Abstract
Presentation of a prototype lipid antigen α-Galactosylceramide (αGC) was examined on primary epithelial cells derived from mouse lungs and on bronchoalveolar lavage (BAL) cells that essentially comprise alveolar macrophages. Presence of CD1d molecules coupled to αGC was demonstrated on both types of cells pre-treated with αGC, suggesting that both cell types are equipped to present lipid antigens. Internalization of Mycobacterium bovis Bacillus Calmette–Guérin (BCG: a prototype pathogen), a pre-requisite to the processing and presentation of protein as well as lipid antigens, was clearly demonstrated in primary lung epithelial (PLE) cells as well as BAL cells. Both PLE and BAL cells expressed CD1d molecule and a significant up-regulation of its expression occurred upon infection of these cells with BCG. Besides CD1d, the expression of other important molecules that participate in lipid antigen presentation pathway (i.e. microsomal triglyceride transfer protein (MTTP), scavenger receptor B1 (SR-B1) and Saposin) was also significantly upregulated in PLE and BAL cells upon BCG infection. In situ up-regulation of CD1d expression on lung epithelial cells was also demonstrated in the lungs of mice exposed intra-tracheally to BCG. Taken together these results suggest that lung epithelial cells may have the ability to present lipid antigens and this pathway seems to get significantly upregulated in response to BCG infection.
Highlights
Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb), remains one of the deadliest diseases worldwide, in spite of tremendous advances in the understanding of host-pathogen interactions [1]
Presentation of lipid antigens by primary lung epithelial cells We have previously shown that the LA-4 cells could present αGC lipid moiety through the CD1d pathway in vitro [26]
Airborne pathogens reach lung alveoli through the inspired air and come in contact with alveolar epithelial cells and alveolar macrophages. These two types of lung cells are amongst the very first host cells to interact with the airborne pathogens like Mycobacterium tuberculosis
Summary
Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb), remains one of the deadliest diseases worldwide, in spite of tremendous advances in the understanding of host-pathogen interactions [1]. Lung provides the primary site of infection for Mtb, where the bacterium gains entry through the inhaled air [1,2]. Macrophages interact with and respond to the invading pathogen [1]. Lipid antigen presentation in mouse primary lung epithelial cells from Indian Council of Medical Research, New Delhi. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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