摘要：

Invasive nontyphoidal Salmonella (iNTS) infections are commonly associated with Plasmodium falciparum infections, but the immunologic basis for this linkage is poorly understood. We hypothesized that P. falciparum infection compromises the hosts' humoral and cellular immunity to NTS which increases their susceptibility to iNTS infection. We prospectively recruited children aged between 6 and 60 months at a Community Health Centre in Blantyre, Malawi and allocated them to the following groups; febrile with uncomplicated malaria, febrile malaria-negative, non-febrile malaria-negative. S Typhimurium (STm)-specific; serum bactericidal activity (SBA) and blood bactericidal activity (WBBA), complement C3 deposition and neutrophil respiratory burst activity (NRBA) were measured. SBA to STm was reduced in febrile P. falciparum infected (Median -0.201og10, IQR [-1.85, 0.32]) compared to non-febrile malaria-negative (Median -1.42log10, IQR [-2.0, -0.47], p=0.052). In relation to SBA, C3 deposition on STm was significantly reduced in febrile P. falciparum infected (Median 7.5%, IQR [4.1, 15.0]) compared to non-febrile malaria-negative (Median 29%, IQR [11.8, 48.0], p=0.048). WBBA to STm was significantly reduced in febrile P. falciparum infected (Median 0.25log10, IQR [-0.73, 1.13], p=0.0001) compared to non-febrile malaria-negative (Median -1.0log10, IQR [-1.68, -0.16]). In relation to WBBA, STm-specific NRBA was reduced in febrile P. falciparum infected (Median 8.8% IQR [3.7, 20], p=0.0001) compared to non-febrile malaria-negative (Median 40.5% IQR [33, 65.8]). P. falciparum infection impairs humoral and cellular immunity to STm in children during malaria episodes, which may explain the increased risk of iNTS observed in children from malaria endemic settings. The mechanisms underlying humoral immunity impairment are incompletely understood and should be explored further.

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