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No holes barred: invasion of the intestinal mucosa by Mycobacterium avium subsp. paratuberculosis.
|Title||No holes barred: invasion of the intestinal mucosa by Mycobacterium avium subsp. paratuberculosis.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Bannantine JP, Bermudez LE|
|Journal||Infection and immunity|
|Date Published||2013 Nov|
|Keywords||Animals, Bacterial Proteins, Epithelial Cells, Host-Pathogen Interactions, Humans, Intestinal Mucosa, Macrophages, Mutation, Mycobacterium avium subsp. paratuberculosis, Signal Transduction, Tight Junctions, Virulence Factors|
The infection biology of Mycobacterium avium subsp. paratuberculosis has recently crystallized, with added details surrounding intestinal invasion. The involvement of pathogen-derived effector proteins such as the major membrane protein, oxidoreductase, and fibronectin attachment proteins have been uncovered. Mutations constructed in this pathogen have also shed light on genes needed for invasion. The host cell types that are susceptible to invasion have been defined, along with their transcriptional response. Recent details have given a new appreciation for the dynamic interplay between the host and bacterium that occurs at the outset of infection. An initial look at the global expression pathways of the host has shown a circumvention of the cell communication pathway by M. avium subsp. paratuberculosis, which loosens the integrity of the tight junctions. We now know that M. avium subsp. paratuberculosis activates the epithelial layer and also actively recruits macrophages to the site of infection. These notable findings are summarized along with added mechanistic details of the early infection model. We conclude by proposing critical next steps to further elucidate the process of M. avium subsp. paratuberculosis invasion.
|Alternate Journal||Infect. Immun.|