scholarly journals Non‐invasive Salmonella typhimurium mutants are avirulent because of an inability to enter and destroy M cells of ileal Peyer's patches

1997 ◽  
Vol 24 (4) ◽  
pp. 697-709 ◽  
Author(s):  
Kristi L. Penheiter ◽  
Nitin Mathur ◽  
Dobie Giles ◽  
Thomas Fahlen ◽  
Bradley D. Jones
1994 ◽  
Vol 180 (1) ◽  
pp. 15-23 ◽  
Author(s):  
B D Jones ◽  
N Ghori ◽  
S Falkow

Salmonella species are known to initiate infection of mammalian hosts by penetrating the intestinal epithelium of the small bowel. These bacteria preferentially interact with Peyer's patches which are collections of lymphoid follicles making up the gut-associated lymphoid tissue. We infected murine ligated intestinal loops with invasive and noninvasive Salmonella typhimurium strains for 30, 60, 120, and 180 min and examined the infected tissue by transmission electron microscopy. Within 30 min, we found that invasive S. typhimurium exclusively entered M cells found within the follicle-associated epithelium (FAE) of the Peyer's patches. Initially, interactions between invasive bacteria and enterocytes adjacent to the M cells were not found. Invasion of M cells was associated with the ability of the bacteria to invade tissue culture cells. S. typhimurium mutants, which were noninvasive for tissue culture cells, could not be found in ligated loops associated with M cells or enterocytes after incubations of 30, 60, 120, or 180 min. At 60 min, internalized invasive S. typhimurium were cytotoxic for the M cells. Destruction of an M cell formed a gap in the FAE which allowed organisms to invade enterocytes adjacent to the dead cell. Later in the infection process (120 and 180 min), the presence of bacteria beneath the FAE correlated with changes in the cytoarchitecture of the lymphoid follicle. In addition, replicating Salmonella began to enter both the apical and basolateral surfaces of enterocytes adjacent to infected M cells.


2013 ◽  
Vol 6 (5) ◽  
pp. 1027-1037 ◽  
Author(s):  
A Kobayashi ◽  
D S Donaldson ◽  
C Erridge ◽  
T Kanaya ◽  
I R Williams ◽  
...  

2010 ◽  
Vol 341 (3) ◽  
pp. 417-427 ◽  
Author(s):  
Feyzullah Beyaz ◽  
Emel Ergün ◽  
Alev G. Bayraktaroğlu ◽  
Levent Ergün

2010 ◽  
Vol 78 (8) ◽  
pp. 3570-3577 ◽  
Author(s):  
Luiz E. Bermudez ◽  
Mary Petrofsky ◽  
Sandra Sommer ◽  
Raúl G. Barletta

ABSTRACT Mycobacterium avium subsp. paratuberculosis, the agent of Johne's disease, infects ruminant hosts by translocation through the intestinal mucosa. A number of studies have suggested that M. avium subsp. paratuberculosis interacts with M cells in the Peyer's patches of the small intestine. The invasion of the intestinal mucosa by M. avium subsp. paratuberculosis and Mycobacterium avium subsp. hominissuis, a pathogen known to interact with intestinal cells, was compared. M. avium subsp. paratuberculosis was capable of invading the mucosa, but it was significantly less efficient at dissemination than M. avium subsp. hominissuis. B-cell knockout (KO) mice, which lack Peyer's patches, were used to demonstrate that M. avium subsp. paratuberculosis enters the intestinal mucosa through enterocytes in the absence of M cells. In addition, the results indicated that M. avium subsp. paratuberculosis had equal abilities to cross the mucosa in both Peyer's patch and non-Peyer's patch segments of normal mice. M. avium subsp. paratuberculosis was also shown to interact with epithelial cells by an α5β1 integrin-independent pathway. Upon translocation, dendritic cells ingest M. avium subsp. paratuberculosis, but this process does not lead to efficient dissemination of the infection. In summary, M. avium subsp. paratuberculosis interacts with the intestinal mucosa by crossing both Peyer's patches and non-Peyer's patch areas but does not translocate or disseminate efficiently.


2004 ◽  
Vol 78 (2) ◽  
pp. 947-957 ◽  
Author(s):  
Amy B. Hutchings ◽  
Anna Helander ◽  
Katherine J. Silvey ◽  
Kartik Chandran ◽  
William T. Lucas ◽  
...  

ABSTRACT Reovirus type 1 Lang (T1L) adheres to M cells in the follicle-associated epithelium of mouse intestine and exploits the transport activity of M cells to enter and infect the Peyer's patch mucosa. Adult mice that have previously cleared a reovirus T1L infection have virus-specific immunoglobulin G (IgG) in serum and IgA in secretions and are protected against reinfection. Our aim in this study was to determine whether secretory IgA is sufficient for protection of Peyer's patches against oral reovirus challenge and, if so, against which reovirus antigen(s) the IgA may be directed. Monoclonal antibodies (MAbs) of the IgA isotype, directed against the σ1 protein of reovirus T1L, the viral adhesin, were produced and tested along with other, existing IgA and IgG MAbs against reovirus T1L outer capsid proteins. Anti-σ1 IgA and IgG MAbs neutralized reovirus T1L in L cell plaque reduction assays and inhibited T1L adherence to L cells and Caco-2BBe intestinal epithelial cells in vitro, but MAbs against other proteins did not. Passive oral administration of anti-σ1 IgA and IgG MAbs prevented Peyer's patch infection in adult mice, but other MAbs did not. When anti-σ1 IgA and IgG MAbs were produced in mice from hybridoma backpack tumors, however, the IgA prevented Peyer's patch infection, but the IgG did not. The results provide evidence that neutralizing IgA antibodies specific for the σ1 protein are protective in vitro and in vivo and that the presence of these antibodies in intestinal secretions is sufficient for protection against entry of reovirus T1L into Peyer's patches.


2013 ◽  
Vol 41 (1) ◽  
pp. 100-104 ◽  
Author(s):  
Rodrigo Prado Martins ◽  
Valentina Lorenzi ◽  
Cristina Arce ◽  
Concepción Lucena ◽  
Ana Carvajal ◽  
...  

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