Esophageal mucosa in HIV infection: A"deeper" look at this little spoken organ

Although the esophagus is a common site of opportunistic infection in AIDS patients, little is known about the impact of HIV as well as opportunistic infection in the esophageal mucosa. Our aim is to analyze the esophageal immune profile in HIV+ patients with different immunological status with and without the opportunistic Candida infection.

Immunohistochemistry to CD4⁺ and CD8⁺ T-cells, γ-interferon, transforming growth factor-β, interleukin (IL)-4, IL-6, IL-13, and IL-17 was performed in esophageal samples of 40 chronically HIV+ patients under highly active antiretroviral therapy (16 with Candida esophagitis, 12 virologically non-supressed with blood CD4 count < 500, and 12 virologically suppressed with blood CD4 count > 500; the latter two groups without esophageal candidiasis). The controls were 12 HIV-negative healthy individuals.

Esophageal CD4⁺ T-cell expression in HIV+ patients did not differ from the control group (P = 0.50). Mucosal CD8⁺ T-cell expression was significantly increased in HIV+ patients (P = 0.0018). Candida esophagitis and virologically non-supressed HIV+ patients with CD4 < 500 showed an increased expression of IL-17 and IL-6 with fewer expressions of γ-interferon, more attenuated in the latter group. Transforming growth factor-β was increased only in virologically suppressed HIV+ patients with CD4 > 500. IL-4 and IL-13 were similar to the control group.

In contrast to CD8⁺ T-cell expression, esophageal CD4⁺ T-cell expression does not reflect the HIV+ patient's immunological status. T-helper 17 (Th17) response seems to play a role in the esophageal mucosa of virologically non-supressed HIV+ patients with blood CD4 < 500. Candida esophagitis showed a Th1/Th17 response but seems to be dominantly regulated by the Th17 pathway.