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Pathogenic bacterial species associated with endodontic infection evade innate
immune control by disabling neutrophils
#MMPMID25024367
Matsui A
; Jin JO
; Johnston CD
; Yamazaki H
; Houri-Haddad Y
; Rittling SR
Infect Immun
2014[Oct]; 82
(10
): 4068-79
PMID25024367
show ga
Endodontic infections, in which oral bacteria access the tooth pulp chamber, are
common and do not resolve once established. To investigate the effects of these
infections on the innate immune response, we established a mouse subcutaneous
chamber model, where a mixture of four oral pathogens commonly associated with
these infections (endodontic pathogens [EP]), i.e., Fusobacterium nucleatum,
Streptococcus intermedius, Parvimonas micra, and Prevotella intermedia, was
inoculated into subcutaneously implanted titanium chambers. Cells that
infiltrated the chamber after these infections were primarily neutrophils;
however, these neutrophils were unable to control the infection. Infection with a
nonpathogenic oral bacterial species, Streptococcus mitis, resulted in
well-controlled infection, with bacterial numbers reduced by 4 to 5 log units
after 7 days. Propidium iodide (PI) staining of the chamber neutrophils
identified three distinct populations: neutrophils from EP-infected chambers were
intermediate in PI staining, while cells in chambers from mice infected with S.
mitis were PI positive (apoptotic) or negative (live). Strikingly, neutrophils
from EP-infected chambers were severely impaired in their ability to phagocytose
and to generate reactive oxygen species in vitro after removal from the chamber
compared to cells from S. mitis-infected chambers. The mechanism of neutrophil
impairment was necrotic cell death as determined by morphological analyses. P.
intermedia alone could induce a similar neutrophil phenotype. We conclude that
the endodontic pathogens, particularly P. intermedia, can efficiently disable and
kill infiltrating neutrophils, allowing these infections to become established.
These results can help explain the persistence of endodontic infections and
demonstrate a new virulence mechanism associated with P. intermedia.
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