Exposure to Triclosan Augments the Allergic Response to Ovalbumin in a Mouse Model of Asthma
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV. Toxicological Sciences
(Impact Factor: 3.85).
11/2012; 132(1). DOI: 10.1093/toxsci/kfs328
During the last decade there has been a remarkable and unexplained increase in the prevalence of asthma. These studies were conducted to investigate the role of dermal exposure to triclosan, an endocrine-disrupting compound, on the hypersensitivity response to ovalbumin (OVA) in a murine model of asthma. Triclosan has had widespread use in the general population as an antibacterial and antifungal agent and is commonly found in consumer products such as soaps, deodorants, toothpastes, shaving creams, mouth washes, and cleaning supplies. For these studies, BALB/c mice were exposed dermally to concentrations of triclosan ranging from 0.75-3% (0.375-1.5 mg/mouse/day) for 28 consecutive days. Concordantly, mice were intraperitoneally injected with OVA (0.9 μg) and aluminum hydroxide (0.5 mg) on days 1 and 10 and challenged with OVA (125 μg) by pharyngeal aspiration on days 19 and 27. Compared to the animals exposed to OVA alone, increased spleen weights, OVA-specific IgE, Interleukin (IL)-13 cytokine levels, and lung eosinophils were demonstrated when mice were co-exposed to OVA and triclosan. Statistically significant increases in OVA-specific and non-specific airway hyperreactivity (AHR) were observed for all triclosan co-exposed groups when compared to the vehicle and OVA controls. In these studies exposure to triclosan alone was not demonstrated to be allergenic, however; co-exposure with a known allergen resulted in enhancement of the hypersensitivity response to that allergen, suggesting that triclosan exposure may augment the allergic responses to other environmental allergens.
Available from: Christine G Parks
- "Similar results have been observed in female mice, where exposure to triclosan enhanced the hypersensitivity response to an allergen (Anderson et al. 2013). While it is unclear how triclosan could be related to the development of autoimmunity, and why the association was only seen in males in our study, the enhancement of certain T cell responses is thought to be strongly associated with development of autoimmunity and autoimmune disease related to environmental exposures (Selmi et al. 2012). "
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ABSTRACT: Potential associations between background environmental chemical exposures and autoimmunity are understudied.
Our exploratory study investigated exposure to individual environmental chemicals and selected mixtures in relation to the presence of antinuclear antibodies (ANA), a widely used biomarker of autoimmunity, in a representative sample of the U.S.
This cross-sectional analysis used data on 4340 participants from the National Health and Nutrition Examination Survey (1999-2004), of whom 14% were ANA positive, to explore associations between ANA and concentrations of dioxins, dibenzofurans, polychlorinated biphenyls, organochlorines, organophosphates, phenols, metals, and other environmental exposures and metabolites measured in participants' serum, whole blood, or urine. For dioxin-like compounds with toxic equivalency factors, we developed and applied a new statistical approach to study selected mixtures. Lognormal models and censored-data methods produced estimates of chemical associations with ANA in males, nulliparous females, and parous females that were adjusted for confounders and accommodated concentrations below detectable levels.
Several associations between chemical concentration and ANA positivity were observed, but only the association in males exposed to triclosan remained statistically significant after correcting for multiple comparisons (mean concentration ratio = 2.8; 95% confidence interval = 1.8,4.5; p < 10(-5)).
These data suggest that background levels of most xenobiotic exposures typical in the U.S. population are not strongly associated with ANA. Future studies should ideally reduce exposure misclassification by including prospective measurement of the chemicals of concern, and track changes in ANA and other autoantibodies over time.
- "Several studies have used ovalbumin for induction of allergy to investigate the effects of allergy in different situations. It has been shown to be a reliable allergen in animal studies. "
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ABSTRACT: This randomized trial was undertaken to investigate the effect of experimentally induced allergy on orthodontic induced root resorption.
A total of 30 Wistar rats were divided randomly into test and control groups. Starting from the first 3 days, the rats in the test group were injected intra-peritoneally by 2 mg ovalbumin as allergen and 0.5 mg Alume as adjuvant. Afterward only allergen was injected once a week. The control group was injected by normal saline. After 21 days, Wistar immunoglobulin E was measured and peripheral matured eosinophil was counted. A total of 50 g nickel-titanium closed coil spring was ligated between right incisor and first molar. All animals were sacrificed after 14 days. The mesial root of the right and left first molar was dissected in a horizontal plane. The specimens were divided into four groups considering whether force and/or ovalbumin was applied or not. Root resorption was measured and compared among these groups. Repeated measures analysis of variance (ANOVA), and Bonferoni tests were used to analyze the data. The level of significance was determined at 0.05.
In general, the differences were insignificant (P < 0.05). As the only exception, the group in which both ovalbumin and force were applied had significantly more root resorption than the group in which neither force nor ovalbumin was applied (P > 0.001).
Allergy may increase the susceptibility to root resorption. Application of light force, periodical monitoring of root resorption and control of allergy are advisable.
Available from: Mark H. Kaplan
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ABSTRACT: Pulmonary viral infections can exacerbate or trigger the development of allergic airway diseases via multiple mechanisms depending upon the infectious agent. Respiratory vaccinia virus transmission is well established, yet the effects of allergic airway disease on the host response to intra-pulmonary vaccinia virus infection remain poorly defined. As shown here BALB/c mice with preexisting airway disease infected with vaccinia virus developed more severe pulmonary inflammation, higher lung virus titers and greater weight loss compared with mice inoculated with virus alone. This enhanced viremia was observed despite increased pulmonary recruitment of CD8(+) T effectors, greater IFNγ production in the lung, and high serum levels of anti-viral antibodies. Notably, flow cytometric analyses of lung CD8(+) T cells revealed a shift in the hierarchy of immunodominant viral epitopes in virus inoculated mice with allergic airway disease compared to mice treated with virus only. Pulmonary IL-10 production by T cells and antigen presenting cells was detected following virus inoculation of animals and increased dramatically in allergic mice exposed to virus. IL-10 modulation of host responses to this respiratory virus infection was greatly influenced by the localized pulmonary microenvironment. Thus, blocking IL-10 signaling in virus-infected mice with allergic airway disease enhanced pulmonary CD4(+) T cell production of IFNγ and increased serum anti-viral IgG1 levels. In contrast, pulmonary IFNγ and virus-specific IgG1 levels were reduced in vaccinia virus-treated mice with IL-10 receptor blockade. These observations demonstrate that pre-existing allergic lung disease alters the quality and magnitude of immune responses to respiratory poxviruses through an IL-10-dependent mechanism.
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