Inflammatory response in rat lungs with recurrent exposure to welding fumes

Abstract

As chronic exposure to welding fumes causes pulmonary diseases, such as pneumoconiosis, public concern has increased regarding continued exposure to these hazardous gases in the workplace. In a previous study, the inflammatory response to welding fume exposure was analysed in rat lungs in the case of recurrent exposure and recovery periods. Thus using lung samples, well-annotated by histological observation and biochemical analysis, this study examines the gene expression profiles to identify phenotype-anchored genes corresponding to lung inflammation and the repair phenomenon after recurrent welding fume exposure. Seven genes (Mmp12, Cd5l, LOC50101, LOC69183, Spp1, and Slc26a4) were found to be significantly up-regulated according to the severity of the lung injury. In addition, the transcription and translation of Trem2, which was up-regulated in response to the repair process, were validated using a real-time polymerase chain reaction, Western blotting, and immunohistochemistry. The differentially expressed genes in the exposure and recovery groups were also classified using k-means and hierarchical clustering, plus their toxicological function and canonical pathways were further analysed using Ingenuity Pathways Analysis Software. As a result, this comprehensive and integrative analysis of the transcriptional changes that occur during repeated exposure provides important information on the inflammation and repair processes after welding-fume-induced lung injury.

Immunotoxicology of arc welding fume: Worker and experimental animal studies

“…In addition, triggering receptor expressed on myeloid cells 2 (Trem2), γ-2a immunoglobulin heavy chain (IgG-2a), immunoglobulin heavy chain-1a (Igh-1a), and immunoglobulin heavy locus (Igh) were increased after an exposure and recovery protocol. A second 30-day MMA-SS fume inhalation exposure verified that this gene sub-set was predominant in the response and that the lung showed a lack of adaptation to a repeated exposure Oh et al, 2011). In mice, many of these same genes were altered after GMA welding fume aspiration and inhalation exposure (Zeidler-Erdely et al, 2010, 2011c, which suggests a consistency across rodent species and a general response to welding fume-induced lung injury.…”

“…Results of lung gene expression studies in both mice and rats indicate a strong immunologic transcriptional response to welding fume (Oh et al, 2009(Oh et al, , 2011Yang et al, 2009;Zeidler-Erdely et al, 2010). A 30-day inhalation exposure to MMA-SS fume in rats resulted in marked changes in several immune-related genes, including matrix metalloproteinase-12 (Mmp12), Cd 5 moleculelike (Cd5l), chemokine (C-C motif) ligand 7 (Ccl7), C-X-C motif chemokine 5 (Cxcl5), and secreted phosphoprotein 1 (Spp1).…”

Physicochemical Characterization of Simulated Welding Fumes from a Spark Discharge System

“…Others have developed robotic welders to generate fumes. Oh et al (2012) used a rotating stainless disc as a base metal and a welding rod restrained in the welding rod holder support to simulate SMAW fume, known informally as stick welding. Similarly, Zimmer et al (2002) used a welding fume generation system comprised of a rotating cylinder as the base material.…”

Inhibitors of pendrin anion exchange identified in a small molecule screen increase airway surface liquid volume in cystic fibrosis

“…Pendrin up-regulation is seen in: 1) airway epithelial cultures chronically exposed to cytokines, including IL-4, IL-13, and IL-17A; 2) rodent models of inflammatory lung disease, including allergen (ovalbumin)-induced asthma, chronic obstructive pulmonary disease, infection, and industrial toxin exposure; and 3) humans with rhinovirus infection, asthma, cystic fibrosis (CF), rhinitis, and chronic rhinosinusitis (10,11,(17)(18)(19)(20)(21)(22)(23)(24)(25). Pendrin knockout is also associated with reduced lung inflammation in a murine model of Bordetella pertussis lung infection (26).…”