Background: Some chemical compounds in the environment worsen allergic inflammation. In this study, we examined whether organic solvents induce the production of thymic stromal lymphopoietin (TSLP) which elicits Th2-type immune responses. Methods: Organic solvents were painted on the earlobes of BALB/c mice. The expression of TSLP in the ear was determined by ELISA. Results: Xylene and toluene, but not chloroform or ethyl acetate, induced the expression of mRNA for TSLP in the earlobe tissue. Among the aromatic compounds, xylene, especially m-xylene, and trimethylbenzene caused apparent TSLP production. The level of TSLP in the xylene-treated earlobes reached a maximum at 24 h, and TSLP was expressed in epithelial tissues. Production of TSLP was unaffected in mast cell-deficient W/Wv mice but apparently diminished in TNF-α knockout mice and IL-4 receptor knockout mice. Repeated painting of xylene for 7 days induced an increase in the weight of cervical lymph nodes and expression of OX40 ligand, both of which were inhibited in TSLP receptor knockout mice. Xylene promoted the picryl chloride-induced thickening of the ear and IL-4 production, which were reversed in TSLP receptor knockout mice. Conclusion: Xylene induced TSLP production, resulting in an exacerbation of allergic inflammation. Thus, xylene might be a good tool for examining the roles of TSLP in eliciting allergy in experimental animals.
We used a PCR method to develop a diagnostic assay for the detection of cytomegalovirus (CMV) DNA in infantile hepatitis, which has been suggested to be associated with CMV infection. CMV DNA was detected in 25 (58.1%) of 43 patients with elevated serum alanine aminotransferase (ALT) levels but no jaundice, and no hepatitis B or C as assessed by conventional PCR. None of the samples from 97 healthy infants tested positive for CMV DNA. We assayed CMV DNA quantitatively in blood using a real-time PCR system that allowed reproducible detection of at least 10 copies of CMV DNA. When 1 microg of DNA from each blood sample was used in this system, a good correlation was obtained between the calculated and measured copy numbers of CMV DNA. This system detected CMV DNA in 29 patients (67.4%) with liver dysfunction. Serial studies in patients with liver dysfunction revealed that CMV DNA copy number decreased, ultimately to below 10, as the ALT levels normalized. In contrast, no CMV DNA copies were detectable by the real-time system in any of the samples from control subjects. These results highlight the usefulness of detecting CMV DNA in the diagnosis of infantile hepatitis and indicate that the real-time quantitative PCR assay may be a valuable tool for monitoring CMV-associated infantile hepatitis.
Background Thymic stromal lymphopoietin (TSLP) plays critical roles in the induction and exacerbation of allergic diseases. We tested various chemicals in the environment and found that xylene and 1,2,4-trimethylbenzene induced the production of TSLP in vivo. These findings prompted us to search for additional chemicals that induce TSLP production. In this study, we examined whether fatty acids could induce the production of TSLP in vivo and exacerbate allergic inflammation. Methods Various fatty acids and related compounds were painted on the ear lobes of mice and the amount of TSLP in the homogenate of ear lobe tissue was determined. The effects of nonanoic acid on allergic inflammation were also examined. Results Octanoic acid, nonanoic acid, and decanoic acid markedly induced TSLP production, while a medium-chain aldehyde and alcohol showed only weak activity. Nonanoic acid induced the production of TSLP with a maximum at 24 h. TSLP production was even observed in nonanoic acid-treated C3H/HeJ mice that lacked functional toll-like receptor 4. The aryl hydrocarbon receptor agonist β-naphthoflavone did not induce TSLP production. Nonanoic acid promoted sensitization to ovalbumin, resulting in an enhancement in the cutaneous anaphylactic response. In addition, painting of nonanoic acid after the sensitization augmented picryl chloride-induced thickening of the ear, which was reversed in TSLP receptor-deficient mice. Conclusion Nonanoic acid and certain fatty acids induced TSLP production, resulting in the exacerbation of allergic inflammation. We propose that TSLP-inducing chemical compounds such as nonanoic acid be recognized as chemical allergo-accelerators.
Exposure to several chemical compounds in the environment might worsen allergies. However, it remains unclear which chemicals except for contact-sensitizing compounds modify inflammatory and immune responses and how. Thymic stromal lymphopoietin (TSLP), an IL-7-like cytokine produced mainly by epithelial cells, plays important roles in the initiation of allergic inflammation. We found that the painting of xylene on ear lobes induced production of TSLP and exacerbated the picryl chloride-induced allergic dermatitis. Thus, there are chemical compounds in the environment which do not have contact-sensitizing activity but cause the production of TSLP and on exacerbation of allergic dermatitis.
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