Skip to main content
ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Infectious Bacterial Diseases Research » Research » Publications at this Location » Publication #293662

Title: No holes barred: Invasion of the intestinal mucosa by Mycobacterium avium subspecies paratuberculosis

item Bannantine, John
item BERMUDEZ, LUIZ - Oregon State University

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/6/2013
Publication Date: 11/1/2013
Publication URL:
Citation: Bannantine, J.P., Bermudez, L.E. 2013. No holes barred: Invasion of the intestinal mucosa by Mycobacterium avium subsp. paratuberculosis. Infection and Immunity. 81(11):3960-3965.

Interpretive Summary: This article examines the early events that occur during intestinal infection of cows with Mycobacterium avium subspecies paratuberculosis, the agent that causes Johne’s disease. These early events include attachment to the intestinal lining followed by uptake into either M cells or epithelial cells, both of which line the intestinal wall. This uptake triggers a series of events that ultimately lead to the pathogen’s entry into the surrounding tissues (called the lamina propria) where macrophages are waiting to engulf and attempt to destroy the bacterium. However, it is well-known that pathogenic mycobacteria can survive in macrophages and the bacteria later collects in the nearby lymph node tissues. These important early events establish a long and chronic disease for the animal. A short discussion is included on how these events might be circumvented to prevent establishment of infection, and thereby, disease. This article is of primary interest to researchers working on this disease as well as other mycobacterial diseases.

Technical Abstract: The infection biology of Mycobacterium avium subspecies paratuberculosis (MAP) has recently crystalized 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. For example, the interaction of fibronectin and milk with MAP proteins and their effect on invasion of epithelial cells has been elucidated. An initial look at the global expression pathways of the host has shown a circumvention of the cell communication pathway by MAP, which loosens the integrity of the tight junctions. We now know that MAP activates the epithelial layer and also actively recruits macrophages to the site of infection. These notable findings are summarized along with added mechanistic details to the early infection model.