Highly increased numbers of leukocytes in inflamed gingiva from patients with HIV infection

Myint, Maung Maung; Steinsvoll, Svein; Yuan, Zuan-Ning; Johne, Berit; Helgeland, Kristen; Schenck, Karl

doi:10.1097/00002030-200201250-00013

Cited by 30 publications

(37 citation statements)

References 49 publications

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“…Recently, cytokine-like activities have been ascribed to MRPs (19,21,22), which are released during inflammatory episodes by neutrophils and monocytes (54 -57). High levels of MRPs have been detected in the serum of patients suffering from bronchitis and tuberculosis (7,16,26), as well as in patients suffering from AIDS (27)(28)(29)(30)(31)(32). The presence of these proteins in HIV-1 seropositive patients was correlated with an increased viral load and a decrease in the number of circulating CD4-expressing T lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Transcription and Virus Production Are Both Accentuated by the Proinflammatory Myeloid-Related Proteins in Human CD4+ T Lymphocytes

Ryckman

Robichaud

Roy

et al. 2002

The Journal of Immunology

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S100A8, S100A9, and S100A12, collectively known as myeloid-related proteins (MRPs), are highly expressed by the myeloid cell lineage and are found in the extracellular milieu during infections and inflammatory conditions. Recent data showed high levels of MRPs in the serum of HIV type 1 (HIV-1)-infected patients which correlated with disease progression and low CD4+ counts. Therefore, we set out to investigate the effect of MRPs on HIV-1 replication. We observed a 4- to 5-fold induction of virus production in J1.1, a human T lymphoid cell line latently infected with HIV-1, following treatment with MRPs. Using luciferase-based reporter gene assays, we demonstrated that MRPs induce a dose- and time-dependent activation of the HIV-1 long terminal repeat promoter region that could be blocked by specific anti-MRP polyclonal Abs and by physical denaturation of these proteins. The MRP-mediated induction was acting through the HIV-1 enhancer sequence and was dependent upon NF-κB activity. These latter results were also confirmed by EMSA experiments conducted in Jurkat cells and freshly isolated PBMCs. In conclusion, we demonstrate that MRPs induce HIV-1 transcriptional activity and viral replication in infected CD4+ T-lymphocytes at concentrations similar to those found in the serum of HIV-1-infected patients.

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Section: Discussionmentioning

confidence: 99%

HIV-1 Transcription and Virus Production Are Both Accentuated by the Proinflammatory Myeloid-Related Proteins in Human CD4+ T Lymphocytes

Ryckman

Robichaud

Roy

et al. 2002

The Journal of Immunology

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“…HIV-infected patients with chronically inflamed gingivae have increased numbers of mucosal macrophages and PMNs, demonstrating that HIV infection does not prevent a normal innate mucosal immune response by these cells (306). Although recruitment of phagocytes to the oral epithelium does not appear to be perturbed by HIV infection, their anticandidal properties could be impaired either directly by HIV infection or by altered stimulation by cytokines.…”

Section: Perturbed Mucosal Immune Defense Mechanisms Against C Albicmentioning

confidence: 99%

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

2004

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Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal

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“…adr.sagepub.com Downloaded from include human herpesvirus 6 and 8, herpes simplex virus 1/2 (HSV-1/2), Epstein-Barr virus, human papilloma virus, several protozoan parasites, bacteria, and the fungus Candida albicans. Although the composition of the oral flora is relatively unaffected by HIV infection, HIV-positive individuals endure increased colonization and tissue invasion of oral epithelium by coinfecting pathogens (Myint et al, 2002). Coinfection might be attributable to reduced saliva flow rates, which are often observed in early HIV-1 disease (Lin et al, 2003).…”

Section: Questionmentioning

confidence: 99%

Innate Immunity Including Epithelial and Nonspecific Host Factors

et al. 2011

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The majority of HIV infections are initiated at mucosal sites. The oral mucosal tissue has been shown to be a potential route of entry in humans and primates. Whereas HIV RNA, proviral DNA, and infected cells are detected in the oral mucosa and saliva of infected individuals, it appears that the oral mucosa is not permissive for efficient HIV replication and therefore may differ in susceptibility to infection when compared to other mucosal sites. Since there is no definitive information regarding the fate of the HIV virion in mucosal epithelium, there is a pressing need to understand what occurs when the virus is in contact with this tissue, what mechanisms are in play to determine the outcome, and to what degree the mechanisms and outcomes differ between mucosal sites. Workshop 1B tackled 5 important questions to define current knowledge about epithelial cell-derived innate immune agents, commensal and endogenous pathogens, and epithelial cells and cells of the adaptive immune system and how they contribute to dissemination or resistance to HIV infection. Discovering factors that explain the differential susceptibility and resistance to HIV infection in mucosal sites will allow for the identification and development of novel protective strategies.

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Highly increased numbers of leukocytes in inflamed gingiva from patients with HIV infection

Cited by 30 publications

References 49 publications

HIV-1 Transcription and Virus Production Are Both Accentuated by the Proinflammatory Myeloid-Related Proteins in Human CD4+ T Lymphocytes

HIV-1 Transcription and Virus Production Are Both Accentuated by the Proinflammatory Myeloid-Related Proteins in Human CD4+ T Lymphocytes

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Innate Immunity Including Epithelial and Nonspecific Host Factors

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