Cytomegalovirus induction of tumor necrosis factor-alpha by human monocytes and mucosal macrophages.

Abstract

Cytomegalovirus (CMV) is a major cause of inflammatory organ disease in immunosuppressed persons. To elucidate the mechanisms of CMV-induced inflammation, we investigated whether tumor necrosis factor-a (TNF-a) was involved in the pathogenesis of CMV colitis in patients with AIDS. In in situ hybridization experiments, TNF-a mRNA was shown to be abundantly present in colonic mucosa from AIDS patients with CMV colitis but not in colonic mucosa from control (AIDS and normal) subjects. The TNF-a transcripts, identified in macrophage-like cells containing cytomegalic inclusions, were positively associated with CMV, but not HIV-1, within the mucosa.

The Human Cytomegalovirus UL26 Protein Antagonizes NF-κB Activation

“…WT HCMV infection induced more TNF-a production than mock-infected cells (Fig. 2F), which agrees with previous reports (44,45). Cells infected with ⌬U L 26 induced a similar amount of TNF-␣ (Fig.…”

Tumour necrosis factor- production during cytomegalovirus infection in immunosuppressed rats

“…Recently, increased serum TNF concentrations were observed in liver transplant patients suffering from CMV disease (Tilg et al, 1991). Moreover, TNF-~ mRNA was shown to be abundant in the colonic mucosa from AIDS patients with CMV colitis (Smith et al, 1992).…”

Macrophages in Vaginal but Not Intestinal Mucosa Are Monocyte-Like and Permissive to Human Immunodeficiency Virus Type 1 Infection

“…Robust HIV-1 replication in vaginal macrophages indicates the cells are a likely source of virus in the female genital tract during HIV-1 infection. In addition, the susceptibility of macrophages in the vaginal mucosa to HIV-1 suggests the potential contribution of vaginal macrophages to heterosexual HIV-1 transmission, particularly in the presence of genital infections that enhance CCR5 expression (8,60,43), HIV-1 replication (32), and cytokine production that in turn could enhance HIV-1 replication (20,34,47). Finally, the findings presented here suggest that the cellular reservoir of HIV-1 during chronic infection may extend to vaginal macrophages.…”