J Respir Med Lung Dis | Volume 1, Issue 1 | Case Report | Open Access
Michael Roth*
Department of Pulmonary Cell Research and Clinics of Pneumology, University Hospital Basel, Switzerland
*Correspondance to: Michael Roth
Fulltext PDFThe C1q-receptor functions as a stress response protein, a cellular calcium regulator, and as a cell death mediator. Thereby it contributes to carcinogenesis and controls innate immunity and. First described as an intracellular protein, the C1q-receptor also integrates into the cell membrane and mediates the response to extracellular stimuli including collagen degradation fragments, bacterial wall proteins and complement proteins. However, its role in chronic inflammatory diseases has not been investigated in details. Recent evidence suggests that in chronic inflammatory lung diseases the C1q-receptor contributes to infection induced exacerbation, which is the major cause of increased morbidity and mortality. In isolated human airway smooth muscle cells, the C1q-receptorregulates translation control and thus, can function on the level of epigenetic protein control. In this function, the C1q-receptor deregulation may lead to hyperplasia of airway smooth muscle cells, which is well documented in asthma. Furthermore, there are studies indicating that the C1q-receptor is a positive regulator for a number of asthma relevant pro-inflammatory cytokines, growth factors, and extracellular matrix compounds. In regard to asthma exacerbation, it is interesting to know that several bacteria and viruses encode for their own specific C1q-receptor or the C1q-receptor -like protein, which interacts with its binding proteins on the host cells just as a host own C1q-receptor. Thereby, the micro-organisms C1q-receptor can hijack the host cellular regulation system. This review presents supportive data for the hypothesis that deregulation of the C1q-receptor is a major event leading to multiple asthma specific pathologies of the airway.
Roth M. The C1q-Receptor - Calreticulin - Contributes to the Pathogenesis of Asthma. J Respir Med Lung Dis. 2016; 1(1): 1002.