Does environmental endotoxin exposure prevent asthma?

Douwes, Jeroen; Pearce, Neil; Heederik, Dick

doi:10.1136/thorax.57.1.86

Cited by 128 publications

(89 citation statements)

References 84 publications

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“…Findings from epidemiological studies are less consistent [74]. Whereas some reports suggest a protective effect of endotoxins on the development of allergies [57,[75][76][77], others found that the exposure to endotoxins constitutes a risk factor for respiratory symptoms [78][79][80][81][82][83][84], which might depend on the amount of exposure [85].…”

Section: Endotoxinsmentioning

confidence: 75%

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Respiratory health and indoor air pollutants based on quantitative exposure assessments

et al. 2012

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We reviewed the main epidemiological studies that evaluate the respiratory effects of indoor air pollutants quantitatively in industrialised countries. Consistent results support short-term (aggravation) and, although more rarely, long-term (prevalence augmentation) effects on asthma, chronic bronchitis and chronic obstructive pulmonary disease (COPD) in indoor settings with poor air quality. Environmental tobacco smoke is one of the most important risks for respiratory symptoms and diseases worldwide. The evidence is also reliable for indoor nitrogen dioxide and particulate matter, which have been associated with asthma, bronchitis and COPD. Whereas formaldehyde and volatile organic compounds seem to be the main pollutants in indoor settings, relevant papers on their respiratory effects are still scarce, and limited to asthma and bronchitis. Moulds have been associated with an increased risk of asthma and COPD. Contradictory results have been found between endotoxins and asthma. The role of phthalates, persistent organic pollutants and flame retardants in respiratory diseases remains to be established. Results from rural areas of industrialised countries indicate that exposure to some indoor bio-contaminants might be protective in early life, while it is associated with adverse respiratory adverse effects in adulthood. Studies focusing on indoor air pollutants should be developed to better understand their involvement in the inception and aggravation of respiratory diseases.

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Section: Endotoxinsmentioning

confidence: 75%

“…Several questions are still unanswered. It has been shown that endotoxin could not only modulate the immune system but also lead to or exacerbate asthma through inflammation [74]. Such observations suggest that these compounds might have protective or adverse effects according to atopic status.…”

Section: Endotoxinsmentioning

confidence: 98%

Respiratory health and indoor air pollutants based on quantitative exposure assessments

et al. 2012

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“…Recent epidemiological studies have implicated endotoxin as a protective factor against the development of asthma. [33][34][35] Independent analysis (Aldevron, Fargo, ND) of our grade V OVA demonstrated that the 1% solution contained 0.6 to 4.1 g/ml of lipopolysaccharide (LPS) endotoxin. Based on the ratio of our calculated OVA inhalation dose to aerosol concentration (80 g/10 mg/ml), we estimate that the mice could have inhaled between 5 and 35 ng/day of endotoxin.…”

Section: Discussionmentioning

confidence: 99%

Chronic Inhaled Ovalbumin Exposure Induces Antigen-Dependent but Not Antigen-Specific Inhalational Tolerance in a Murine Model of Allergic Airway Disease

