Abstract
Mycobacterium avium is a human and animal pathogen that infects the host through the mucosal surfaces. Past work has demonstrated that the bacterium can interact with both the respiratory and gastrointestinal tracts. Those surfaces in the body are covered by a bilayer of a glycoprotein, mucin, which works as a physical barrier and a gel which contains antibacterial and antivirus properties. This current work shows that different strains of M. avium, in contrast to Escherichia coli, Pseudomonas aeruginosa, and Listeria monocytogenes, are not able to bind to mucins, MUC2 and MUC5b, the main mucins in the gastrointestinal and respiratory tracts, respectively. The lack of binding is due to the characteristics of the cell wall and is impaired by altering lipids, proteins, or glycolipids. M. avium, in contrast to E. coli, interacts with epithelial cells equally in the presence or absence of the mucin, suggesting that the cell wall of the pathogen can facilitate the bacterial movement through the mucin layer, towards the mucosal wall. In conclusion, the study has shown that M. avium can avoid the mucin barrier, which explains its ability to interact with the mucosal epithelium, even in absence of motion-related structures.
Highlights
Mycobacteriumavium subsp. hominissuis (M. avium) is an environmental bacteria associated with the infection of individuals with underlying lung conditions such as bronchiectasis, cystic fibrosis, and emphysema [1, 2]
Mucin is present in two layers, one adjacent to the mucosal surface, which is rich in antimicrobial peptides, and a more external layer, where bacteria are encountered [10, 11]. e same arrangement appears to be present in the airways [12]
Because the role of mucins has not been studied with regards to M. avium infection, we hypothesized that the mucin is probably ineffective in its role to separate mycobacteria from the mucosal layer of cells, likely due to the lipid content of the mycobacterial surface, facilitating the bacterium movements toward the mucosal wall. e results of the present investigation support the hypothesis that the M. avium surface protects the bacterium against the action of mucins
Summary
Mycobacteriumavium subsp. hominissuis (M. avium) is an environmental bacteria associated with the infection of individuals with underlying lung conditions such as bronchiectasis, cystic fibrosis, and emphysema [1, 2]. M.avium interacts with the host mucosal cells once in the airways or in the GI tract. As a step in the process of interaction with the airway or the GI mucosa, pathogens need to bypass the mucin layer, both in the respiratory tract as well as the intestinal tract. E authors showed that MUC2 production is critical for host protection during attachment and effacing bacterial infections (Escherichia coli and Citrobacter rodentium) but limits the overall bacterial pathogens and commensal numbers associated with the mucosal surface. E abilities of secreted mucins to regulate mucocellular clearances are dependent on their polymer structures formed through disulfide bonds Pathogenic bacteria such as enterotoxic Escherichia coli produces a protein, EatA, that degrades the intestinal mucin [17], and can migrate towards and bind to the mucosal surface. Because the role of mucins has not been studied with regards to M. avium infection, we hypothesized that the mucin is probably ineffective in its role to separate mycobacteria from the mucosal layer of cells, likely due to the lipid content of the mycobacterial surface, facilitating the bacterium movements toward the mucosal wall. e results of the present investigation support the hypothesis that the M. avium surface protects the bacterium against the action of mucins
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