The nematode Caenorhabditis elegans has become a model system for studying the disease interaction between pathogens and the host. To determine whether the transparent nematode could serve as a useful model for Mycobacterium avium subspecies hominissuis (MAH) infection of the intestinal tract, worms were fed MAH and assayed for the effects of the bacterial infection on the worm. It was observed during feeding that viable MAH increases in the intestinal lumen in a time dependent manner. Ingestion of MAH was deemed non-toxic to worms as MAH-fed populations have similar survival curves to those fed E. coli strain OP50. Pulse-chase analysis using E. coli strain OP50 revealed that MAH colonize the intestinal tract, as viable MAH remain within the intestine after the assay. Visualization of intestinal MAH using histology and transmission electron microscopy demonstrates that MAH localizes to the intestinal lumen, as well as establishes direct contact with intestinal epithelium. Bacterial colonization appears to have a detrimental effect on the microvilli of the intestinal epithelial cells. The MAH ΔGPL/4B2 strain with a mutation in glycopeptidolipid production is deficient in binding to human epithelial cells (HEp-2), as well as deficient in its ability to bind to and colonize the intestinal tract of C. elegans as efficiently as wild-type MAH. These data indicate the C. elegans may serve as a useful model system for MAH pathogenesis and in determining the mechanisms used by MAH during infection and colonization of the intestinal epithelium.

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.