Schramm

Puddington

et al. 2004

The American Journal of Pathology

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Sensitized mice acutely challenged with inhaled ovalbumin (OVA) develop allergic airway inflammation, characterized by OVA-specific IgE production, airway eosinophilia, increased pulmonary B and T lymphocytes, and airway hyperreactivity. In this study, a chronic exposure model was developed and two distinct patterns of response were observed. Discontinuous inhalational exposure to OVA (6 weeks) produced airway inflammation and hyperreactivity that were similar to acute (10 days) responses. Continuous inhalational exposure to OVA (6 or 11 weeks) resulted in attenuation of airway eosinophilia and hyperresponsiveness without reduction of OVA-specific IgE and IgG 1 levels. The inhibition of airway inflammation was dependent on continuous exposure to antigen, because continuously exposed mice with attenuated inflammatory responses redeveloped allergic airway disease if the OVA aerosols were interrupted and then restarted (11-week-discontinuous). Inhalational tolerance induced by continuous OVA exposure demonstrated bystander suppression of cockroach allergen-mediated airway eosinophilia. These findings may be attributed to changes in production of the anti-inflammatory cytokine interleukin-10 during continuous OVA aerosol exposure. The symptomatic and asymptomatic allergic responses in human asthmatics could be explained by similar variable or discontinuous exposures to aeroantigens. Throughout the past 40 years, the prevalence of allergic disease, including atopic dermatitis, hay fever, and asthma, has risen dramatically in the developed world. This disturbing trend is documented best for asthma. 1,2 A wealth of clinical and experimental data suggests that allergic asthma is due to an aberrant lung immune response mediated through T-helper type 2 cells (Th2 cells) and associated cytokine-signaling pathways. The normal lung is able to distinguish between airborne antigens associated with infectious agents, to which an immunological response is generated, and harmless inhaled antigens, which are usually ignored. In the asthmatic lung, some of these normally harmless antigens activate specific Th2 cells and elicit an inflammatory response characterized by Th2 cytokine production, eosinophilic airway inflammation, airway hyperresponsiveness, and bronchoconstriction. These pulmonary responses may be accompanied by systemic allergic sensitization, manifested by elevated titers of antigen-specific IgE. The mechanisms that control CD4 ϩ T lymphocyte polarization to allergenic Th2 phenotypes are incompletely understood but seem to involve genetic predispositions, local factors such as pre-existing cytokine concentrations and inflammation, and antigenic factors (ie, potency, dose, and duration of exposure).Several investigators have used mouse models to investigate the mechanisms of inhalational tolerance to antigens 3,4 or of allergic airway sensitization. [5][6][7][8][9][10] However, these responses have typically been assessed in isolation from each other. We have recently demonstrated that C57BL/6J mice undergo a biphasic...

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“…Bacterial endotoxin in indoor environment has also been suggested to play a role in the development of atopy and asthma. However, it is currently not clear whether endotoxin has a protective or inducing effect, or both, depending on timing and dose of exposure (Martinez and Holt, 1999;Gereda et al, 2000;Gehring et al, 2001Gehring et al, , 2002Park et al, 2001;Douwes et al, 2002). Longterm exposure to allergens, fungi and endotoxin is generally assessed by measuring these agents in house dust at one point in time.…”

Section: Introductionmentioning

confidence: 99%

Reproducibility of allergen, endotoxin and fungi measurements in the indoor environment

Heinrich

Hölscher

Douwes

et al. 2003

J Expo Sci Environ Epidemiol

100

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Measurements of biocontaminants in settled house dust once a year are commonly used to assess long-term exposure. To examine stability over time and seasonal variation, we measured concentrations of mite and cat allergens, endotoxin and mold spores in living room floor dust in 745 German homes collected twice a year in two different seasons. The study population consisted of adults and children living in five different areas in Germany. All dust samples were collected in a standardized manner from the living room floor and taken during the years 1995 to 1998. The median interval between the two dust samplings was approximately 7 months. Mite and cat allergens were measured in settled house dust by monoclonal antibodies, endotoxin by the limulus amebocyte lysate method, and total spore counts by cultural methods. Crude Pearson's correlation coefficients between logtransformed concentrations in the first and second dust samples ranged between 0.65 and 0.75 for allergens, 0.59 for endotoxin and only 0.06 for total spore counts. The strongest and most consistent seasonal effects were observed for fungi with highest levels in July-September. Cat allergen concentrations were found consistently to be increased in January-March. Mite allergens did not show a strong and consistent seasonal pattern. We conclude that repeated measurements of mite and cat allergens and endotoxin in settled house dust improve the estimate for annual mean concentrations. However, even a single observation of these biocontaminants may be a good proxy for a 1-year exposure since repeated measures were highly correlated. However, repeated measurements of fungi levels were only weakly correlated and thus repeated observations for assessment of annual means of total spore counts are needed.

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Does environmental endotoxin exposure prevent asthma?

Cited by 128 publications

References 84 publications

Respiratory health and indoor air pollutants based on quantitative exposure assessments

Respiratory health and indoor air pollutants based on quantitative exposure assessments

Chronic Inhaled Ovalbumin Exposure Induces Antigen-Dependent but Not Antigen-Specific Inhalational Tolerance in a Murine Model of Allergic Airway Disease

Reproducibility of allergen, endotoxin and fungi measurements in the indoor environment

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