Is toll like receptor 4 a common pathway hypothesis for development of lung cancer and idiopathic pulmonary fibrosis?

Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause, occurring primarily in older adults and limited to the lungs. IPF is a disease with similarities and links to cancer biology whose main event is aberrant cell proliferation. Although toll like receptors (TLRs) are essential for protective immunity, inappropriate TLR responses contribute to inflammation. Chronic inflammation is one of the risk factors and features of cancer. It can affect any stage of tumorigenesis and migration of cancer cell.Aim of workTo investigate the key role of TLR4 expression in the development and progression of lung cancer and IPF and its contribution as a common pathway in the development of both.MethodsThis study included 16 IPF patients, 20 lung cancer patients and 23 control subjects. All patients were subjected to full history taking, detailed clinical examination, radiological assessment, bronchoscopic biopsies and serum samples for measurement of TLR4 expression. TLR4 was measured in serum of all control subjects and in bronchoscopic biopsies for only five of them.ResultsTLR4 expression was higher in serum and tissue biopsies of IPF and lung cancer patients than that in the control group; however the highest level of LTR4 expression in serum was observed in the IPF group and the highest level in tissue biopsy was observed in the lung cancer group. TLR4 levels were not significantly different between the three studied groups. There was a significant association between TLR4 expression in tissue biopsy and distant metastasis among NSCLC cases (p = 0.006).ConclusionOur results support that TLR4 pathway may be a common contribution to both diseases. There was association between distant metastasis and TLR4 expression. Further studies are needed to evaluate the TLR4 prognostic value for tumor progression and its expression in precancerous lesions.