3 research outputs found
Sociodemographic Predictors of Rural Poverty: A Regional Analysis
The focus of the present study is to determine the extent to which the socio-demographic variables of education, occupation, number of children, race, sex, age, and willingness to travel for employment and predictors of a rural family\u27s level of poverty. Discriminant analysis is employed to assess the accuracy of these variables in - discriminating between poor and nonpoor families randomly selected from thirty low income, rural counties in ten contiguous southeastern states. The results are supportive of previous studies as these variables are found to be statistically significant discriminants between the poor and the nonpoor. The profile of a rural poor head of household is a poorly educated, semi-skilled, female, black, farm resident who tends to be old, have a large number of children, and be less willing to travel for employment outside of one\u27s immediate area
IL-33–Dependent Type 2 Inflammation during Rhinovirus-induced Asthma Exacerbations In Vivo
IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo
Rationale:
Rhinoviruses are the major cause of asthma
exacerbations; however, its underlying mechanisms are poorly
understood. We hypothesized that the epithelial cell–derived
cytokine IL-33 plays a central role in exacerbation pathogenesis
through augmentation of type 2 inflammation.
Objectives:
To assess whether rhinovirus induces a type 2
inflammatory response in asthma
in vivo
and to define a role for IL-33
in this pathway.
Methods:
We used a human experimental model of rhinovirus
infection and novel airway sampling techniques to measure IL-4, IL-5,
IL-13, and IL-33 levels in the asthmatic and healthy airways during
a rhinovirus infection. Additionally, we cultured human T cells and type
2 innate lymphoid cells (ILC2s) with the supernatants of rhinovirus-
infected bronchial epithelial cells (BECs) to assess type 2 cytokine
production in the presence or absence of IL-33 receptor blockade.
Measurements and Main Results:
IL-4, IL-5, IL-13, and IL-33 are
all induced by rhinovirus in the asthmatic airway in vivo and relate to
exacerbation severity. Further, induction of IL-33 correlates with
viral load and IL-5 and IL-13 levels. Rhinovirus infection of human
primary BECs induced IL-33, and culture of human T cells and ILC2s
with supernatants of rhinovirus-infected BECs strongly induced
type 2 cytokines. This induction was entirely dependent on IL-33.
Conclusions:
IL-33 and type 2 cytokines are induced during
a rhinovirus-induced asthma exacerbation in vivo. Virus-induced
IL-33 and IL-33
–
responsive T cells and ILC2s are key mechanistic
links between viral infection and exacerbation of asthma. IL-33
inhibition is a novel therapeutic approach for asthma exacerbations