HIV alters immune response in lungs

HIV infection alters the functioning of the immune system in the lungs, researchers working in Malawi have found, but not to such an extent that it could lead to a deficiency in innate pulmonary immune function. The research is published in the October 15^th edition of the Journal of Infectious Diseases.

Bacterial pneumonia and invasive pneumococcal disease are common in HIV-positive individuals and the specific immune defects rendering HIV-infected patients more susceptible to such diseases are not fully understood and innate immune responses in the lung fluid of HIV-positive patients have not been described.

Investigators therefore compared concentrations of innate pulmonary immune factors in patients with HIV with HIV-negative patients. The concentrations measured were lactoferrin, lysozyme, immunoglobulins, and secretory leukocyte protease inhibitor.

A total of 45 individuals were recruited to the study. Of these, 16 were HIV-positive with no history of pulmonary disease, eleven were HIV-positive with a history of invasive pneumococcal disease and the remaining 18 individuals were HIV-negative controls. All 45 individuals were well at the time of the study with no active pulmonary disease.

Samples of bronchoalveolar lavage were obtained during a bronchoscopy examination.

The percentage of bronchoalveolar lavage cells which were lymphocytes was significantly higher in the HIV-positive patients (21%) than HIV-negative individuals (11%, p = 0.02).

Concentrations of beta-chemokine were also significantly higher in the HIV-infected patients than HIV-uninfected individuals (p < 0.001). Concentrations were undetectable in the HIV-negatives, a mean of 57pg/ml in HIV-infected individuals with a CD4 cell count above 200 cells/mm³ and a mean of 130pg/ml in HIV-positive patients with a CD4 cell count below 200 cells/mm³.

The investigators found that beta-chemokine concentrations were correlated with HIV viral load in bronchoalveolar lavage (p < 0.001), but not with viral load in blood.

Lysozyme concentrations were higher in HIV-positive patients than the HIV-negative controls (p = 0.03). There was no significant relationship between lysozyme concentrations and viral load in either bronchoalveolar lavage or blood.

Although concentrations of secretory leukocyte protease inhibitor in pulmonary fluid did not differ significantly between the three groups of patients, however in further statistical analysis they found that that secretory leukocyte protease inhibitor concentrations were significantly correlated to HIV viral load in the bronchoalveolar lavage of HIV-positive patients (p = 0.01), but not plasma viral load.

Lactoferrin concentrations were lower in HIV-positive individuals than the study members who were HIV-uninfected (p = 0.04). There was no correlation between concentrations and viral load in pulmonary fluid or plasma.

Immunoglobulin concentrations in pulmonary fluid were, as the investigators expected, significantly higher in HIV-positive patients. The investigators also found that concentrations were higher in HIV patients with a history of lung disease than those who were well. Once again, a correlation was established between immunoglobulin levels in pulmonary fluid, but not for plasma.

“The present study has described altered concentrations of innate immune factors in bronchoalveolar lavage fluid from HIV-infected subjects” conclude the investigators, who add, “inappropriately low lysozyme concentrations in the subjects with AIDS may have been relevant to their susceptibility to pneumococcal disease, but no clear defect in pulmonary innate immunity was demonstrated in this group.”