Mechanisms of asthma and allergic inflammationClara cell 16-kd protein downregulates TH2 differentiation of human naive neonatal T cells
Section snippets
Subjects
Sixty-four healthy Swedish infants born in 2001-2003 at the Sahlgrenska University Hospital (Göteborg, Sweden) were involved in the study. These children formed part of a prospective birth cohort study (IMMUNOFLORA). Inclusion criteria were normal pregnancy without expected complications and expected vaginal delivery at term (at least 38 weeks' gestational age). The parental history of allergy was recorded. Blood samples were collected from the umbilical cord and at 4, 18, and 36 months of age,
Levels of CC16 peaked in infants at 4 months of age
To investigate the levels of CC16 in children during the first years of life, we measured the concentrations of CC16 in plasma in cord blood and at 4 and 18 months and 3 years from a cohort of children. The levels of CC16 increased significantly from a median level of 15 ng/mL at birth to a level of 96 ng/mL at the age of 4 months (Fig 1). Thereafter, the levels of CC16 decreased significantly to 20 ng/mL at 18 months and continued to decrease to 7 ng/mL at the age of 3 years. The CC16 levels
Discussion
Previous studies show that the levels of CC16 are lower in asthmatic patients compared with those seen in healthy control subjects. However, it is still not clear whether these differences in CC16 levels have an effect on the immunopathogenic mechanisms of allergic inflammation. In the present study we investigated the levels of CC16 in blood during the first 3 years of life and whether CC16 might have an opportunity to affect T-cell development of children in vitro. We unexpectedly found that
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Lung developmental is altered after inhalation exposure to various concentrations of calcium arsenate
2021, Toxicology and Applied PharmacologyCitation Excerpt :CC16 KO mice have increased expression of IL-13 (Chen et al., 2001). CC16 down regulates TH2 differentiation (Johansson et al., 2007). Our aim has been to determine whether arsenic compounds inhaled during in utero and early postnatal life can result in altered adult lung function and structure.
Secretoglobin 1A member 1 (SCGB1A1) +38A/G polymorphism is associated with asthma risk: A meta-analysis
2013, GeneCitation Excerpt :In the SCGB1A1-deficient mouse model, Chen et al. found that deficiency of SCGB1A1 aggravated pulmonary allergic inflammation through augmentation of the TH2 response, and reconstitution of SCGB1A1 in SCGB1A1-deficient mice was able to reverse the altered phenotypes (Chen et al., 2001; Hung et al., 2004). Recently, Johansson and colleagues suggested that SCGB1A1 had an inhibitory effect on TH2 cell differentiation from human infants by affecting DCs (Johansson et al., 2007). Taken together, this information indicated that SCGB1A1 may play a critical role in the development of asthma.
Clara cell 10-kDa protein inhibits T<inf>H</inf>17 responses through modulating dendritic cells in the setting of allergic rhinitis
2013, Journal of Allergy and Clinical ImmunologyRelation between serum CC16 levels and asthma predictive index in pre-schoolers with recurrent wheezing
2018, Allergologia et ImmunopathologiaCitation Excerpt :Ma et al.32 on 147 Chinese asthmatic children (9–15 years old) showed lower levels of urine CC16 and FVC (but not FEV1) in asthmatic children compared to controls, after adjustment for sex, age, BMI, parental education and smoking status; suggesting that CC16 may be a useful tool or biomarker for investigating lung epithelium integrity among children with asthma or lung injury. A study in healthy Swedish children reported significantly different levels of CC16 in blood according with age (e.g. median levels of 15 ng/ml at birth, 96 ng/ml at 4 months, 20 ng/ml at 18 months, and 7 ng/ml at age of 3 years).33 Four-month-old children with a parental history of allergy had similar levels of CC16 as the children with no parental history of allergy (94 ng/ml vs. 100 ng/ml).33
Supported by the Swedish Research Council, the Vårdal Foundation, Cancer-och Allergifonden, the Sahlgrenska Academy at Göteborg University, the Swedish Asthma and Allergy Association Research Foundation, Frimurare Barnhusdirektionen, Åke Wibergs stiftelse, and Konsul Th. C. Berghs stiftelse.
Disclosure of potential conflict of interest: The authors have declared that they have no conflict of interest.