Background: Exposure to microorganisms elicts the production of cytokines.
These soluble factors enhance several innate immune functions and regulate
the ensuing specific immune response aimed at limiting the spread of infect
ion.
Aim: This study was undertaken to quantify the plasma levels of pro-inflamm
atory cytokines during the course of primary Listeria monocytogenes and Cam
pylobacter jejuni infection. Using an in vivo infection the relationship be
tween endogenous cytokines and the bacterial number in the liver of infecte
d animals was examined.
Methods: C57BL/6 mice were infected by the intraperitoneal route. At differ
ent time points we determined the number of colony-forming units of bacteri
a in the liver of infected animals and paralled these with the plasma level
s of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha)
and interleukin-6 (IL-6) measured by enzyme immunoassays.
Results: L. monocytogenes infection lasted 10-11 days. IFN-gamma production
occurred in the early phase but was more pronounced after day 4, following
the appearance of specific immunity. The duration of experimental campylob
acteriosis was 15 days. Early IFN-gamma production was not significant but
a progressive rise of this cytokine in plasma was seen during the second we
ek post infection. Mice produced measurable amounts of plasma TNF-alpha imm
ediately after being given viable L. monocytogenes, peaking on day 2-3 when
the greatest number of bacteria was present in the examined organs. During
C. jejuni infection plasma TNF-alpha was produced in a similar manner, but
the highest concentrations were found a few days later than in listeriosis
, in correlation with the different course of campylobacteriosis. The quant
ity of IL-6 increased and decreased in concordance with clearance of L. mon
ocytogenes and the clinical status of the animals. C. jejuni did not promot
e the induction of this cytokine. This is to some extent an unusual finding
. With respect to the role of IL-6 in Th2 responses and antibody production
, the appearance of this cytokine in campylobacteriosis was more expected.
Discussion: During systemic bacterial infection, a network of pro-inflammat
ory cytokines is activated and blood levels of these cytokines are elevated
, albeit inconsistently, with large individual variations and depending on
microbial characteristics and structure.