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• W2022242545 abstract "The vast majority of patients infected with HIV will have pulmonary complications at some point during the course of their illness.1Murray JF Garay SM Hopewell PC Mills J Snider GL Stover DE Pulmonary complications of the acquired immunodeficiency syndrome: an update.Am Rev Respir Dis. 1987; 135: 504-509PubMed Google Scholar Before the widespread use of prophylaxis against Pneumocystis carinii infection, more than 70 percent of HIV-infected individuals eventually developed symptomatic disease from this organism alone,2Murray JF Mills J Pulmonary infectious complications of human immunodeficiency virus infection: part II.Am Rev Respir Dis. 1990; 141: 1582-1598Crossref PubMed Scopus (106) Google Scholar without taking into account the multitude of other infections seen in these patients.2Murray JF Mills J Pulmonary infectious complications of human immunodeficiency virus infection: part II.Am Rev Respir Dis. 1990; 141: 1582-1598Crossref PubMed Scopus (106) Google Scholar, 3Murray JF Mills J Pulmonary infectious complications of human immunodeficiency virus infection: part I.Am Rev Respir Dis. 1990; 141: 1356-1372Crossref PubMed Google Scholar Even after infectious causes have been excluded, many of these patients have noninfectious pulmonary disorders such as Kaposi's sarcoma, nonspecific or lymphocytic interstitial pneumonitis, and lymphocytic alveolitis.1Murray JF Garay SM Hopewell PC Mills J Snider GL Stover DE Pulmonary complications of the acquired immunodeficiency syndrome: an update.Am Rev Respir Dis. 1987; 135: 504-509PubMed Google Scholar Why are pulmonary complications so prevalent in HIV-infected individuals? A common thread connecting many of the complications listed above is that host immune and/or inflammatory responses contribute significantly to the pathogenesis and resulting manifestations of the disease process. Evidence is accumulating that mononuclear phagocytes, including alveolar macrophages, are activated in HIV-infected patients, even during the early asymptomatic phase of the disease. The result is a potentially enhanced capacity to initiate inflammatory4Buhl R Jaffe JA Holroyd KJ Borok Z Roum JH Mastrangeli A et al.Activation of alveolar macrophages in asymptomatic HIV-infected individuals.J Immunol. 1993; 150: 1019-1028PubMed Google Scholar and immune5Twigg HL Lipscomb MF Yoffe B Barbaro DJ Weissler JC Enhanced accessory cell function by alveolar macrophages from patients infected with the human immunodeficiency virus: potential role for depletion of CD4+ cells in the lung.Am J Respir Cell Mol Biol. 1989; 1: 391-400Crossref PubMed Scopus (24) Google Scholar responses. Activated alveolar macrophages are uniquely located within the alveolar space to initiate these responses since nowhere else in the body are cells of the immune system exposed to such an abundant variety of antigenic challenges—either from the environment, as inhaled particles, or from circulating antigens as they traffic through the pulmonary microvasculature. Thus, any augmentation of alveolar macrophage function threatens to impair the balance between stimulatory and inhibitory signals received by inflammatory and immune cells within the lung. In this context, the article by Lipschik et al in this issue of Chest (see page 763) is most interesting. These investigators demonstrated increased concentrations of interleukin (IL)-8 and phospholipase A2 in broncho-alveolar lavage (BAL) fluid from HIV-infected patients with P carinii pneumonia and nonspecific interstitial pneumonitis, as well as in asymptomatic individuals. Their work adds IL-8 to the growing list of alveolar macrophage-derived cytokines found to be secreted in increased amounts in HIV-infected patients, including IL-l,6Twigg HL Iwamoto GK Soliman DM Role of cytokines in alveolar macrophage accessory cell function in HIV-infected individuals.J Immunol. 1992; 149: 1462-1469PubMed Google Scholar IL-6,6Twigg HL Iwamoto GK Soliman DM Role of cytokines in alveolar macrophage accessory cell function in HIV-infected individuals.J Immunol. 1992; 149: 1462-1469PubMed Google Scholar, 7Trentin L Garbisa S Zambello R Agostini C Caenazzo C Di Francesco C et al.Spontaneous production of IL-6 by alveolar macrophages of HIV-1 seropositive patients.J Infect Dis. 1992; 166: 731-737Crossref PubMed Scopus (52) Google Scholar granulocyte-macrophage colony-stimulating factor (GM-CSF),8Agostini C Trentin L Zambello R Bulian P Caenazzo C Cipriani A et al.Release of granulocyte-macrophage colony-stimulating factor by alveolar macrophages in the lung of HIV-1-infected patients.J Immunol. 1992; 149: 3379-3385PubMed Google Scholar and tumor necrosis factor.9Agostini C Zambello R Trentin L Garbisa S Francia Di Celle P Bulian P et al.Alveolar macrophages from patients with AIDS and AIDS-related complex constitutively synthesize and release tumor necrosis factor alpha.Am Rev Respir Dis. 1991; 144: 195-201Crossref PubMed Scopus (41) Google Scholar Importantly, enhanced secretion of these cytokines can occur in the absence of any recognized inflammatory or infectious process, as well as in response to low concentrations of nonspecific stimuli (ie, LPS, phorbol esters). This implies that alveolar macrophages from HIV-infected individuals not only spontaneously synthesize and secrete these factors but also possess the ability to respond in an augmented fashion to stimuli that would otherwise have minimal or no effects on nonactivated cells. The mechanisms behind enhanced cytokine secretion by alveolar macrophages in HIV-infected persons are not clear. Intriguing possibilities include activation of alveolar macrophages by HIV with subsequent enhanced ability to respond to specific infectious agents (including HIV proteins themselves, such as gpl20) or nonspecific stimuli (which normally have minimal effects on resting alveolar macrophages), and direct upregulation of cytokine gene transcription in alveolar macrophages induced by viral proteins. Lipschik and colleagues speculate that high BAL IL-8 concentrations recruit neutrophils found in the lower respiratory tract of individuals with P carinii pneumonia and nonspecific interstitial pneumonitis. Here we begin to enter murky waters. Many investigators have documented derangements in BAL cellular profiles in HIV-infected patients. Most documented abnormalities involve increases in the cellular components of BAL, including alveolar macrophages,8Agostini C Trentin L Zambello R Bulian P Caenazzo C Cipriani A et al.Release of granulocyte-macrophage colony-stimulating factor by alveolar macrophages in the lung of HIV-1-infected patients.J Immunol. 