Functional activity of polymorphonuclear neutrophils (PMN) was tested in 63 HIV-1 infected patients. PMN chemiluminescence (CL) and intracellular enzyme activity were both depressed in patients at all stages of infection, though this depression was more pronounced in AIDS patients. We found no such depression when cells were incubated in the presence of autologous serum. PMN phagocytosis in the presence of serum was reduced in the early stage of HIV infection (LAS) but was in the normal range in AIDS patients. No differences in PMN functional activity between patients with LAS and those with dermatological disorders were found. The appearance of recurrent upper respiratory tract infection was associated with reduced PMN CL. The most pronounced changes in PMN activity were observed in patients with severe, recurrent bacterial pneumonia and Pneumocystis carinii pneumonia. A lower level of PMN activity was found in patients with infection progressing rapidly towards AIDS than in patients with a relatively stable course of infection. Thus, PMN CL may be regarded as a predictive factor for the progression of HIV infection.

The aim of this study was to determine whether polymorphonuclear neutrophils (PMN) can modify the immune response in HIV cases. Supernatants of PMN (PMNS) from 33 HIV-infected patients (16 with lymphoadenopathy syndrome, 17 with AIDS-related complex) were tested for their influence on the functional activity of lymphocytes and monocytes from 6 healthy donors. PMNS from another 6 healthy donors comprised a control group. It was found that PMNS from HIV-infected patients, but not from healthy donors, induced suppression of lymphocyte proliferative response and down-regulation of CD8 receptor expression on lymphocytes. Decrease of NK-cell cytotoxicity in the presence of PMNS from HIV-infected patients was the same as that from healthy donors. PMNS did not influence the production of anti-HIV antibody by lymphocytes from HIV-infected patients, as well as non-specific IgG by lymphocytes from healthy donors. PMNS effect on functional activity of lymphocytes was blocked completely after treatment of PMN by catalase and superoxide dismutase. At the same time PMNS from HIV-infected patients but not from healthy donors induced increased production of TNF-alpha by monocytes and up-regulation of monocyte phagocytosis. These effects were independent of catalase and superoxide dismutase and were not abrogated by antibody against IL-1, IL-8, TNF-alpha, IFN-gamma or IFN-alpha.

SUMMARYThe influence of mononuclear cell supernatants (MNCS) from nine healthy donors and 35 HIVinfected patients (1.7 with lymphoadenopathy syndrome (LAS), 15 with ARC and three with AIDS) on functional activity of polymorphonuclear neutrophils (PMN) from healthy donors was investigated. MNC after short-term cultivation (24 h) produced factors which enhanced chemiluminescence (CL) and chemotaxis of PMN. This augmentation did not depend on stimulation of MNC by mitogens (lipopolysaccharide Escherichia coli (LPS) and concanavalin A (Con A)) or on activation of PMN by FMLP. After 48 h of cultivation only MNC stimulated by LPS produced these factors. MNCS from HIV-infected patients provoked a more pronounced augmentation of PMN CL compared with MNCS from healthy subjects. This enhancement was observed in patients at all stages of infection, but was more pronounced in patients with LAS. MNCS impact on PMN CL was not connected with proliferative activity of MNC but was correlated with the level of CD4 cells. It was shown that removal of adherent cells from MNC fraction resulted in decreased MNCS impact. Treatment of MNCS by antibody to IL-Ip, IL-8, interferon-alpha (IFN-oc) and tumour necrosis factor-alpha (TNF-a) did not decrease MNCS impact on PMN CL.

The impact of the sera from 64 HIV-1-infected patients on the functional activity of polymorphonuclear neutrophils (PMN) from 9 healthy donors was investigated. Augmentation of PMN oxygen radical production in the presence of sera from HIV-infected patients (PMN chemiluminescence) was demonstrated. This enhancement was connected with intracellular generation of chemiluminescence (CL). A significant correlation between this enhancement and stages of HIV infection was not found. The presence of the sera from HIV-infected patients in the incubation media led to a decrease of PMN phagocytosis. It was found that contrary impact of the sera on PMN CL and phagocytosis was connected with different factors. The decrease of PMN phagocytosis correlated with the level of complement and was independent of other factors. At the same time the increase of PMN CL was not connected with the level of complement activity but correlated with the level of anti-HIV antibody and circulating immune complexes. The reasons for this phenomenon are unclear. It was suggested that one of the serum factors which caused increase of PMN CL is HIV or HIV compounds.

Leukocytes from donors and subjects with terminal complement component deficiency were incubated for 30 rain at 37~ in autologous serum with or without meningococcal lipopolysaccharide (LPS), followed by treatment with monoclonal antibodies to membrane-attack complexes (MAC) and complement inhibitors and cytofluorometry. After incubation in normal serum, about 97% granulocytes and 65% lymphocytes expressed CD55 and CD59. MAC were detected on only 5% of both types of cells. After incubation with the serum and meningococcal LPS, up to 40% granulocytes expressed MAC, expression of CD55 was decreased, and of CD59 virtually did not change. MAC were not detected in cells incubated in the serum with terminal complement component deficiency. LPS-dependent MAC-mediated hyperactivation of granulocytes may play an unfavorable role in meningococcal infection.