Author/Authors :
Sohrabi, Nooshin Mycology Research Centre - Faculty of Veterinary Medicine - Tehran University, Tehran , Khosravi, Ali Reza Mycology Research Centre - Faculty of Veterinary Medicine - Tehran University, Tehran , Hassan, Zuhair Mohammad Immunology Department - School of Medicine - Tarbiat Modares University, Tehran , Mahdavi, Mehdi Immunology Department - School of Medicine - Tarbiat Modares University, Tehran , Tebianian, Majid Immunology Department - School of Medicine - Tarbiat Modares University, Tehran , Amini, Abbas Ali Immunology Department - School of Medicine - Tehran University of Medical Sciences, Tehran
Abstract :
Objective(s)
Using a cancer murine model of invasive aspergillosis (IA), we investigated the expression of TLR-2,
Dectin-1 and the level of cytokine production by CD4+ T helper cells in different groups of mice (with or
without cancer), also, the effect of invasive aspergillosis on the immune response pattern of cancer mice.
Materials and Methods
Patterns of susceptibility and resistance to infection obtained with different groups of mice injected with
Aspergillus fumigatus conidia. TLR-2 and Dectin-1 analyzed applying flowcytometry and cytokine
production of cultured splenocytes by ELISA method.
Results
Cancer mice that challenged with A. fumigatus conidia showed significant increase in TLR-2 and Dectin-1
levels compared with the two other control groups (normal mice challenged with A. fumigatus and
non-infected cancer mice). Moreover, it showed insignificant decrease in IFN-γ and IL-10 levels and
insignificant increase in TNF-α level. The data demonstrated remarkable rise in IL-4 level and the mortality
of cancer mice that intravenously infected with A. fumigatus.
Conclusion
Probably IA causes stimulation in innate immunity and Th2 cells, also some disorganization in cytokine
production in CD4+ T helper cells. We hypothesize that concomitance of IA and cancer may change the
microenvironment for local or systemic immune responses. Other complementary studies could help
supporting our hypothesis.
Keywords :
Toll-like receptor 2 , Dectin 1 , Cancer Cytokines , Aspergillosis