1992; 149: 3379-3385PubMed Google Scholar lymphocytes,10Guillon JM Autran B Denis M Fouret P Plata F Mayaud CM et al.Human immunodeficiency virus-related lymphocytic alveolitis.Chest. 1988; 94: 1264-1270Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar, 11Agostini C Poletti V Zambello R Trentin L Siviero F Spiga L et al.Phenotypical and functional analysis of bronchoalveolar lavage lymphocytes in patients with HIV infection.Am Rev Respir Dis. 1988; 138: 1609-1615Crossref PubMed Scopus (46) Google Scholar natural killer cells,11Agostini C Poletti V Zambello R Trentin L Siviero F Spiga L et al.Phenotypical and functional analysis of bronchoalveolar lavage lymphocytes in patients with HIV infection.Am Rev Respir Dis. 1988; 138: 1609-1615Crossref PubMed Scopus (46) Google Scholar and neutrophils.8Agostini C Trentin L Zambello R Bulian P Caenazzo C Cipriani A et al.Release of granulocyte-macrophage colony-stimulating factor by alveolar macrophages in the lung of HIV-1-infected patients.J Immunol. 1992; 149: 3379-3385PubMed Google Scholar, 12Agostini C Zambello R Trentin L Poletti V Spiga L Gritti F et al.Prognostic significance of the evaluation of bronchoalveolar lavage cell populations in patients with HIV-1 infection and pulmonary involvement.Chest. 1991; 100: 1601-1606Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar Cells accumulate in the alveolar space predominantly by two mechanisms: recruitment of cells from the vascular compartment and in situ proliferation. Cytokines play critical roles in both mechanisms, from potential recruitment of neutrophils and lymphocytes induced by IL-8 and IL-1,13Hunninghake GW Glazier AJ Monick MM Dinarello CA Interleukin-1 is a chemotactic factor for human T-lymphocytes.Am Rev Respir Dis. 1987; 135: 66-71PubMed Google Scholar respectively, to augmented in situ proliferation of alveolar macrophages and lymphocytes promoted by GM-CSF, IL-1, and IL-6.6Twigg HL Iwamoto GK Soliman DM Role of cytokines in alveolar macrophage accessory cell function in HIV-infected individuals.J Immunol. 1992; 149: 1462-1469PubMed Google Scholar, 8Agostini C Trentin L Zambello R Bulian P Caenazzo C Cipriani A et al.Release of granulocyte-macrophage colony-stimulating factor by alveolar macrophages in the lung of HIV-1-infected patients.J Immunol. 1992; 149: 3379-3385PubMed Google Scholar From the above discussion, it is apparent that BAL fluid from HIV-seropositive patients can be a veritable “cytokine soup,” containing increased concentrations of any number of different cytokines and cells. Thus, it is not surprising that the lung is so frequently involved in these individuals. The increased concentration of cytokines and the resultant increase in cellular components render the alveolar space an ideal medium for immune and inflammatory reactions in response to specific and nonspecific antigenic challenges. More important, increases in cytokine and cell concentrations can occur spontaneously, thus causing symptoms in the absence of recognized pulmonary disease. It is important to recognize that augmented cytokine secretion and increased number of immune cells in the alveolar space do not necessarily translate into enhanced immunologic function. Clearly, HIV infection is characterized by impaired immune responses to various infectious agents. It is likely that cytokines with negative regulatory functions are similarly upregulated in the alveolar space. For example, despite the ability of alveolar macrophages from HIV-infected patients to stimulate T-cell proliferation5Twigg HL Lipscomb MF Yoffe B Barbaro DJ Weissler JC Enhanced accessory cell function by alveolar macrophages from patients infected with the human immunodeficiency virus: potential role for depletion of CD4+ cells in the lung.Am J Respir Cell Mol Biol. 1989; 1: 391-400Crossref PubMed Scopus (24) Google Scholar and their enhanced ability to secrete cytokines which enhance B-cell proliferation and differentiation, their ability to induce immunoglobulin secretion from normal B cells is markedly impaired compared with normal alveolar macrophages (David Wilkes, M.D., unpublished observations). This finding could be explained by increased concentrations of negative regulatory cytokines, such as transforming growth factor β, secreted by alveolar macrophages in HIV infection. In summary, the cellular constituents of the lower respiratory tract in HIV-infected individuals are likely to depend on the prevailing cytokine profile in the alveolar milieu, which in turn is affected by many variables, including the presence or absence of specific infectious agents, the degree of infection of alveolar macrophages by HIV, and the degree of chronic immune stimulation by potential environmental antigens. The presence of increased cytokine levels and cell numbers in the alveolar space can be expected to have multiple clinical consequences depending on which of these components are upregulated and which are downregulated. Dissecting which cytokines and cellular components contribute to specific diseases in HIV-infected patients will require careful studies similar to that of Lipschik and coworkers to bridge the arenas of basic science and clinical medicine." @default.
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