Our findings strongly indicate that IAV coinfection compromises the host's ability to control Mtb infection via the production of IL-10 which was rapidly induced upon viral infection.
This review briefly discusses patterns of selected cytokine (IL-6, IL-8, IL-10, TNF-α and INF-γ) responses associated with infections caused by Plasmodium, intestinal parasites as well as a Plasmodium-helminth co-infection.
Our findings further imply a convergent mechanism of inhibition of TLR signaling by <i>T. gondii</i> and IL-10 and suggest potential negative consequences of HIV/<i>T. gondii</i> coinfection.
Antigens from the tapeworm Hymenolepis diminuta and the nematode Trichuris muris caused an anti-inflammatory response with M2-type polarization, reduced macrophage phagosome maturation and ability to activate T cells, along with increased Mtb burden, especially in T. muris exposed cells which also induced the highest IL-10 production upon co-infection.
An increase of messenger RNA (mRNA) expression of Th1- (IFN-γ, IL-12, TNF-α) and Th2-related cytokines (IL-10) mainly in groups PC-E and TE was observed, however, without statistically significant differences between co-infection and single infection with Eimeria.
Our findings suggest that common IL-10 (-1082, -819 and -592) genotypes/haplotypes do not influence the degree of HAI and response to combination therapy or susceptibility to HCV infection with and without S. mansoni co-infection.