CONTEXT: Sulfur mustard (SM) is known as an effective chemical agent and was used in the 1980s during the Iran-Iraq war against Iranians. At the present time, there are more than 40,000 people suffering from pulmonary lesions due to mustard gas in Iran. Though much is known about the gross pathology of SM damage, the molecular and cellular basis for this pathology is not well understood. OBJECTIVE: One of the most important protein groups involved in inflammatory responses is nuclear factor κB protein (NF-κB1) family. They belong to the category of DNA-binding protein factors necessary for transcription of many proinflammatory molecules. In our research, we examined the role of NF-κB1/RelA in the pathophysiology of the lung. MATERIALS AND METHODS: We investigated 10 normal individuals and 20 SM induced patients. Expression of NF-κB1/RelA in controls and the SM exposed samples was measured by real-time polymerase chain reaction and localization of NF-κB1 protein was detected by immunohistochemistry staining. RESULTS: Our results revealed that expression levels of NF-κB1 and RelA were upregulated 0.64-6.50 fold and 0.83-8.34 fold, respectively, in the SM exposed patients in comparison with control samples. DISCUSSION AND CONCLUSION: As far as we know, this is the first finding of induction of NF-κB in patients exposed to SM. NF-κB1/RelA may play a major role in inflammation induced by mustard gas or even in cell survival in the bronchial wall of affected patients.
CONTEXT: Sulfur mustard (SM) is known as an effective chemical agent and was used in the 1980s during the Iran-Iraq war against Iranians. At the present time, there are more than 40,000 people suffering from pulmonary lesions due to mustard gas in Iran. Though much is known about the gross pathology of SM damage, the molecular and cellular basis for this pathology is not well understood. OBJECTIVE: One of the most important protein groups involved in inflammatory responses is nuclear factor κB protein (NF-κB1) family. They belong to the category of DNA-binding protein factors necessary for transcription of many proinflammatory molecules. In our research, we examined the role of NF-κB1/RelA in the pathophysiology of the lung. MATERIALS AND METHODS: We investigated 10 normal individuals and 20 SM induced patients. Expression of NF-κB1/RelA in controls and the SM exposed samples was measured by real-time polymerase chain reaction and localization of NF-κB1 protein was detected by immunohistochemistry staining. RESULTS: Our results revealed that expression levels of NF-κB1 and RelA were upregulated 0.64-6.50 fold and 0.83-8.34 fold, respectively, in the SM exposed patients in comparison with control samples. DISCUSSION AND CONCLUSION: As far as we know, this is the first finding of induction of NF-κB in patients exposed to SM. NF-κB1/RelA may play a major role in inflammation induced by mustard gas or even in cell survival in the bronchial wall of affected patients.