Editorial
doi: 10.1016/j.jaci.2021.05.004.
Epub 2021 May 14.
Environmental endotoxin exposure and asthma
Affiliations
- PMID: 34000345
- PMCID: PMC9706490
- DOI: 10.1016/j.jaci.2021.05.004
Item in Clipboard
Editorial
Environmental endotoxin exposure and asthma
J Allergy Clin Immunol.
2021 Jul.
No abstract available
Keywords: Allergy; LPS; asthma; endotoxin; inflammation; innate immunity.
Conflict of interest statement
Conflict of Interest Statement: The research studies by the author that are described in this manuscript were funded by the U.S. National Institutes of Health, Centers for Disease Control and Prevention, and Housing and Urban Development. The author has no conflicts of interest to disclose.
Figures
Geometric mean airborne endotoxin and reservoir dust endotoxin in a variety of settings. Figure 1A. Airborne endotoxin concentration (EU/m3) measured in 23 environments using the kinetic chromogenic Limulus amoebocyte lysate assay in our laboratory. It is noteworthy that endotoxin concentrations vary more than 10,000-fold across these locations and circumstances. Squares denote outdoor environments, circles denote indoor domestic and office locations, red triangles denote agricultural settings from multiple studies. Figure 1B. Reservoir dust endotoxin load (EU/m2) measured in residences using the kinetic chromogenic Limulus amoebocyte lysate assay. Squares denote data from the National Survey of Lead and Allergens in Housing (NSLAH), the circle denotes data from the National Health and Nutrition Examination Survey (NHANES). All assays were conducted in our University of Iowa Laboratory. CAFO: concentrated animal feeding operation; NYC: New York City.
Four strains of mice (C57Bl/6, TLR-3Lps-d, MD-2−/−, and CD-14−/−) were exposed to 300 EU of lipoöligosaccharide from Neisseria meningitidis alone (LOS) or complexed with MD-2 (LOS:MD-2) or received vehicle control (CNTL) by intranasal instillation. Neutrophils (Figure 2A) and cytokines (TNF-α, Figure 2B and IL-6, Figure 2C) in bronchoalveolar lavage were measured. Mice deficient in CD-14 did not mount an inflammatory response to the LOS alone nor to the monomeric LOS:MD-2 complex. Similarly, TLR-4 deficient mice had limited responses. The MD-2−/− mice did not respond to the LOS but demonstrated a robust response to the LOS:MD-2 showing that exogenously-administered MD-2 complexed with endotoxin could restore the pathway to inflammation.