Macrophage Mannose Receptor CD206 Predicts Prognosis in Community-acquired Pneumonia

Tsuchiya, Kazuo; Suzuki, Yuzo; Yoshimura, Katsuhiro; Yasui, Hideki; Karayama, Masato; Hozumi, Hironao; Furuhashi, Kazuki; Enomoto, Noriyuki; Fujisawa, Tomoyuki; Nakamura, Yutaro; Inui, Naoki; Yokomura, Koushi; Suda, Takafumi

doi:10.1038/s41598-019-55289-2

Cited by 34 publications

(30 citation statements)

References 34 publications

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“…The steady-state AMs express CD206 (a mannose receptor, which is a C-type lectin and serves as a PRR) and β-glucan specific receptor (Dectin-1), which are also expressed by alternatively-activated macrophages (AAMs) or M2 as their definitive markers (150,151). The serum CD206 (sCD206) levels increases in the patients of community-acquired pneumonia (CAP) with the increase in its severity [pneumonia severity index (PSI)], which can be used for CAP prognosis (152). Also, the infiltration of CD206 + macrophages increases in the lungs of patients with fatal pneumonia.…”

Section: Pulmonary Macrophages During Bacterial Pneumonia and Associamentioning

confidence: 99%

Pulmonary Innate Immune Response Determines the Outcome of Inflammation During Pneumonia and Sepsis-Associated Acute Lung Injury

2020

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The lung is a primary organ for gas exchange in mammals that represents the largest epithelial surface in direct contact with the external environment. It also serves as a crucial immune organ, which harbors both innate and adaptive immune cells to induce a potent immune response. Due to its direct contact with the outer environment, the lung serves as a primary target organ for many airborne pathogens, toxicants (aerosols), and allergens causing pneumonia, acute respiratory distress syndrome (ARDS), and acute lung injury or inflammation (ALI). The current review describes the immunological mechanisms responsible for bacterial pneumonia and sepsis-induced ALI. It highlights the immunological differences for the severity of bacterial sepsis-induced ALI as compared to the pneumonia-associated ALI. The immune-based differences between the Gram-positive and Gram-negative bacteria-induced pneumonia show different mechanisms to induce ALI. The role of pulmonary epithelial cells (PECs), alveolar macrophages (AMs), innate lymphoid cells (ILCs), and different pattern-recognition receptors (PRRs, including Toll-like receptors (TLRs) and inflammasome proteins) in neutrophil infiltration and ALI induction have been described during pneumonia and sepsis-induced ALI. Also, the resolution of inflammation is frequently observed during ALI associated with pneumonia, whereas sepsis-associated ALI lacks it. Hence, the review mainly describes the different immune mechanisms responsible for pneumonia and sepsis-induced ALI. The differences in immune response depending on the causal pathogen (Gram-positive or Gram-negative bacteria) associated pneumonia or sepsis-induced ALI should be taken in mind specific immune-based therapeutics.

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Section: Pulmonary Macrophages During Bacterial Pneumonia and Associamentioning

confidence: 99%

Pulmonary Innate Immune Response Determines the Outcome of Inflammation During Pneumonia and Sepsis-Associated Acute Lung Injury

2020

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“…Increased sMR levels were also observed in patients with a wide variety of inflammatory diseases, such as pulmonary tuberculosis ( 59 ), pulmonary fibrosis ( 60 ), multiple myeloma ( 61 , 62 ), rheumatoid arthritis ( 63 ), chronic joint inflammation ( 64 ), pneumonia ( 65 , 66 ), interstitial lung disease ( 67 , 68 ) and gastric cancer ( 69 ). Strikingly, in these studies, sMR levels positively correlated with disease severity and mortality.…”

