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M1 macrophage features in severe Plasmodium falciparum malaria patients with pulmonary oedema

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Abstract Background Pulmonary oedema (PE) is a serious complication of Plasmodium falciparum malaria which can lead to acute lung injury in severe cases. Lung macrophages are activated during malaria infection due to a complex host-immune response. The molecular basis for macrophage polarization is still unclear but understanding the predominant subtypes could lead to new therapeutic strategies where the diseases present with lung involvement. The present study was designed to study the polarization of lung macrophages, as M1 or M2 macrophages, in the lungs of severe P. falciparum malaria patients, with and without evidence of PE. Methods Lung tissue samples, taken from patients who died from severe P. falciparum malaria, were categorized into severe malaria with PE and without PE (non-PE). Expression of surface markers (CD68+, all macrophages; CD40+, M1 macrophage; and CD163+, M2 macrophage) on activated lung macrophages was used to quantify M1/M2 macrophage subtypes. Results Lung injury was demonstrated in malaria patients with PE. The expression of CD40 (M1 macrophage) was prominent in the group of severe P. falciparum malaria patients with PE (63.44 ± 1.98%), compared to non-PE group (53.22 ± 3.85%, p < 0.05), whereas there was no difference observed for CD163 (M2 macrophage) between PE and non-PE groups. Conclusions The study demonstrates M1 polarization in lung tissues from severe P. falciparum malaria infections with PE. Understanding the nature of macrophage characterization in malaria infection may provide new insights into therapeutic approaches that could be deployed to reduce lung damage in severe P. falciparum malaria.
Title: M1 macrophage features in severe Plasmodium falciparum malaria patients with pulmonary oedema
Description:
Abstract Background Pulmonary oedema (PE) is a serious complication of Plasmodium falciparum malaria which can lead to acute lung injury in severe cases.
Lung macrophages are activated during malaria infection due to a complex host-immune response.
The molecular basis for macrophage polarization is still unclear but understanding the predominant subtypes could lead to new therapeutic strategies where the diseases present with lung involvement.
The present study was designed to study the polarization of lung macrophages, as M1 or M2 macrophages, in the lungs of severe P.
falciparum malaria patients, with and without evidence of PE.
Methods Lung tissue samples, taken from patients who died from severe P.
falciparum malaria, were categorized into severe malaria with PE and without PE (non-PE).
Expression of surface markers (CD68+, all macrophages; CD40+, M1 macrophage; and CD163+, M2 macrophage) on activated lung macrophages was used to quantify M1/M2 macrophage subtypes.
Results Lung injury was demonstrated in malaria patients with PE.
The expression of CD40 (M1 macrophage) was prominent in the group of severe P.
falciparum malaria patients with PE (63.
44 ± 1.
98%), compared to non-PE group (53.
22 ± 3.
85%, p < 0.
05), whereas there was no difference observed for CD163 (M2 macrophage) between PE and non-PE groups.
Conclusions The study demonstrates M1 polarization in lung tissues from severe P.
falciparum malaria infections with PE.
Understanding the nature of macrophage characterization in malaria infection may provide new insights into therapeutic approaches that could be deployed to reduce lung damage in severe P.
falciparum malaria.

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