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. 2014 Jul;69(7):1830-3.
doi: 10.1093/jac/dku047. Epub 2014 Feb 28.

Induction of human plasmablasts during infection with antibiotic-resistant nosocomial bacteria

Victor I Band  1 , Chris Ibegbu  2 , Surinder Pal Kaur  2 , Stephanie M Cagle  3 , Ronald Trible  4 , Crystal L Jones  1 , Yun F Wang  5 , Colleen S Kraft  4 , Susan M Ray  3 , Jens Wrammert  2 , David S Weiss  6
Affiliations

Induction of human plasmablasts during infection with antibiotic-resistant nosocomial bacteria

Victor I Band et al. J Antimicrob Chemother. 2014 Jul.

Abstract

Objectives: Nosocomial pathogens such as Acinetobacter baumannii are a growing public health threat, due in part to their increasing resistance to antibiotics. Since some strains are resistant to all available antibiotics, novel therapies are urgently needed. Plasmablasts are short-lived B cells found in the blood that can be collected and harnessed to produce therapeutic antibodies. We set out to determine whether plasmablasts are induced during infection with A. baumannii and other nosocomial pathogens.

Methods: We obtained blood samples from patients infected with antibiotic-resistant nosocomial pathogens, and analysed their plasmablast response by flow cytometry.

Results: We observed a strong induction of plasmablasts in patients with antibiotic-resistant A. baumannii infection. Furthermore, plasmablasts were also induced in response to other drug-resistant nosocomial pathogens.

Conclusions: These data suggest that plasmablasts may be broadly harnessed to develop therapeutic antibodies to combat otherwise untreatable antibiotic-resistant infections.

Keywords: Acinetobacter baumannii; antibody therapy; nosocomial infections.

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Figures

Figure 1.
Figure 1.
A. baumannii infection induces cycling human plasmablasts. (a) Peak plasmablast levels (percentage of CD27+ CD38+ plasmablasts of total CD3− CD20− lymphocytes) observed in healthy controls (n = 5) and patients with A. baumannii infection (n = 13). (b) Percentage of recently proliferated plasmablasts (Ki-67+) in observed peak plasmablast samples from healthy controls (n = 5) and patients with A. baumannii infection (n = 8). (c) Average percentage of plasmablasts across all samples from A. baumannii-infected patients 0–7, 8–16 or ≥17 days after culture positivity (n = 13). (d) Time course of plasmablast levels from an A. baumannii-infected patient (isolate 5). Flow cytometry plots were gated for lymphocytes by forward and side scatter, and then as CD3− CD20−. Graphs shown represent contour plots indicating areas of higher cell density. Square gates represent cells defined as plasmablasts, with the percentage of cells within the gate quantified. *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001.
Figure 2.
Figure 2.
Plasmablast induction during infection with diverse antibiotic-resistant nosocomial bacteria. Peak plasmablast levels (percentage of CD27+ CD38+ plasmablasts of total CD3− CD20− lymphocytes) observed in healthy controls and patients with the indicated bacterial infections.
See this image and copyright information in PMC

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