Increased IgG but normal IgA anti-pneumococcal protein antibodies in lung of HIV-infected adults

Collins, Andrea; Batrawy, Sherouk El; Gordon, Stephen B.; Ferreira, Daniela M.

doi:10.1016/j.vaccine.2013.04.062

Cited by 9 publications

(5 citation statements)

References 20 publications

(15 reference statements)

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“…However, previous studies have reported HIV-associated impairment of function of these two cell subsets in peripheral blood 19– 21 . Consistent with what has been observed in the systemic circulation, hyperglobulinemia has been reported in BAL fluid of HIV-infected adults 22, 23 , but the antibodies have impaired opsonic function 24 . It is plausible that the HIV-associated increase in B cells in the lung results in increased antibody production and BAL fluid hyperglobulinemia.…”

Section: Discussionsupporting

confidence: 81%

B cell, CD8 + T cell and gamma delta T cell infiltration alters alveolar immune cell homeostasis in HIV-infected Malawian adults

Mwale¹,

Hummel²,

Mvaya³

et al. 2017

Wellcome Open Res

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Background: HIV infection is associated with increased risk to lower respiratory tract infections (LRTI). However, the impact of HIV infection on immune cell populations in the lung is not well defined. We sought to comprehensively characterise the impact of HIV infection on immune cell populations in the lung. Methods: Twenty HIV-uninfected controls and 17 HIV-1 infected ART-naïve adults were recruited from Queen Elizabeth Central Hospital, Malawi. Immunophenotyping of lymphocyte and myeloid cell populations was done on bronchoalveolar lavage fluid and peripheral blood cells. Results: We found that the numbers of CD8 + T cells, B cells and gamma delta T cells were higher in BAL fluid of HIV-infected adults compared to HIV-uninfected controls (all p<0.05). In contrast, there was no difference in the numbers of alveolar CD4 + T cells in HIV-infected adults compared to HIV-uninfected controls (p=0.7065). Intermediate monocytes were the predominant monocyte subset in BAL fluid (HIV-, 63%; HIV+ 81%), while the numbers of classical monocytes was lower in HIV-infected individuals compared to HIV-uninfected adults (1 × 10 5 vs. 2.8 × 10 5 cells/100ml of BAL fluid, p=0.0001). The proportions of alveolar macrophages and myeloid dendritic cells was lower in HIV-infected adults compared to HIV-uninfected controls (all p<0.05). Conclusions: Chronic HIV infection is associated with broad alteration of immune cell populations in the lung, but does not lead to massive depletion of alveolar CD4 + T cells. Disruption of alveolar immune cell homeostasis likely explains in part the susceptibility for LRTIs in HIV-infected adults.

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Section: Discussionsupporting

confidence: 81%

B cell, CD8 + T cell and gamma delta T cell infiltration alters alveolar immune cell homeostasis in HIV-infected Malawian adults

Mwale¹,

Hummel²,

Mvaya³

et al. 2017

Wellcome Open Res

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“…Immunoglobulins in lung fluid can be derived from the blood by transudation or could be synthesized locally by cells within the lymphoid tissue in the respiratory tract. Furthermore, lung lining fluid antibodies are important in mucosal defense where the lungs are continually exposed to antigenic material, including during bacterial and viral infection (84)(85)(86). We detected both IgM and IgG SVV-specific antibodies in BAL fluid beginning at 10 dpi, which correlated with peak B cell proliferation and supports local secretion of antibodies.…”

Section: Discussionmentioning

confidence: 58%

Intrabronchial Infection of Rhesus Macaques with Simian Varicella Virus Results in a Robust Immune Response in the Lungs

