Title: Association of interleukin-33 and thymic stromal lymphopoietin levels with the development of idiopathic pulmonary fibrosis

Transcription

1 Author s response to reviews Title: Upregulation of interleukin-33 and thymic stromal lymphopoietin levels in the lungs of idiopathic pulmonary fibrosis Authors: Jong-Uk Lee (lajoal@nate.com) Hun Soo Chang (hschang@sch.ac.kr) Hyeon Ju Lee (1204thgml@naver.com) Chang An Jung (jca8836@naver.com) Da Jeong Bae (dnwls75@naver.com) Hyun Ji Song (songhj0404@naver.com) Jong Sook Park (newstart1221@naver.com) Soo-Taek Uh (uhs@schmc.ac.kr) Young Hoon Kim (welkim@schmc.ac.kr) Ki-Hyun Seo (khseo@schmc.ac.kr) Choon-Sik Park (mdcspark@daum.net) Version: 3 Date: 21 Dec 2016 Author s response to reviews: Title: Association of interleukin-33 and thymic stromal lymphopoietin levels with the development of idiopathic pulmonary fibrosis Manuscript ID: PULM-D Dear Dr. Isis E Fernandez, Editor in Chief I wish to express my sincere appreciation to the reviewers and editors for their constructive comments on the manuscript. As recommended, we have attempted to address the comments of editors in a point by point response.

2 We believe that the revision have increased the overall quality of the manuscript and hope that our results fulfill the high standards of BMC Pulmonary Medicine With my best regards, Choon-Sik Park, M.D., Ph.D., Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, 1174, Jung-Dong, Wonmi-Ku, Bucheon, Kyeonggi-Do, , Korea Tel: , Fax: , Choon-Sik Park;

3 Editor Comments: Thanks for the resubmission to BMC pulmonary medicine. The manuscript has benefit from the review process, increasing its quality. However, some language editing is necessary to finalize the process. The paragraph below is confusing and would benefit of rephrasing. Especially: 1. The initial onset of IPF and secondary pulmonary fibrosis Could be rephrased to: The initial injury process and secondary fibrosis development R: We change the sentence according to the editor comment as follow: Previously sentence: The initial onset of IPF and secondary pulmonary fibrosis likely begins as the result of alveolar epithelial injury due to exposure to environmental triggers, including cigarette smoke [3], particles [4], occupational dust [5], or chemical fumes [5], radiotherapy [6], chemotherapy [6], and endogenous triggers, including obstructive sleep apnea, chronic graft-versus-host disease and connective tissue disease followed by abnormal repair.

4 The initial injury process and secondary fibrosis development likely begins as the result of [6], and endogenous triggers, including obstructive sleep apnea, chronic graft-versus-host disease and connective tissue disease followed by abnormal repair. 2. chemotherapy [6], and endogenous triggers, including obstructive sleep apnea, chronic graft-versus-host disease and connective tissue disease followed by abnormal repair Could be rephrased to: chemotherapy [6]. Endogenous triggers, include obstructive sleep apnea, chronic graft-versus-host disease and connective tissue disease. Connective tissue disease is not a trigger of IPF, but of non-ipf ILD, specifically CTD-ILD. R: We change the sentence as follow: Previously sentence: The initial injury process and secondary fibrosis development likely begins as the result of [6], and endogenous triggers, including obstructive sleep apnea, chronic graft-versus-host disease and connective tissue disease followed by abnormal repair. The initial injury process and secondary fibrosis development likely begins as the result of [6]. Endogenous triggers, include obstructive sleep apnea, chronic graft-versus-host disease and connective tissue disease followed by abnormal repair. 3. The reviewer specified: I think that they are rather confounders in multifactorial genesis of IPF not IPF cofounders. Please address accordingly. R: We delete the sentence as follow:

5 Previously sentence: Microbial agents such as Epstein Barr virus [7], herpes virus [8], and certain bacterial species [9, 10], as well as gastroesophageal reflux [11], have been suggested as cofounders of IPF. These triggers are capable of inducing both innate and adaptive immune responses [12]. These triggers are capable of inducing both innate and adaptive immune responses [7].