title: Activation of beta-chemokines and CCR5 in persons infected with human immunodeficiency virus type 1 and tuberculosis.
abstract: Tuberculosis (TB) in human immunodeficiency virus type 1 (HIV-1)-infected persons is associated with progression of HIV-1 disease. The expression of macrophage inflammatory protein (MIP)-1alpha and CCR5 was assessed in HIV-1-infected patients with pulmonary TB (HIV-1/PTB) and without PTB (HIV-1/C), PTB patients not infected with HIV-1 (PTB), and control subjects. Mycobacterium tuberculosis (MTB)-induced MIP-1alpha production was lower in peripheral blood mononuclear cells (PBMC) of HIV-1/PTB patients than in those of PTB patients (P< .05) and was lower in PBMC of HIV-1/C patients than in those of control subjects (P< .005). However, MIP-1alpha production was higher in PBMC of HIV/PTB patients than in those of HIV-1/C patients (P< .01). The pattern of MTB-induced RANTES production was similar to that of MIP-1alpha. However, MTB induced greater expression of mRNA for CCR5 in PBMC of HIV-1/PTB patients than in those of HIV-1/C patients (P< .04). Furthermore, the MTB-induced HIV p24 antigen level in PBMC of HIV-1/PTB patients with a CD4 cell count <500 cells/microL was higher (P< .05) than that in HIV-1/C patients. Thus, perturbations in chemokine pathways in HIV-1/PTB patients may accelerate HIV-1 disease.
authors.affiliation: Department of Internal Medicine, Makerere University Medical School, Kampala, Uganda.
authors.forename: H
authors.initials: H
authors.lastname: Mayanja-Kizza
authors.forename: A
authors.initials: A
authors.lastname: Wajja
authors.forename: M
authors.initials: M
authors.lastname: Wu
authors.forename: P
authors.initials: P
authors.lastname: Peters
authors.forename: G
authors.initials: G
authors.lastname: Nalugwa
authors.forename: F
authors.initials: F
authors.lastname: Mubiru
authors.forename: H
authors.initials: H
authors.lastname: Aung
authors.forename: G
authors.initials: G
authors.lastname: Vanham
authors.forename: C
authors.initials: C
authors.lastname: Hirsch
authors.forename: C
authors.initials: C
authors.lastname: Whalen
authors.forename: J
authors.initials: J
authors.lastname: Ellner
authors.forename: Z
authors.initials: Z
authors.lastname: Toossi
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000276:immunology*; D002478:Cells, Cultured; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis; D019742:Chemokines, CC / Q000378:metabolism*; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D015658:HIV Infections / Q000150:complications / Q000276:immunology*; D015497:HIV-1; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis*; D012333:RNA, Messenger; D019713:Receptors, CCR5 / Q000378:metabolism*; D014397:Tuberculosis, Pulmonary / Q000150:complications / Q000276:immunology*
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019742:Chemokines, CC; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D019713:Receptors, CCR5