Bronchoalveolar lavage cell pattern from healthy human lung

Heron, Michiel; Grutters, Jan C.; Dam-Molenkamp, K. M. ten; Hijdra, Daniëlle; Heugten-Roeling, A. van; Claessen, Anke M. E.; Ruven, Henk J.T.; Bosch, Jules M.M. van den; Velzen‐Blad, Heleen van

doi:10.1111/j.1365-2249.2011.04529.x

Cited by 81 publications

(78 citation statements)

References 35 publications

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“…Alveolar macrophages are the most common cell type within airways and are the front line of defense in pulmonary bacterial infections (25). These innate immune cells have multiple mechanisms by which they clear bacteria from airways: phagocytosis, respiratory burst (26), AMP production (27), and extracellular trap formation (28).…”

Section: Resultsmentioning

confidence: 99%

Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

et al. 2015

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f Cigarette smoking is the leading preventable cause of death, disease, and disability worldwide. It is well established that cigarette smoke provokes inflammatory activation and impairs antimicrobial functions of human immune cells. Here we explore whether cigarette smoke likewise affects the virulence properties of an important human pathogen, Staphylococcus aureus, and in particular methicillin-resistant S. aureus (MRSA), one of the leading causes of invasive bacterial infections. MRSA colonizes the nasopharynx and is thus exposed to inhalants, including cigarette smoke. MRSA exposed to cigarette smoke extract (CSE-MRSA) was more resistant to macrophage killing (4-fold higher survival; P < 0.0001). CSE-MRSA demonstrated reduced susceptibility to cell lysis (1.78-fold; P ‫؍‬ 0.032) and antimicrobial peptide (AMP) (LL-37) killing (MIC, 8 M versus 4 M). CSE modified the surface charge of MRSA in a dose-dependent fashion, impairing the binding of particles with charge similar to that of AMPs by 90% (P < 0.0001). These changes persisted for 24 h postexposure, suggesting heritable modifications. CSE exposure increased hydrophobicity by 55% (P < 0.0001), which complemented findings of increased MRSA adherence and invasion of epithelial cells. CSE induced upregulation of mprF, consistent with increased MRSA AMP resistance. S. aureus without mprF had no change in surface charge upon exposure to CSE. In vivo, CSE-MRSA pneumonia induced higher mouse mortality (40% versus 10%) and increased bacterial burden at 8 and 20 h postinfection compared to control MRSA-infected mice (P < 0.01). We conclude that cigarette smoke-induced immune resistance phenotypes in MRSA may be an additional factor contributing to susceptibility to infectious disease in cigarette smokers.

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Section: Resultsmentioning

confidence: 99%

Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

et al. 2015

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“…Pure populations of neutrophils are not usually encountered in vivo ; instead neutrophils are usually encountered as part of a heterogenous mixture of leukocytes and epithelial cells (Farrera and Fadeel, 2013; Heron et al, 2012; Nicu and Loos, 2016; Werner et al, 2011). Since these other cell types also express Fc receptors, pathogen recognition receptors, and/or selectins (Golebski et al, 2015; van Tongeren et al, 2015), we sought to determine whether the relationship described in Equation 1 could accurately measure neutrophil content in a heterogenous sample containing nasal epithelial cells.…”

Section: Resultsmentioning

confidence: 99%

“…Similarly, burn injuries are also rich in neutrophils and epithelial cells, making burned skin samples a good candidate for examination by this method. However, other leukocytes highly express CD16, CD18, and CD62L, and are abundant in the lungs during inflammation (Ghoneim et al, 2013; Heron et al, 2012), so this method is unlikely to be accurate with BALF. A recent study of BALF in various human diseases found that neutrophils typically made up only 6% of BALF cell content, while alveolar macrophages and lymphocytes constituted 86% (Wojtan et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, a protective host response to an infection must orchestrate a balanced innate effector response that is more predominantly associated with infection clearance. Flow cytometry and histological staining remain the two most important methods for assessing neutrophil numbers during infection or inflammatory disease (Heron et al, 2012). However, histological staining can yield only a qualitative estimate of cell abundance, and flow cytometry must be performed on fresh samples because notoriously-fragile neutrophils rupture during various freezing procedures.…”

Section: Introductionmentioning

confidence: 99%

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A PCR-based method for quantifying neutrophils in human nasal secretions

