Parnpen ViriyavejakulVasant KhachonsaksumetChuchard PunsawadMahidol UniversityWalailak University2018-11-092018-11-092014-03-17Malaria Journal. Vol.13, No.1 (2014)147528752-s2.0-84899087895https://repository.li.mahidol.ac.th/handle/123456789/33981Background: Liver involvement in severe Plasmodium falciparum infection is commonly a significant cause of morbidity and mortality among humans. The clinical presentation of jaundice often reflects a certain degree of liver damage. This study investigated the liver pathology of severe P. falciparum malaria as well as the regulation and occurrence of apoptosis in cellular components of formalin-fixed, paraffin-embedded liver tissues. Methods. The liver tissues used in the study came from patients who died from P. falciparum malaria with hyperbilirubinaemia (total bilirubin (TB) ≥ 51.3 μmol/L or 3 mg/dl) (12 cases), P. falciparum malaria without hyperbilirubinaemia (TB < 51.3 μmol/L) (10 cases); and patients who died due to accidents, whose liver histology was normal (the control group) (10 cases). The histopathology of the liver tissue was studied by routine histology method. Caspase-3 and nuclear factor kappa B (NF-κB) p65 expressions were determined using immunohistochemistry. Results: The severity of liver histopathology, occurrence of apoptosis and NF-κB p65 activation in P. falciparum malaria were associated with higher TB level. Significant correlations were found between NF-κB p65 expression and apoptosis in Kupffer cells and lymphocytes in the portal tracts. Conclusions: Hyperplastic Kupffer cells and portal tract inflammation are two main features found in the liver tissues of severe P. falciparum malaria cases. In addition, NF-κB is associated with Kupffer cells and lymphocyte apoptosis in severe P. falciparum malaria. © 2014 Viriyavejakul et al.; licensee BioMed Central Ltd.Mahidol UniversityImmunology and MicrobiologyMedicineArticleSCOPUS10.1186/1475-2875-13-106