Forty individuals were enrolled comprising 20 active and untreated cases of VL and 20
non-VL individuals from the endemic region of Bihar, India. The patients with VL were segregated
into two groups of 10 well-nourished and 10 malnourished participants. Patients’ blood samples
were directed against a crude Leishmania donovani extract (soluble leishmanial antigen) and
phorbol 12-myristate-13-acetate plus ionomycin. The transendothelial cell adherence migration
abilities of the PMNs and monocytes directed against these antigens were determined in wholeblood
assays by flow cytometry. The chemokine (interleukin [IL]-8, macrophage inflammatory
protein [MIP]-1 a) and cytokine support (tumor necrosis factor -a, interferon [IFN]-g, IL-10), which
could be significant in transendothelial cell migration, and efficacies of antileishmanial phagocytic
function and reactive oxygen species (ROS) generation were also determined.
Results: Severe hindrance in the adherence of innate immune cells to the endothelial wall due to
Leishmania parasites, as revealed by decreased shedding of L-selectin (CD62 L) and down-regulation
of CD11 b expression on the surface of the PMNs and monocytes, occurred in malnourished VL
patients. The production of MIP-1 a and IL-8 in response to L. donovani antigen was reduced in
malnourished patients. In contrast, malnutrition in VL patients significantly reduced the IFN-g and
TNF-a produced by these immune cells, whereas the levels of IL-10 were significantly elevated.
Malnourished VL patients were observed with severely dysfunctional PMNs and monocytes in terms
of ROS activity that could not be recovered by stimulation with L. donovani antigen.
Conclusions: Malnutrition linked to VL can be a decisive factor in the dynamics of L. donovani
evasion of innate immune cell function in VL patients.
Forty individuals were enrolled comprising 20 active and untreated cases of VL and 20
non-VL individuals from the endemic region of Bihar, India. The patients with VL were segregated
into two groups of 10 well-nourished and 10 malnourished participants. Patients’ blood samples
were directed against a crude Leishmania donovani extract (soluble leishmanial antigen) and
phorbol 12-myristate-13-acetate plus ionomycin. The transendothelial cell adherence migration
abilities of the PMNs and monocytes directed against these antigens were determined in wholeblood
assays by flow cytometry. The chemokine (interleukin [IL]-8, macrophage inflammatory
protein [MIP]-1 a) and cytokine support (tumor necrosis factor -a, interferon [IFN]-g, IL-10), which
could be significant in transendothelial cell migration, and efficacies of antileishmanial phagocytic
function and reactive oxygen species (ROS) generation were also determined.
Results: Severe hindrance in the adherence of innate immune cells to the endothelial wall due to
Leishmania parasites, as revealed by decreased shedding of L-selectin (CD62 L) and down-regulation
of CD11 b expression on the surface of the PMNs and monocytes, occurred in malnourished VL
patients. The production of MIP-1 a and IL-8 in response to L. donovani antigen was reduced in
malnourished patients. In contrast, malnutrition in VL patients significantly reduced the IFN-g and
TNF-a produced by these immune cells, whereas the levels of IL-10 were significantly elevated.
Malnourished VL patients were observed with severely dysfunctional PMNs and monocytes in terms
of ROS activity that could not be recovered by stimulation with L. donovani antigen.
Conclusions: Malnutrition linked to VL can be a decisive factor in the dynamics of L. donovani
evasion of innate immune cell function in VL patients.
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