Activation of beta-chemokines and CCR5 in persons infected with human immunodeficiency virus type 1 and tuberculosis

J Infect Dis. 2001 Jun 15;183(12):1801-4. doi: 10.1086/320724. Epub 2001 May 17.

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • AIDS-Related Opportunistic Infections / immunology*
  • Cells, Cultured
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5 / biosynthesis
  • Chemokines, CC / metabolism*
  • Disease Progression
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • HIV Infections / complications
  • HIV Infections / immunology*
  • HIV-1*
  • Humans
  • Leukocytes, Mononuclear / immunology
  • Macrophage Inflammatory Proteins / biosynthesis*
  • RNA, Messenger
  • Receptors, CCR5 / metabolism*
  • Tuberculosis, Pulmonary / complications
  • Tuberculosis, Pulmonary / immunology*

Substances

  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5
  • Chemokines, CC
  • Macrophage Inflammatory Proteins
  • RNA, Messenger
  • Receptors, CCR5