Alveolar macrophages (AMs) harvested from 32 HIV-infected patients with respiratory riddles (opportunistic pulmonary infections.

Alveolar macrophages (AMs) harvested from 32 HIV-infected patients with respiratory riddles (opportunistic pulmonary infections, n = 12; other lung disease, n = 20) and 13 healthy rules were stained with a panel of 15 monoclonal antibodies directed against surface antigens implicated in lonely dwelling function. Antigen expression was quantified from flow cytometry and expressed as relative linear median fluorescence intensity (RLMFI). in succession AMs of patients, as compared with sways there was a significant enhancement of HLA DP (121 [+ or -] 15 v 65 [+ or -] 09 p = 001 M [+ or -] SEM RLMFI units), CD11b (34 [+ or -] 05 v 17 [+ or -] 04 p = 0014) CD11c (89 [+ or -] 10 v 48 [+ or -] 08 p = 00046) CD14 (21 [+ or -] 03 v 10 [+ or -] 02 p = 00009) and CD33 (17 [+ or -] 01 v 10 [+ or -] 02 p = 00093) No significant differences could be established for HLA-DR (369 [+ or -] 58 v 309 [+ or -] 75 NS) HLA-DQ (34 [+ or -] 03 v 31 [+ or -] 06 NS) CD54 (19 [+ or -] 03 v 12 [+ or -] 01 NS) CD13 (25 [+ or -] 06 v 15 [+ or -] 03 NS) CD36 (14 [+ or -] 02 v 09 [+ or -] 03 NS) CD71 (103 [+ or -] 19 v 89 [+ or -] 18 NS) CD25 (08 [+ or -] 00 v 09 [+ or -] 01 NS) 27E10 (11 [+ or -] 01 v 08 [+ or -] 03 NS) RM3/1 (19 [+ or -] 04 v 15 [+ or -] 04 NS) and CD4 (15 [+ or -] 03 v 10 [+ or -] 00 NS) The expression of CD14 and CD11b yet not of HLA class II antigens and CD71 was increased in the smaller solitary abode; squalid population compared with the larger, thus suggesting monocyte recruitment. The increased expression of HLA-DP, CD11c CD14 and CD33 upon the patients' AMs was independent of smoking habits. The extent of immunodeficiency as indicated by means of the absolute peripheral CD4 esteem the character of HIV-related pulmonary disease, and the prophylactic use of pentamidine or zidovudine did not significantly modify the antigen expression pattern. It is conclud that HIV infection may lead, most numerous probably indirectly, to enhanced expression of surface antigens from local upregulation and/or recruitment of monocytes from the peripheral circulation. The functional significance of enhanced marker expression requires further clarification.

Deficient monocyte/macrophage function has been adviseed to be a leading cause of opportunistic disease in HIV-infected patients.[1] However, evidence to support this idea is far from conclusive. mostly investigations have been carried without on peripheral blood monocytes (PBMs) In these studies, defective function has not been consistently found

Chemotaxis of PBM from patients with AIDS and lymphadenopathy syndrome was reported to be decreased through some[2,3] but not all authors.[4] However, in vitro infection of normal PBM with HIV-1 clearly overpowered their chemotactic activity.[5] Phagocytosis of latex particles,[3,6] and phagocytosis and intracellular killing of pathogens so as opsonized Candida albicans,[4] Toxoplasma gondii,[7,8] or Chlamydia psittaci[7] by the agency of AIDS PBMs were reported to be intact. succeeding to incubation with HIV case protein gp120, normal alveolar macrophages (AMs) demonstrated decreased internalization of Cryptococcus neoformans, unless binding of the yeast was not altered.[9] Although PBM from patients with lymphadenopathy syndrome showed decreased superoxide anion production,[3] AIDS PBM were normal in this respect[410] The accessory capacity of PBM from patients with AIDS and AIDS-related tangled skein proved to be either reduced[11] or in the normal range,[12] whereas it was substantially enhanced in AMs from these patients.[12] In a fresh study in asymptomatic HIV-positive patients, evidence for AM activation, increased spontaneous release of superoxide anion, has been reported.[13]

Since pulmonary disease continues to be a major determinant of morbidity and mortality in HIV-infected patients, the subject of attention of local lung defense mechanisms is of paramount importance. The goal of the not away study was to measure AM membrane marker expression by means of flow cytometry. As in the case of functional studies, surface marker analysis of small cavitys of the monocyte/macrophage lineage from HIV-infected patients has been performed predominantly with PBMs[614-18] An additional aim was to elucidate the purport of prophylactic pentamidine inhalation onward surface antigen expression. To this extremity we have quantified 15 surface markers implicated in confined apartment functions on AMs harvested from HIV-infected patients and healthy tenders The markers can be broadly classified into five functional clusters with some overlap among the groups: (1) markers reflecting antigen presenting capacity (HLA-DR, DP DQ);[1930] (2) adhesion markers (CD11bc CD54);[21-25] (3) markers identifying lately recruited monocytes (CD11b, CD13, CD14 CD33 CD36);[2627] (4) activation markers (CD11bc CD71 CD25);[28] and (5) markers defining the stage of inflammatory changes (27E10 RM 3/1)[29]

METHODS

Patients and Controls

Bronchoalveolar lavage (BAL) fluid was obtained from a total of 32 consecutive nonselected HIV-infected patients presenting with respiratory symptoms (cough or mild dyspnea or both) Bronchoscopy including lavage and transbronchial biopsy, was indicated to obtain a diagnosis of suspected infections or noninfectious pulmonary disease. Patients unwilling to go through the procedure and those in whom the BAL retrieval rate was less than 30 percent were exclud from the contemplation Pertinent clinical and laboratory data were aggregateed from the patients' charts. WR- and CDC-staging was updated according to the actual bronchoscopic, histologic, and microbiologic findings.

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