Levels of macrophage inflammatory protein 1 alpha (MIP-1 alpha) and MIP-1 beta in intervillous blood plasma samples from women with placental malaria and human immunodeficiency virus infection.
Macrophage inflammatory protein-1 alpha (MIP-1 alpha) and MIP-1 beta play an important role in modulating immune responses. To understand their importance in immunity to placental malaria (PM) and in human immunodeficiency virus (HIV)-PM coinfection, we investigated levels of these chemokines in the placental intervillous blood plasma (IVB plasma) and cord blood plasma of HIV-negative PM-negative, HIV-negative PM-positive, HIV-positive PM-negative, and HIV-positive PM-positive women. Compared to HIV-negative PM-negative women, the MIP-1 beta concentration in IVB plasma was significantly elevated in HIV-negative PM-positive women and HIV-positive PM-positive women, but it was unaltered in HIV-positive PM-negative women. Also, PM-infected women, irrespective of their HIV status, had significantly higher levels of MIP-1 beta than HIV-positive PM-negative women. The MIP-1 alpha level was not altered in association with either infection. The IVB plasma levels of MIP-1 alpha and MIP-1 beta positively correlated with the cord blood plasma levels of these chemokines. As with IVB plasma, only cord plasma from PM-infected mothers had significantly elevated levels of MIP-1 beta compared to PM-negative mothers, irrespective of their HIV infection status. MIP-1 beta and MIP-1 alpha levels in PM-positive women were positively associated with parasite density and malaria pigment levels. Regardless of HIV serostatus, the IVB MIP-1 beta level was significantly lower in women with PM-associated anemia. In summary, an elevated level of MIP-1 beta was associated with PM. HIV infection did not significantly alter these two chemokine levels in IVB plasma.
Chaisavaneeyakorn
Sujittra
S
Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Public Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 30333, USA.
Moore
Julie M
JM
Mirel
Lisa
L
Othoro
Caroline
C
Otieno
Juliana
J
Chaiyaroj
Sansanee C
SC
Shi
Ya Ping
YP
Nahlen
Bernard L
BL
Lal
Altaf A
AA
Udhayakumar
Venkatachalam
V
D000328:Adult; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D015331:Cohort Studies; D004198:Disease Susceptibility; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005786:Gene Expression Regulation; D015658:HIV Infections / Q000097:blood*; D006420:Hemeproteins / Q000032:analysis* / Q000502:physiology; D006801:Humans; D007630:Kenya / Q000453:epidemiology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D008288:Malaria / Q000097:blood*; D010922:Placenta Diseases / Q000097:blood*; D010949:Plasma; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000097:blood*; D012189:Retrospective Studies; D018417:Th1 Cells / Q000276:immunology
D054405:Chemokine CCL3; D054407:Chemokine CCL4; D006420:Hemeproteins; D019402:Macrophage Inflammatory Proteins; C020753:hemozoin