Loss of Humoral and Cellular Immunity to Invasive Nontyphoidal Salmonella during Current or Convalescent Plasmodium falciparum Infection in Malawian Children

Autor: Queen Dube, Tonney S. Nyirenda, James T. Nyirenda, Kondwani C. Jambo, Robert S. Heyderman, Chisomo L. Msefula, Henry C. Mwandumba, Wilson L. Mandala, Melita A. Gordon, Janet Storm, Dumizulu L. Tembo
Jazyk: angličtina
Rok vydání: 2017
Předmět:
Male
Salmonella typhimurium
0301 basic medicine
Malawi
Cellular immunity
Neutrophils
Clinical Biochemistry
wc_269
susceptibility
Salmonella
Interquartile range
Immunology and Allergy
Prospective Studies
Spotlight
Malaria
Falciparum

Respiratory Burst
Immunity
Cellular

3. Good health
Child
Preschool

Salmonella Infections
Female
Disease Susceptibility
Antibody
qw_520
Microbiology (medical)
Blood Bactericidal Activity
Salmonella Vaccines
qw_568
Immunology
malaria
Biology
03 medical and health sciences
children
Immunity
parasitic diseases
medicine
Humans
Infant
Plasmodium falciparum
Complement System Proteins
medicine.disease
biology.organism_classification
immunity
Immunity
Humoral

wc_750
030104 developmental biology
qx_135
Bacteremia
Humoral immunity
biology.protein
Clinical Immunology
ws_440
Malaria
Zdroj: CLINICAL AND VACCINE IMMUNOLOGY
Clinical and Vaccine Immunology : CVI
ISSN: 1556-6811
Popis: 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 humoral and cellular immunity of the host to NTS, which increases the susceptibility of the host 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, and nonfebrile malaria negative. Levels of Salmonella enterica serovar Typhimurium-specific serum bactericidal activity (SBA) and whole-blood bactericidal activity (WBBA), complement C3 deposition, and neutrophil respiratory burst activity (NRBA) were measured. Levels of SBA with respect to S . Typhimurium were reduced in febrile P. falciparum -infected children (median, −0.20 log10 [interquartile range {IQR}, −1.85, 0.32]) compared to nonfebrile malaria-negative children (median, −1.42 log10 [IQR, −2.0, −0.47], P = 0.052). In relation to SBA, C3 deposition on S . Typhimurium was significantly reduced in febrile P. falciparum -infected children (median, 7.5% [IQR, 4.1, 15.0]) compared to nonfebrile malaria-negative children (median, 29% [IQR, 11.8, 48.0], P = 0.048). WBBA with respect to S . Typhimurium was significantly reduced in febrile P. falciparum -infected children (median, 0.25 log10 [IQR, −0.73, 1.13], P = 0.0001) compared to nonfebrile malaria-negative children (median, −1.0 log10 [IQR, −1.68, −0.16]). In relation to WBBA, S . Typhimurium-specific NRBA was reduced in febrile P. falciparum -infected children (median, 8.8% [IQR, 3.7, 20], P = 0.0001) compared to nonfebrile malaria-negative children (median, 40.5% [IQR, 33, 65.8]). P. falciparum infection impairs humoral and cellular immunity to S . Typhimurium in children during malaria episodes, which may explain the increased risk of iNTS observed in children from settings of malaria endemicity. The mechanisms underlying humoral immunity impairment are incompletely understood and should be explored further.
Databáze: OpenAIRE