. Author manuscript; available in PMC: 2013 Jul 1.

Published in final edited form as: J Allergy Clin Immunol. 2012 May 2;130(1):83–90.e4. doi: 10.1016/j.jaci.2012.03.020

Table 4.

Longitudinal analysis for FEV₁ (%pred) and C1orf100 expression levels in CAMP

	Model 1	Model 2

Intercept^†	96.1% (2.9)	96.2% (2.9)
*C1orf100*^‡	−0.36% (0.08)^**	−0.44% (0.09)^**
Budesonide^§	3.63% (1.6)^*	3.23% (1.6)^*
*C1orf100^budesonide^\|\|	– –	0.32% (0.16)^*

Models from adjusted longitudinal analysis for percent-predicted FEV₁. Model 1 shows main effects of C1orf100 expression level and treatment with inhaled budesonide. Model 2 also includes the interaction term. Numbers represent β coefficients from mixed-effects regression models with standard errors in parentheses.

P<0.05,

^**

P<0.001.

^†

Children in CAMP with the lowest levels of C1orf100 ~ and no budesonide treatment had FEV₁ ~96.2%.

^‡

C1orf100 gene expression levels as log-intensity values. There was a drop of ~0.4% in FEV₁ for each log increase in C1orf100 level.

^§

Children receiving budesonide had an FEV₁ ~3.2–3.6% higher than those not on budesonide.

^||

Children with higher C1orf100 levels had a greater response to budesonide: for each log increase in the level, treatment improved their FEV₁ by ~0.3% more than those with lower expression levels of the gene.

In summary, higher expression levels of C1orf100 were associated with lower FEV₁; budesonide improved FEV₁ and also partially reversed the reduction in FEV₁ associated with higher C1orf100 levels.