Haberthur

Meyer

Arnold

et al. 2014

J Virol

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Varicella-zoster virus (VZV) is the etiological agent of varicella (chickenpox) and herpes zoster (shingles). Primary VZV infection is believed to occur via the inhalation of virus either in respiratory droplets or from shedding varicella lesions or by direct contact with infectious vesicular fluid. However, the ensuing immune response in the lungs remains incompletely understood. We have shown that intrabronchial inoculation of rhesus macaques with simian varicella virus (SVV), a homolog of VZV, recapitulates the hallmarks of acute and latent VZV infection in humans. In this study, we performed an in-depth analysis of the host immune response to acute SVV infection in the lungs and peripheral blood. We report that acute SVV infection results in a robust innate immune response in the lungs, characterized by the production of inflammatory cytokines, chemokines, and growth factors as well as an increased frequency of plasmacytoid dendritic cells (DCs) that corresponded with alpha interferon (IFN-␣) production and a rapid decrease in viral loads in the lungs. This is followed by T and B cell proliferation, antibody production, T cell differentiation, and cytokine production, which correlate with the complete cessation of viral replication. Although terminally differentiated CD8 T cells became the predominant T cell population in bronchoalveolar lavage cells, a higher percentage of CD4 T cells were SVV specific, which suggests a critical role for these cells in the resolution of primary SVV infection in the lungs. Given the homology between SVV and VZV, our data provide insight into the immune response to VZV within the lung. IMPORTANCEAlthough primary VZV infection occurs primarily via the respiratory route, the host response in the lungs and its contribution to the cessation of viral replication and establishment of latency remain poorly understood. The difficulty in accessing lung tissue and washes from individuals infected with VZV has hampered efforts to address this knowledge gap. SVV infection of rhesus macaques is an important model of VZV infection of humans; therefore, we utilized this animal model to gain a comprehensive view of the kinetics of the immune response to SVV in the lung and its relationship to the resolution of acute infection in respiratory tissues. These data not only advance our understanding of host immunity to VZV, a critical step in developing new vaccines, but also provide additional insight into immunity to respiratory pathogens. P rimary infection with varicella-zoster virus (VZV), a neurotropic alphaherpesvirus, occurs primarily through the inhalation of virus-laden saliva droplets (1, 2) or airborne virions from varicella lesions (3) or by contact with infectious vesicular fluid (4). The incubation period of varicella can range from 10 to 21 days and usually results in a benign self-limiting disease characterized by the appearance of vesicular exanthem, fever, and malaise (5). Current evidence suggests VZV can infect and replicate within the respiratory mucosal epithelium....

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“…Alveolar macrophages (AM) release GM-CSF and further induce the accumulation of macrophages and neutrophils in the lungs of HIV-infected subjects [114], and an increased amount of total and pneumococcal-specific Ab in the alveolar space [101, 115, 116]. However, due to the immune deficiency, opportunistic bacterial infections can create an inflammatory environment facilitating viral replication through up-regulation of cytokines and chemokines, which enhance HIV infection and replication, and perhaps promote viral egress from latent reservoirs [19, 117, 118]. HIV infection also impairs immune responses within the respiratory tract as well as M mannose receptor C-type lectin-mediated phagocytosis through the inhibition of Cdc42 and Rho activation, leading to a susceptibility of S. pneumonia infection in HIV infection [119].…”

Section: Introductionmentioning

confidence: 99%

Humoral immune responses to Streptococcus pneumoniae in the setting of HIV-1 infection

Zhang

Wan

et al. 2015

Vaccine

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Streptococcus pneumonia (pneumococcus) remains one of the most commonly identified causes of bacterial infection in the general population, and the risk is 30-100 fold higher in HIV-infected individuals. Both innate and adaptive host immune responses to pneumococcal infection are important against pathogen invasion. Pneumococcal-specific IgA antibody (Ab) is key to control infection at the mucosal sites. Ab responses against pneumococcal infection by B cells can be generated through T cell-dependent or T cell-independent pathways. Depletion of CD4+ T cells is a hallmark of immunodeficiency in HIV infection and this defect also contributes to B cell dysfunction, which predisposes to infections such as the pneumococcus. Two pneumococcal vaccines have been demonstrated to have potential benefits for HIV-infected patients. One is a T cell dependent 13-valent pneumococcal conjugate vaccine (PCV13); the other is a T cell independent 23-valent pneumococcal polysaccharide vaccine (PPV23). However, many questions remain unknown regarding these two vaccines in the clinical setting in HIV disease. Here we review the latest research regarding B cell immune responses against pneumococcal antigens, whether derived from potentially invading pathogens or vaccinations, in the setting of HIV-1 infection.

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Increased IgG but normal IgA anti-pneumococcal protein antibodies in lung of HIV-infected adults

Cited by 9 publications

References 20 publications

B cell, CD8 + T cell and gamma delta T cell infiltration alters alveolar immune cell homeostasis in HIV-infected Malawian adults

B cell, CD8 + T cell and gamma delta T cell infiltration alters alveolar immune cell homeostasis in HIV-infected Malawian adults

Intrabronchial Infection of Rhesus Macaques with Simian Varicella Virus Results in a Robust Immune Response in the Lungs

Humoral immune responses to Streptococcus pneumoniae in the setting of HIV-1 infection

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