Idiopathic pulmonary fibrosis (IPF) is a fatal chronic interstitial lung disease with no established treatment and is characterized by progressive scarring of the lung tissue and an irreversible decline in lung function. Chronic inflammation has been demonstrated to be the pathological basis of fibrosis. Emerging studies have revealed that most interleukin-17 (IL-17) isoforms are essential for the mediation of acute and chronic inflammation via innate and adaptive immunity. Overexpression or aberrant expression of IL-17 cytokines contributes to various pathological outcomes, including the initiation and exacerbation of IPF. Here, we aim to provide an overview of IL-17 family members in the pathogenesis of IPF.

Idiopathic pulmonary fibrosis (IPF) is a progressive fatal lung disease with a limited therapeutic strategy. Mitochondrial oxidative stress in macrophages is directly linked to IPF. Elamipretide(SS-31) is a mitochondrion-targeted peptide that has been shown to be safe and beneficial for multiple diseases. However, whether SS-31 alleviates IPF is unclear. In the present study, we used a bleomycin (BLM)-induced mouse model followed by SS-31 injection every other day to investigate its role in IPF and explore the possible mechanism. Our results showed that SS-31 treatment significantly suppressed BLM-induced pulmonary fibrosis and inflammation, with improved histological change, and decreased extracellular matrix deposition and inflammatory cytokines release. Impressively, the expression percentage of IL-1β and IL-18 was downregulated to lower than half with SS-31 treatment. Mechanistically, SS-31 inhibited IL-33- or lipopolysaccharide(LPS)/IL-4-induced production of IL-1β and IL-18 in macrophages by suppressing NOD-like receptor thermal protein domain associated protein 3(NLRP3) inflammasome activation. Nuclear factor erythroid 2-related factor 2(Nrf2) was dramatically upregulated along with improved mitochondrial function after SS-31 treatment in activated macrophages and BLM-induced mice. Conversely, there was no significant change after SS-31 treatment in Nrf2−/− mice and macrophages. These findings indicated that SS-31 protected against pulmonary fibrosis and inflammation by inhibiting the Nrf2-mediated NLRP3 inflammasome in macrophages. Our data provide initial evidence for the therapeutic efficacy of SS-31 in IPF.

To delineate the features of multi-detector computed tomography (MDCT) images and clinical characteristics of pancreatic solid pseudopapillary tumors (SPTs) of the pancreas in asymptomatic patients and compare these features and characteristics between asymptomatic and symptomatic patients. This work is a retrospective study approved by our institutional review board. MDCT images and clinical data of 109 patients with pathologically proven SPTs obtained from October 2008 to October 2016 were reviewed. Patients were categorized into two groups: asymptomatic patients and patients with symptomatic disease. Cases were reviewed to determine the reason for detection, intervention, shape, diameter, location, calcification, encapsulation, internal composition, CT attenuation, enhancement pattern, and tumor pathology. Clinical factors and imaging features were also compared between groups. Statistical analysis was performed using χ2 and t-tests. Data from 49 asymptomatic and 60 symptomatic patients were collected. Asymptomatic SPTs were identified most frequently during routine health examination (18 patients, 36.7%), various screening purposes (12 patients, 24.5%), and traumatic injury (9 patients, 18.4%). Except for a smaller tumor size (5.8 cm in asymptomatic SPTs vs. 7.4 cm in symptomatic SPTs, P = 0.023), the clinical factors or imaging features of asymptomatic patients were very similar to those of symptomatic patients. The current research is the first single-center study to characterize SPTs in asymptomatic patients. Asymptomatic SPTs are gradually being identified with greater frequency. Although generally smaller in size than that in symptomatic patients, an asymptomatic pancreatic mass with the typical imaging features of SPT may be found, the treatment for which is similar to that for symptomatic patients. Evaluating asymptomatic SPTs requires further systematic and multi-center trials.