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J Infect Dis. 2014 Nov 1;210(9):1499-507. doi: 10.1093/infdis/jiu280. Epub 2014 May 14.

Impaired colonic B-cell responses by gastrointestinal Bacillus anthracis infection.

Author information

1
Department of Infectious Diseases and Pathology Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine.
2
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville.

Abstract

Ingestion of Bacillus anthracis spores causes gastrointestinal (GI) anthrax. Humoral immune responses, particularly immunoglobulin A (IgA)-secreting B-1 cells, play a critical role in the clearance of GI pathogens. Here, we investigated whether B. anthracis impacts the function of colonic B-1 cells to establish active infection. GI anthrax led to significant inhibition of immunoglobulins (eg, IgA) and increased expression of program death 1 on B-1 cells. Furthermore, infection also diminished type 2 innate lymphoid cells (ILC2) and their ability to enhance differentiation and immunoglobulin production by secreting interleukin 5 (IL-5). Such B-1-cell and ILC2 dysfunction is potentially due to cleavage of p38 and Erk1/2 mitogen-activated protein kinases in these cells. Conversely, mice that survived infection generated neutralizing antibodies via the formation of robust germinal center B cells in Peyer's patches and had restored B-1-cell and ILC2 function. These data may provide additional insight for designing efficacious vaccines and therapeutics against this deadly pathogen.

KEYWORDS:

B-1 cells; Bacillus anthracis; anthrax toxin; type 2 innate lymphoid cells

PMID:
24829464
PMCID:
PMC4271052
DOI:
10.1093/infdis/jiu280
[Indexed for MEDLINE]
Free PMC Article

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