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Centre de Recherche en Infectiologie, Université Laval, Quebec City, Québec, Canada
Host-derived chemoattractant factors are suggested to play crucial
roles in leukocyte recruitment elicited by inflammatory stimuli in
vitro and in vivo. However, in the case of acute bacterial infections,
pathogen-derived chemoattractant factors are also present, and it has
not yet been clarified how cross-talk between chemoattractant receptors
orchestrates diapedesis of leukocytes in this context of complex
chemoattractant arrays. To investigate the role of chemokine
(host-derived) and formyl peptide (pathogen-derived) chemoattractants
in leukocyte extravasation in life-threatening infectious diseases, we
used a mouse model of pneumococcal pneumonia. We found an increase in
mRNA expression of eight chemokines (RANTES, macrophage-inflammatory
protein (MIP)-1
, MIP-1
, MIP-2, IP-10, monocyte chemoattractant
protein (MCP)-1, T cell activation 3, and KC) within the lungs
during the course of infection. KC and MIP-2 protein expression closely
preceded pulmonary neutrophil recruitment, whereas MCP-1 protein
production coincided more closely than MIP-1 with the kinetics of
macrophage infiltration. In situ hybridization of MCP-1 mRNA suggested
that MCP-1 expression started at peribronchovascular regions and
expanded to alveoli-facing epithelial cells and infiltrated
macrophages. Interestingly, administration of a neutralizing Ab against
MCP-1, RANTES, or MIP-1 alone did not prevent macrophage
infiltration into infected alveoli, whereas combination of the three
Abs significantly reduced macrophage infiltration without affecting
neutrophil recruitment. The use of an antagonist to
N-formyl peptides,
N-t-Boc-Phe-D-Leu-Phe-D-Leu-Phe,
reduced both macrophages and neutrophils significantly. These data
demonstrate that a complex chemokine network is activated in response
to pulmonary pneumococcal infection, and also suggest an important role
for fMLP receptor in monocyte/macrophage recruitment in that
model.
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