Biology Reference
In-Depth Information
CONCLUSION
Most HIV-infected individuals will experience pulmonary complications during
the course of HIV-1 related disease, especially in the absence of HAART and
speci®c chemoprophylaxis. In the lungs, AM represent the most abundant pul-
monary immune cell and represent an important ®rst-line-host defense cell.
Through its capacity to serve as an essential component of innate immunity,
and the capacity to mediate subsequent acquired immune response, AM are
important mediators in healthy individuals. Increasingly, growing evidence
suggests that in addition to CD4 T-lymphocyte depletion in the lungs (which
parallels the decline in the peripheral blood), AM from HIV-infected individ-
uals demonstrate a variety of functional alterations, all of which may impact on
the clinical consequences of HIV-1-related disease. Clearly, impaired innate and
altered acquired immune function may impair critical functions and lead to
susceptibility to opportunistic pathogens and infection and inability to ade-
quately clear pulmonary infections.
Although much has been learned in recent years, many unanswered ques-
tions related to AM function in HIV-1 infection remain. Clearly, studying AM
rather than peripheral blood±derived macrophages is important. Continued use
of powerful tools, including ¯ow cytometry, will allow a greater understanding
of the function of these important cells, and hopefully lead to novel therapeutic
interventions such as immunomodulation of these cells to assist in host defense
function.
REFERENCES
Abbud RA, Finegan CK, Guay LA, Rich EA. 1995. Enhanced production of human im-
munode®ciency virus type 1 by in vitro-infected alveolar macrophages from otherwise healthy
cigarette smokers. J Infect Dis 172: 859±863.
Agostini C, Zambello R, Trentin L, Garbisa S, DiCelle PF, Bulian P, Onisto M, Poletti V, Spiga L,
Raise E, Foa R, Semenzato G. 1991a. Alveolar macrophages from patients with AIDS and
AIDS-related complex constitutively synthesize and release tumor necrosis factor alpha. Am Rev
Resp Dis 144: 195±201.
Agostini C, Zambello R, Trentin L, Poletti V, Spiga L, Gritti F, Cipriani A, Salmaso L, Cadrobbi
P, Semenzato G. 1991b. Prognostic signi®cance of the evaluation of bronchoalveolar lavage
populations in patients with HIV-1 infection and pulmonary involvement. Chest 100: 1601±
1606.
Agostini C, Trentin L, Zambello R, Builian P, Caenazzo C, Cipriani A, Candrobbi P, Garbisa S,
Semenzato G. 1992. Release of granulocyte-macrophage colony-stimulating factor by alveolar
macrophages in the lung of HIVl-1-infected patients. A mechanism accounting for macrophage
and neutrophil accumulation. J Immunol 149: 3379±3385.
Agostini C, Trentin L, Zambello R, Bulian P, Garbisa S, Cipriani A, Cadrobbi P, Semenzato
G. 1993a. Alveolar macrophages in HIV-1 infection express accessory molecules, activation
markers, and release increased biological response modi®ers. Chest 103: 108S±111S.
Agostini C, Trentin L, Zambello R, Semenzato G. 1993b. HIV-1 and the lung. Infectivity, patho-
genic mechanisms and cellular immune responses taking place in the lower respiratory tract. Am
Rev Respir Dis 147: 1038±1049.
