title: 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.
abstract: 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.
authors.affiliation: 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.
authors.forename: Sujittra
authors.initials: S
authors.lastname: Chaisavaneeyakorn
authors.forename: Julie M
authors.initials: JM
authors.lastname: Moore
authors.forename: Lisa
authors.initials: L
authors.lastname: Mirel
authors.forename: Caroline
authors.initials: C
authors.lastname: Othoro
authors.forename: Juliana
authors.initials: J
authors.lastname: Otieno
authors.forename: Sansanee C
authors.initials: SC
authors.lastname: Chaiyaroj
authors.forename: Ya Ping
authors.initials: YP
authors.lastname: Shi
authors.forename: Bernard L
authors.initials: BL
authors.lastname: Nahlen
authors.forename: Altaf A
authors.initials: AA
authors.lastname: Lal
authors.forename: Venkatachalam
authors.initials: V
authors.lastname: Udhayakumar
mesh_terms: 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
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D006420:Hemeproteins; D019402:Macrophage Inflammatory Proteins; C020753:hemozoin