Cutting Edge: Brucella abortus Exploits a Cellular Prion Protein on Intestinal M Cells as an Invasive Receptor

Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cell...

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Published inThe Journal of immunology (1950) Vol. 189; no. 4; pp. 1540 - 1544
Main Authors Nakato, Gaku, Hase, Koji, Suzuki, Michio, Kimura, Masanobu, Ato, Manabu, Hanazato, Misaho, Tobiume, Minoru, Horiuchi, Motohiro, Atarashi, Ryuichiro, Nishida, Noriyuki, Watarai, Masahisa, Imaoka, Koichi, Ohno, Hiroshi
Format Journal Article
LanguageEnglish
Published United States 15.08.2012
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Abstract Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrPC) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrPC-deficient (Prnp−/−) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer’s patch was significantly lower in Prnp−/− than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrPC on the apical surface of M cells as an uptake receptor.
AbstractList Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrP(C)) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrP(C)-deficient (Prnp(-/-)) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer's patch was significantly lower in Prnp(-/-) than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrP(C) on the apical surface of M cells as an uptake receptor.Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrP(C)) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrP(C)-deficient (Prnp(-/-)) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer's patch was significantly lower in Prnp(-/-) than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrP(C) on the apical surface of M cells as an uptake receptor.
Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrPC) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrPC-deficient (Prnp−/−) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer’s patch was significantly lower in Prnp−/− than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrPC on the apical surface of M cells as an uptake receptor.
Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrPC) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrPC-deficient (Prnp-/-) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer's patch was significantly lower in Prnp-/- than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrPC on the apical surface of M cells as an uptake receptor.
Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrP(C)) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrP(C)-deficient (Prnp(-/-)) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer's patch was significantly lower in Prnp(-/-) than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrP(C) on the apical surface of M cells as an uptake receptor.
Author Nakato, Gaku
Horiuchi, Motohiro
Suzuki, Michio
Kimura, Masanobu
Ato, Manabu
Tobiume, Minoru
Hase, Koji
Hanazato, Misaho
Ohno, Hiroshi
Nishida, Noriyuki
Atarashi, Ryuichiro
Watarai, Masahisa
Imaoka, Koichi
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/22772447$$D View this record in MEDLINE/PubMed
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Snippet Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the...
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SubjectTerms Animals
Brucella abortus
Brucella abortus - metabolism
Brucella abortus - pathogenicity
Brucellosis - metabolism
Intestinal Mucosa - metabolism
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Peyer's Patches - metabolism
PrPC Proteins - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Title Cutting Edge: Brucella abortus Exploits a Cellular Prion Protein on Intestinal M Cells as an Invasive Receptor
URI https://www.ncbi.nlm.nih.gov/pubmed/22772447
https://www.proquest.com/docview/1031161034
https://www.proquest.com/docview/1551616110
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