmentioning

confidence: 99%

Tobacco Smoking as a Risk Factor for Increased Antibiotic Prescription

Steinberg

Akincigil

Kim

et al. 2016

American Journal of Preventive Medicine

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Introduction Antibiotic resistance is rapidly spreading, affecting millions of people and costing billions of dollars. Potential factors affecting antibiotic prescription, such as tobacco use, could dramatically influence this public health crisis. The study determined the magnitude of impact that tobacco use has on antibiotic prescribing patterns. Methods Pooled data were analyzed in 2015 from the 2006–2010 National Ambulatory Medical Care Survey, a cross-sectional survey describing use of ambulatory medical services in the U.S. via healthcare provider–patient encounters. Patients aged >18 years with documented tobacco use status diagnosed with an infection were included (i.e., all encounters in the analysis included an infectious diagnosis of interest). The analytic sample included 8,307 visits, representing 294 million visits nationally. Results Half (49.9%) of encounters that included any infection had an antibiotic prescribed. Adjusted odds of receiving antibiotics among current tobacco users was 1.20 (95% CI=1.02, 1.42), and even higher for encounters of respiratory infections (AOR=1.31, 95% CI =1.05, 1.62). Antibiotic prescription rates were lower among patients aged >65 years, those with comorbid asthma or cancer, non-whites, and those covered by Medicaid and higher for primary care physicians. Conclusions Despite lack of evidence-based rationale, among a national sample of patients with an infectious diagnosis, tobacco users had 20%–30% higher odds of receiving antibiotics than non-tobacco users. This is the first U.S. study to quantify the magnitude of this unsubstantiated practice. Prescribers should understand that tobacco use could be associated with higher antibiotic prescription, which may subsequently increase antimicrobial resistance in the community.

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Section: Discussionmentioning

confidence: 99%

Tobacco Smoking as a Risk Factor for Increased Antibiotic Prescription

Steinberg

Akincigil

Kim

et al. 2016

American Journal of Preventive Medicine

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“…These receptors are believed to be inhibitory receptors as Thompson‐Cree et al . [7] have demonstrated a decrease in IgE‐mediated release of histamine by prior incubation of basophils with nicotine and a nicotine agonist, methyl‐2‐[3‐pyridyl] pyrolidine.…”

Section: Discussionmentioning

confidence: 99%

“…Muscarinic Acetylcholine (ACh) receptors have been characterised on human mast cells, the tissue‐based mediators of immediate hypersensitivity [4–6] and nicotinic ACh receptors are also suspected to exist on these cells and on basophils, their humoral counterparts [7]. As neuromuscular blocking drugs used in anaesthesia act on the nicotinic receptors on the neuro‐muscular junction, we considered the hypothesis that these drugs may also act on a nicotinic receptor on the cells involved in acute anaphylaxis; basophils and mast cells.…”

mentioning

confidence: 99%

Nicotinic acetylcholine receptors on basophils and mast cells

Sudheer¹,

Hall

Donev

et al. 2006

Anaesthesia

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SummaryAnaphylaxis in response to drugs administered during anaesthesia is a rare but potentially catastrophic event. The anaesthetic drugs most commonly associated with anaphylaxis are neuromuscular blocking agents. As these drugs act on the nicotinic acetylcholine receptor of the neuromuscular junction, potentiation of anaphylaxis by a nicotinic receptor on basophils and mast cells is plausible. The aim of this study was to investigate whether nicotinic acetylcholine receptors are present on a human basophil and mast cell lines as their presence may suggest a mechanism of associated anaphylaxis. Nicotinic receptors were demonstrated on a basophil and a mast cell line using an a-bungarotoxin-fluorescein conjugate by flow cytometry and by both conventional and confocal microscopic techniques. The identity of this receptor was confirmed by reverse transcriptase PCR and quantitative PCR.

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“…Sudheer et al [45] reported that the nicotinic antagonist α 7 -bungarotoxin fluorescently bound to the surface of human basophils. Furthermore, in the presence of nicotine, treatment of anti-IgE-stimulated basophils dose-dependently decreased histamine degranulation in human basophils, suggesting that these cells may have functional nAChRs [14]. …”

Section: Introductionmentioning

confidence: 99%

“…Efferent neurons respond to proinflammatory mediators by releasing endogenous acetylcholine (ACh), which then binds to nicotinic ACh receptors (nAChRs) on various structural and immune cells [9,10,14,15,16]. This leads to the modulation of intracellular signaling cascades that control proinflammatory cellular responses [10,14]. nAChRs are a family of ligand-gated, pentameric ion channels, and 17 different subunits (α 1 -α 8 , α 9 , α 10 , β 1 -β 4 , δ, ϵ and γ) have been reported in humans [17,18,19].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Allergen-Induced Basophil Activation by ASM-024, a Nicotinic Receptor Ligand

Watson

Oliveria²,

Nusca³

et al. 2014

Int Arch Allergy Immunol

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Background: Nicotinic acetylcholine receptors (nAChRs) were identified on eosinophils and shown to regulate inflammatory responses, but nAChR expression on basophils has not been explored yet. Objective: We investigated surface receptor expression of nAChR α₄, α₇ and α₁/α₃/α₅ subunits on basophils. Furthermore, we examined the effects of ASM-024, a synthetic nicotinic ligand, on in vitro anti-IgE and in vivo allergen-induced basophil activation. Methods: Basophils were enriched from the peripheral blood of allergic donors and the expression of nAChR subunits and muscarinic receptors was determined. Purified basophils were stimulated with anti-IgE in the presence of ASM-024 with or without muscarinic or nicotinic antagonists for the measurement of CD203c expression and histamine release. The effect of 9 days of treatment with 50 and 200 mg ASM-024 on basophil CD203c expression was examined in the blood of mild allergic asthmatics before and after allergen inhalation challenge. Results: nAChR α₄, α₇ and α₁/α₃/α₅ receptor subunit expression was detected on basophils. Stimulation of basophils with anti-IgE increased CD203c expression and histamine release, which was inhibited by ASM-024 (10^-5 to 10^-³ M, p < 0.05). The effect of ASM-024 was reversed in the presence of muscarinic and nicotinic antagonists. In subjects with mild asthma, ASM-024 inhalation significantly inhibited basophil CD203c expression measured 24 h after allergen challenge (p = 0.03). Conclusion: This study shows that ASM-024 inhibits IgE- and allergen-induced basophil activation through both nicotinic and muscarinic receptors, and suggests that ASM-024 may be an efficacious agent for modulating allergic asthma responses.

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The effect of nicotine on basophil histamine release

Abstract: This study has demonstrated that nicotine agonists inhibit histamine release from human basophils. Further studies examining the effect of smoking on basophil activation are required.

Cited by 8 publications

References 16 publications

Tobacco Smoking as a Risk Factor for Increased Antibiotic Prescription

Tobacco Smoking as a Risk Factor for Increased Antibiotic Prescription

Nicotinic acetylcholine receptors on basophils and mast cells

Inhibition of Allergen-Induced Basophil Activation by ASM-024, a Nicotinic Receptor Ligand

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