Brucella alters the immune response in a prpA-dependent manner.

Abstract

Brucellosis, a disease caused by the gram-negative bacterium Brucella spp., is a widespread zoonosis that inflicts important animal and human health problems, especially in developing countries. One of the hallmarks of Brucella infection is its capacity to establish a chronic infection, characteristic that depends on a wide repertoire of virulence factors among which are immunomodulatory proteins such as PrpA (encoding the proline racemase protein A or hydroxyproline-2-epimerase), involved in the establishment of the chronic phase of the infectious process that we have previously identified and characterized. We report here that, in vivo, Brucella abortus prpA is responsible for an increment in the B-cell number and in the specific antibody response and that these antibodies promote cell infection. We additionally found that Brucella alters the cytokine levels of IFN-γ, IL-10, TGFβ1 and TNFα during the acute phase of the infectious process in a prpA dependent manner.

• Authors: Juan M Spera, Diego J Comerci, Juan E Ugalde
• Journal: Microbial pathogenesis (Microb Pathog) 2014 Feb-Mar Vol. 67-68 Pg. 8-13 ISSN: 1096-1208 [Electronic] England
• PMID: 24508400 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014 Elsevier Ltd. All rights reserved.

Chemical References

• Antibodies, Bacterial
• Bacterial Proteins
• Tumor Necrosis Factor-alpha
• Virulence Factors
• Interleukin-10
• Interferon-gamma
• Amino Acid Isomerases
• proline racemase

Topics

• Amino Acid Isomerases (genetics, immunology)
• Animals
• Antibodies, Bacterial (immunology)
• B-Lymphocytes (immunology)
• Bacterial Proteins (genetics, immunology)
• Brucella abortus (enzymology, genetics, immunology)
• Brucellosis (genetics, immunology, microbiology)
• Female
• Humans
• Interferon-gamma (genetics, immunology)
• Interleukin-10 (metabolism)
• Mice
• Mice, Inbred BALB C
• Tumor Necrosis Factor-alpha (genetics, immunology)
• Virulence Factors (genetics, immunology)