Very low density lipoproteins (VLDL) trigger the release of histamine from human basophils

Gonen, Boas; O'Donnell, P.; Post, Thomas J.; Quinn, Thomas J.; Schulman, Edward S.

doi:10.1016/0005-2760(87)90121-4

Cited by 31 publications

(12 citation statements)

References 29 publications

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“…The mechanism for this hyperreactivity is unclear but may relate to a reduction in airway caliber, which is associated with hyperreactivity, 45 or to alterations in lipid metabolism. 46 The BMI also may be representative of sedentary lifestyles associated with infrequent deep inspirations, which have been shown to increase bronchial hyperreactivity 47 ; however, controlling for a variety of physical activity measures in our study did not alter the results. Alternatively, obese individuals may be at higher risk because they tend to spend more time indoors, 48 thereby leading to more sustained exposure to the indoor allergens associated 2with asthma.…”

Section: Commentcontrasting

confidence: 55%

Prospective Study of Body Mass Index, Weight Change, and Risk of Adult-onset Asthma in Women

Camargo

Weiss²,

Zhang³

et al. 1999

Arch Intern Med

739

578

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Section: Commentcontrasting

confidence: 55%

Prospective Study of Body Mass Index, Weight Change, and Risk of Adult-onset Asthma in Women

Camargo

Weiss²,

Zhang³

et al. 1999

Arch Intern Med

739

578

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“…Histamine plays a role in atherogenesis and HDC expression has been previously associated with atherosclerotic status [29]. Importantly, lipoproteins, in particular very low-density lipoprotein, have been shown to cause secretion of histamine from basophils [30]. HDC may also play a more general role in metabolic syndrome as murine knockouts display hyperleptinemia, obesity, and glucose intolerance [31], [32].…”

Section: Resultsmentioning

confidence: 99%

An Immune Response Network Associated with Blood Lipid Levels

et al. 2010

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While recent scans for genetic variation associated with human disease have been immensely successful in uncovering large numbers of loci, far fewer studies have focused on the underlying pathways of disease pathogenesis. Many loci which are associated with disease and complex phenotypes map to non-coding, regulatory regions of the genome, indicating that modulation of gene transcription plays a key role. Thus, this study generated genome-wide profiles of both genetic and transcriptional variation from the total blood extracts of over 500 randomly-selected, unrelated individuals. Using measurements of blood lipids, key players in the progression of atherosclerosis, three levels of biological information are integrated in order to investigate the interactions between circulating leukocytes and proximal lipid compounds. Pair-wise correlations between gene expression and lipid concentration indicate a prominent role for basophil granulocytes and mast cells, cell types central to powerful allergic and inflammatory responses. Network analysis of gene co-expression showed that the top associations function as part of a single, previously unknown gene module, the Lipid Leukocyte (LL) module. This module replicated in T cells from an independent cohort while also displaying potential tissue specificity. Further, genetic variation driving LL module expression included the single nucleotide polymorphism (SNP) most strongly associated with serum immunoglobulin E (IgE) levels, a key antibody in allergy. Structural Equation Modeling (SEM) indicated that LL module is at least partially reactive to blood lipid levels. Taken together, this study uncovers a gene network linking blood lipids and circulating cell types and offers insight into the hypothesis that the inflammatory response plays a prominent role in metabolism and the potential control of atherogenesis.

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“…Surprisingly, a proportion of non-allergic controls also demonstrated upregulation of CD63, although they do not experience any symptoms. Evidence that basophils and mast cells have receptors for LDL was reported many years ago 36, 37 . We postulate that the likely explanation for this enigmatic finding is that, although VLDL or LDL can cause basophils to upregulate CD63, the quantity of histamine released in non-allergic controls is not sufficient to cause symptoms.…”

Section: Mechanisms Of Anaphylaxismentioning

confidence: 99%

The alpha-gal story: Lessons learned from connecting the dots

Steinke

Platts-Mills

Commins

2015

Journal of Allergy and Clinical Immunology

309

245

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Anaphylaxis is a severe allergic reaction that can be rapidly progressing and fatal; thus, establishing the etiology of anaphylaxis is pivotal to long-term risk management. Our recent work has identified a novel IgE antibody response to a mammalian oligosaccharide epitope, galactose-alpha-1,3-galactose (alpha-gal). IgE to alpha-gal has been associated with two distinct forms of anaphylaxis: i) immediate onset anaphylaxis during first exposure to intravenous cetuximab, and ii) delayed onset anaphylaxis 3–6 hours after ingestion of mammalian food products (e.g., beef and pork). Results of our studies and those of others strongly suggest that tick bites are a cause, if not the only significant cause, of IgE antibody responses to alpha-gal in the southern, eastern and central United States, Europe, Australia and parts of Asia. Typical immune responses to carbohydrates are considered to be T cell-independent, while IgE antibody production is thought to involve sequential class-switching that requires input from T cells. Therefore, establishing the mechanism of the specific IgE antibody response to alpha-gal will be an important aspect to address as this area of research continues.

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Very low density lipoproteins (VLDL) trigger the release of histamine from human basophils

Cited by 31 publications

References 29 publications

Prospective Study of Body Mass Index, Weight Change, and Risk of Adult-onset Asthma in Women

Prospective Study of Body Mass Index, Weight Change, and Risk of Adult-onset Asthma in Women

An Immune Response Network Associated with Blood Lipid Levels

The alpha-gal story: Lessons learned from connecting the dots

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