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Trace Levels of Staphylococcal Enterotoxin Bioactivity Are Concealed in a Mucosal
Niche during Pulmonary Inflammation
#MMPMID26509442
Ménoret A
; Svedova J
; Behl B
; Vella AT
PLoS One
2015[]; 10
(10
): e0141548
PMID26509442
show ga
Pathogen and cellular by-products released during infection or trauma are
critical for initiating mucosal inflammation. The localization of these factors,
their bioactivity and natural countermeasures remain unclear. This concept was
studied in mice undergoing pulmonary inflammation after Staphylococcal
enterotoxin A (SEA) inhalation. Highly purified bronchoalveolar lavage fluid
(BALF) fractions obtained by sequential chromatography were screened for
bioactivity and subjected to mass spectrometry. The Inflammatory and inhibitory
potentials of the identified proteins were measured using T cells assays. A
potent pro-inflammatory factor was detected in BALF, and we hypothesized SEA
could be recovered with its biological activity. Highly purified BALF fractions
with bioactivity were subjected to mass spectrometry. SEA was the only identified
protein with known inflammatory potential, and unexpectedly, it co-purified with
immunosuppressive proteins. Among them was lactoferrin, which inhibited SEA and
anti-CD3/-CD28 stimulation by promoting T cell death and reducing TNF synthesis.
Higher doses of lactoferrin were required to inhibit effector compared to resting
T cells. Inhibition relied on the continual presence of lactoferrin rather than a
programming event. The data show a fraction of bioactive SEA resided in a mucosal
niche within BALF even after the initiation of inflammation. These results may
have clinical value in human diagnostic since traces levels of SEA can be
detected using a sensitive bioassay, and may help pinpoint potential mediators of
lung inflammation when molecular approaches fail.
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