Morris

Khan

Pichichero

2017

Journal of Immunological Methods

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Neutrophil recruitment to the nasopharynx (NP) is a central event in resolution of NP-initiated microbial infections. A vigorous neutrophil response in infected tissues is also associated with the outcome of adverse tissue pathology. Therefore, differences in infection-induced tissue neutrophil numbers may correlate with pathogenesis events. Existing methods of quantifiying neutrophils require evaluation of NP samples within hours of procurement as flow cytometry based cell quantification methods require live neutrophil cells. Therefore, we developed a novel RT-PCR method that could reliably quantify neutrophil counts in frozen NP wash samples. mRNA transcripts of the genes encoding CD16, CD18, and CD62L were identified as neutrophil-specific in NP samples and not significantly variable in response to stimulation by heat killed bacteria, and can be used to derive an accurate assessment of neutrophil content in a sample even in the presence of epithelial cells. Using flow cytometry as a comparator, the method was validated in human NP wash samples. We conclude that this PCR-based method should prove useful for providing a quantitative estimate of neutrophil recruitment to the NP during infection and pathogenesis.

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“…The vast majority (>85%-96%) of cells obtained from healthy human volunteers by BAL are AMs [3,5,35,36]. Most of the lysates from sham-exposed AMs and AMs exposed to virus in the presence of antiyellow fever virus antibody (lanes 2 and 3, respectively), and lysate from AMs exposed to IAV in the presence of nonneutralizing anti-IAV antibody (lane 4).…”

Section: Discussionmentioning

confidence: 99%

Human Alveolar Macrophages May Not Be Susceptible to Direct Infection by a Human Influenza Virus

et al. 2016

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The current studies were undertaken to determine the susceptibility of human alveolar macrophages (AMs) to influenza A virus (IAV) infection in comparison with autologous peripheral blood-derived monocytes-macrophages (PBMs). AMs and PBMs were exposed to IAV in vitro and examined for their ability to bind and internalize IAV, and synthesize viral proteins and RNA. PBMs but not AMs demonstrated binding and internalization of the virus, synthesizing viral proteins and RNA. Exposure of AMs in the presence of a sialidase inhibitor or anti-IAV antibody resulted in viral protein synthesis by the cells. Exposure of AMs to fluorescein isothiocyanate-labeled IAV in the presence of anti-fluorescein isothiocyanate antibody also resulted in viral protein synthesis. Thus, human AMs are apparently not susceptible to direct infection by a human IAV but are likely to be infected indirectly in the setting of exposure in the presence of antibody that binds the challenging strain of IAV.Keywords. human alveolar macrophages; influenza virus; monocytes; macrophages.Human influenza A virus (IAV) predominantly infects the upper airways [1]. In the vast majority of infected individuals, pneumonia does not occur. In the ferret model, infection is confined largely to airway epithelium and is rare in the alveoli [2]. However, isolated ferret alveolar tissues seem to be as susceptible to infection as the airways, suggesting that host defenses prevent viral infection at the alveolar level [2]. Alveolar macrophages (AMs) generally have been considered to be the first leukocyte-based line of defense against respiratory pathogens such as influenza virus [3][4][5][6]. AMs must protect the lungs not only from pathogens but also from constant immunopathological processes due to all types of inhaled material [6], and elimination of AMs in immunized mice can enhance inflammatory responses to antigen [7], suggesting that AMs play a predominantly suppressive role during inflammatory responses in vivo. Our early studies showed that human AMs from healthy volunteer donors differed substantially from autologous peripheral blood blood-derived monocytes-macrophages (PBMs) in support of lymphocyte proliferative responses to both mitogens and antigens, including inactivated IAV [3]. In contrast to significant accessory cell support demonstrated by PBMs, lymphocytes exposed to the inactivated virus in the presence of AMs showed no difference in proliferation compared with the lymphocytes cultured in the absence of any accessory cell. Furthermore, when AMs were added to PBMs plus lymphocytes, with appropriate controls for cell numbers, the AMs suppressed lymphocyte proliferative responses to antigen [8]. Others have reported that human IAV infection of human monocyte and macrophage subpopulations showed increased susceptibility associated with cell differentiation [9]. As differentiated macrophages likely to first encounter IAV, AMs have generally been assessed for infection using immunofluorescent staining for IAV antigens [10][11][12]. van Riel and colleagu...

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Bronchoalveolar lavage cell pattern from healthy human lung

Cited by 81 publications

References 35 publications

Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

A PCR-based method for quantifying neutrophils in human nasal secretions

Human Alveolar Macrophages May Not Be Susceptible to Direct Infection by a Human Influenza Virus

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