Increased Expression of Collagen V and IL-17 during Usual Interstitial Pneumonia.
Chen Zhang, David S Wilkes, Oscar W Cummings. Indiana University, Indianapolis
Background: Usual interstitial pneumonia (UIP)/idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing disease that is a major cause of pulmonary failure in this country. The etiology of UIP is unknown but it is thought to be an autoimmune disorder. Type V collagen [Col(V)] is considered as a sequestered antigen in the normal lung, and immunity to unmasked Col(V) enhanced by cytokine IL-17 contributes to chronic rejection in allograft lungs. We investigated the expression of Col(V) and IL-17 in patients with UIP to understand whether or not they may contribute to the etiology of that disorder as well.
Design: Col(V) and IL-17 protein expression were studied by immunohistochemical stains in 9 cases of UIP, as well as in 3 cases of normal lung. The mRNA expression level of col(V) was also determined by real-time RT-PCR using formalin-fixed paraffin-embedded tissue.
Results: We found that col(V) mRNA expression is increased by 2.64 ± 1.35 folds in the lungs of patients with UIP as compared with that in normal lungs (p=0.02). Col(V) protein expression as determined by immunohistochemistry analysis is also increased in the lungs of UIP patients. Scattered IL17-expressing cells are present in the lungs with UIP, but absent in normal lungs.
Conclusions: Collagen V and IL-17 expressions are both increased in the lungs of patients with UIP, suggesting a possible role for these molecules in the pathogenesis of UIP.
Wednesday, March 2, 2011 9:30 AM
Poster Session V # 258, Wednesday Morning