Functional morphology of microfold cells (M cells) in Peyer’s patches

1986 ◽  
Vol 21 (4) ◽  
pp. 325-334 ◽  
Author(s):  
Yoshinori Fujimura
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.


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