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It is increasingly clear that parasite-derived prostaglandins potently modulate host response and disease progression.
First, a greater insight into the mechanisms that modulate host response may lead to the development of new therapeutic agents.
Thus, eicosanoid production during acute infection appears to modulate host response and disease evolution in favor of progression to the chronic state.
This capability to modulate host response to infection seems to be a key factor for C. burnetii survival in vivo.
In this way C5a promotes murine tumour growth as tumours frequently modulate host response signals from the microenvironment for their own advantage.
It is well documented that parasites have the ability to modulate host response to avoid rejection by the host and by this increase survival.
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Plant pathogens secrete an arsenal of effector molecules that modulate host responses to enable successful infection.
Furthermore, it is known that proteins localized on the mitochondria are targeted by viruses to modulate host responses.
Few other viruses also target CLU to modulate host responses.
The mechanisms by which M.tb persisters modulate host responses to ensure survival remain unclear.
Therefore, lymphocytes modulate host responses to injury/infection but are not required to bring about resolution (ie, clear PMNs and macrophages from inflamed sites).
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