Section: Smr Correlates With Inflammatory Diseases and Induces Macrophage Activationmentioning

confidence: 99%

The Mannose Receptor: From Endocytic Receptor and Biomarker to Regulator of (Meta)Inflammation

et al. 2021

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The mannose receptor is a member of the C-type lectin (CLEC) family, which can bind and internalize a variety of endogenous and pathogen-associated ligands. Because of these properties, its role in endocytosis as well as antigen processing and presentation has been studied intensively. Recently, it became clear that the mannose receptor can directly influence the activation of various immune cells. Cell-bound mannose receptor expressed by antigen-presenting cells was indeed shown to drive activated T cells towards a tolerogenic phenotype. On the other hand, serum concentrations of a soluble form of the mannose receptor have been reported to be increased in patients suffering from a variety of inflammatory diseases and to correlate with severity of disease. Interestingly, we recently demonstrated that the soluble mannose receptor directly promotes macrophage proinflammatory activation and trigger metaflammation. In this review, we highlight the role of the mannose receptor and other CLECs in regulating the activation of immune cells and in shaping inflammatory responses.

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“…These differences were confirmed when we compared the two groups after an infectious challenge with K. pneumoniae , as differences in the infected groups in the same markers were observed as those seen in the vehicle-treated groups. However, in response to infection, marked differences were also observed in the CMP frequency of CD206, TLR4 and Ly-6C, all of which have important host defense functions ( 27 , 28 , 33 , 34 , 51 ).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Toponomes of Alveolar Macrophages From Wild Type and Surfactant Protein A Knockout Mice and Their Response to Infection

et al. 2022

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BackgroundSurfactant protein-A (SP-A) plays a critical role in lung innate immunity by regulating alveolar macrophages (AM), expression of inflammatory mediators, and other host defense proteins. The toponome imaging system (TIS), a serial immunostainer, was used to study the AM toponome because it characterizes the localization of multiple markers and identifies marker combinations in each pixel as combinatorial molecular phenotypes (CMPs). We used TIS to study the AM toponome from wild type (WT) and SP-A knockout (KO) mice and changes following Klebsiella pneumoniae exposure.MethodsWT or KO mice received intratracheal K. pneumoniae or vehicle and AM were obtained by bronchoalveolar lavage after one hour. AM were attached to slides and underwent TIS analysis. Images were analyzed to characterize all pixels. AM CMPs from WT vehicle (n=3) and infected (n=3) mice were compared to each other and to AM from KO (n=3 vehicle; n=3 infected). Histograms provided us with a tool to summarize the representation of each marker in a set of CMPs.ResultsUsing the histograms and other tools we identified markers of interest and observed that: 1) Both comparisons had conserved (present in all group members) CMPs, only in vehicle AM and only in infected AM, or common to both vehicle and infected AM, (i.e., unaffected by the condition). 2) the CMP number decreased with infection in WT and KO versus vehicle controls. 3) More infection-specific CMPs in WT vs KO AM. 4) When AM from WT and KO vehicle or infected were compared, there were more unique CMPs exclusive to the KO AM. 5) All comparisons showed CMPs shared by both groups.ConclusionsThe decrease of CMPs exclusive to infected AM in KO mice may underlie the observed susceptibility of KO mice to infection. However, both KO groups had more exclusive CMPs than the corresponding WT groups, perhaps indicating a vigorous effort by KO to overcome deficits in certain proteins and CMPs that are dysregulated by the absence of SP-A. Moreover, the presence of shared CMPs in the compared groups indicates that regulation of these CMPs is not dependent on either infection or the presence or absence of SP-A.

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Macrophage Mannose Receptor CD206 Predicts Prognosis in Community-acquired Pneumonia

Cited by 34 publications

References 34 publications

Pulmonary Innate Immune Response Determines the Outcome of Inflammation During Pneumonia and Sepsis-Associated Acute Lung Injury

Pulmonary Innate Immune Response Determines the Outcome of Inflammation During Pneumonia and Sepsis-Associated Acute Lung Injury

The Mannose Receptor: From Endocytic Receptor and Biomarker to Regulator of (Meta)Inflammation

Comparison of the Toponomes of Alveolar Macrophages From Wild Type and Surfactant Protein A Knockout Mice and Their Response to Infection

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