Differential expression of IFN-γ, IL-4, IL-10, and IL-1β mRNAs in decalcified tissue sections of mouse lipopolysaccharide-induced periodontitis mandibles assessed by in situ hybridization

Iwasaki, Yuka W.; Hara, Yoshitaka; Koji, Takehiko; Shibata, Yasuaki; Nakane, Paul K.; Kato, Ihachi

doi:10.1007/s004180050234

Cited by 18 publications

(14 citation statements)

References 39 publications

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“…Seymour et al [25] and Gemmell et al [26] proposed that the progression of periodontal diseases is characterized by a shift from a predominantly Th1 to a Th2 cell profile. This hypothesis is supported by some studies [2, 7, 11, 27, 28, 29, 30, 31] but has not been confirmed by others [32, 33]. Ellis et al [10] suggested that progressively lower gingival concentrations of IL-12 and higher IL-6 concentrations associated with increasing sulcular depth not only indicates a shift from a Th1 to a Th2 immunologic phenotype, but also suggests a regulatory role for IL-12 in that shift.…”

Section: Discussionsupporting

confidence: 70%

CD26 Immuno‐Expression and Periodontal Disease Progression

Manna¹,

Costa²,

Gomez³

2001

BioMed Research International

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Immunological mechanisms participate in the pathogenesis of human chronic inflammatory periodontal disease (CIPD). Human CD4+lymphocytes express functionally heterogeneous profiles of cytokine production. CD26 is an integral membrane glycoprotein, that is, a marker of Th1-like cytokine development. The purpose of the present study was to compare the immuno-expression of CD26 receptor in periodontal sites with and without clinical attachment loss (CAL). Five patients with rapidly progressing periodontitis and one with juvenile periodontitis were investigated. Each patient presented at least one site with and without CAL. Ten sites with CAL and nine without any CAL were biopsied, followed by the immunohistochemical identification of the CD26 receptor using the MIB-DS2/7 antibody. The results demonstrated that the percentage of positive cells for this antigen in the periodontal sites with CAL was not significantly different from those without attachment loss. Therefore, Th1 cell impairment may not be directly involved with periodontal attachment loss.

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Section: Discussionsupporting

confidence: 70%

CD26 Immuno‐Expression and Periodontal Disease Progression

Manna¹,

Costa²,

Gomez³

2001

BioMed Research International

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“…Actually, the EDTA-based solutions have been used for the purpose of decalcification of tissues for ISH in many recent studies (Fujii et al 1999;Iwasaki et al 1998), while Morse's solution was utilized by Nomura et al (1993) for detection of OC mRNA in odontoblasts. In our case, the latter solution completed decalcification within 24 h, while the former solution needed 7-8 days to decalcify similar samples.…”

Section: Discussionmentioning

confidence: 99%

Assessment of decalcifying protocols for detection of specific RNA by non-radioactive in situ hybridization in calcified tissues

Shibata

Fujita

Takahashi

et al. 2000

Histochemistry and Cell Biology

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For the best performance of in situ analysis of specific RNA expression in calcified tissues, it is necessary to choose an appropriate protocol to decalcify the tissues. We evaluated the usefulness of various acid-based decalcifying reagents with reference to 28 S rRNA staining by in situ hybridization using a thymine-thymine dimerized oligonucleotide probe. The reagents evaluated were 10% nitric acid, 10% HCl, 5% formic acid, 5% trichloroacetic acid, Morse's solution, Plank-Rychlo's solution, and K-CX solution, all of which are commonly used to decalcify tissues, and their effects on retention of morphology and RNA were compared with EDTA-based solutions. When normal mouse mandible was used as a model tissue, well-preserved morphology of ameloblasts was obtained from sections decalcified with Morse's solution, 10% HCl, Plank-Rychlo's solution, and K-CX solution, and best retention of 28 S rRNA was obtained with 5% formic acid and Morse's solution. We recommend Morse's solution to decalcify tissues to be processed for the rapid analysis of specific RNA expression. Indeed, we detected specific mRNAs strongly in sections treated with Morse's solution, and quantitative analysis showed that the ratio of signal intensities of 28 S rRNA and the specific mRNAs correlated with each other depending on decalcifying solutions.

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“…Another recent report also showed that subchronic LPS injections (20 injections of 5 g at 48-h intervals) into gingiva of mice produced a maximum level of interferon-␥ (INF-␥ ) (a Th1 cytokine) at the tenth injection but that INF-␥ decreased thereafter. IL-4 (a Th2 cytokine) began to increase after the tenth injection (31). Based on these find- Figure 1.…”

Section: Effect Of Home Endotoxin Exposure On Wheeze In the First Yeamentioning

confidence: 92%

House Dust Endotoxin and Wheeze in the First Year of Life

Park

Gold

Spiegelman

et al. 2001

Am J Respir Crit Care Med

337

279

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We examined endotoxin exposure and wheezing episodes during the first year of life in a birth cohort of 499 infants with one or both parents having a history of asthma or allergy. We measured endotoxin in settled dust from the baby's bed, bedroom floor, family room, and kitchen floor within the first 3 mo after birth. The primary outcomes were any wheeze (versus no wheeze), and repeated wheeze (versus one or no report of wheeze). We found a significant univariate association of elevated endotoxin (> or = 100 EU/ mg) in family room dust with increased risk of any wheeze (Relative Risk = 1.29, 95% CI = 1.03-1.62). The association was not confounded by cockroach allergen, lower respiratory illness (croup, bronchitis, bronchiolitis, and pneumonia), smoking during pregnancy, lower birth weight, maternal asthma, presence of dog, and race/ethnicity in a multivariate model; the multivariate relative risk (RR = 1.33) was marginally significant (95% CI: 1.00-1.76, p < 0.05). In a multivariate model, controlling for the above covariates, elevated endotoxin in family room dust was significantly associated with increased risk (RR = 1.56, 95% CI = 1.03-2.38) of repeated wheeze. These results suggest that home endotoxin exposure may independently increase risk of any wheeze and repeated wheeze during the first year of life for children with a familial predisposition to asthma or allergy.

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Differential expression of IFN-γ, IL-4, IL-10, and IL-1β mRNAs in decalcified tissue sections of mouse lipopolysaccharide-induced periodontitis mandibles assessed by in situ hybridization

Cited by 18 publications

References 39 publications

CD26 Immuno‐Expression and Periodontal Disease Progression

CD26 Immuno‐Expression and Periodontal Disease Progression

Assessment of decalcifying protocols for detection of specific RNA by non-radioactive in situ hybridization in calcified tissues

House Dust Endotoxin and Wheeze in the First Year of Life

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