Role of ICAM‐1 in the aggregation and adhesion of human alveolar macrophages in response to TNF‐α and INF‐γ

Sasaki, Masahiro; Namioka, Yuriko; Ito, Tatsuro; Izumiyama, Noriko; Fukui, Sei; Watanabe, Akiko; Kashima, Masayuki; Sano, Mitsuru; Shioya, Takanobu; Miura, Mamoru

doi:10.1080/09629350120102325

Cited by 17 publications

(12 citation statements)

References 25 publications

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“…This protein can be induced by pathogenic cytokines related to autoinflammatory diseases, such as IL-1β, IL-18, and TNF-α. 32 – 34 Indeed, it has been reported that the level of sCD54 was increased in the serum from patients with FMF and patients with Adult Still Disease. 35 , 36 These finding are consistent with our present observation that sCD54 clearly correlates with IL-18 in the serum from FMF patients in attack.…”

Section: Discussionmentioning

confidence: 99%

Multiple Serum Cytokine Profiling to Identify Combinational Diagnostic Biomarkers in Attacks of Familial Mediterranean Fever

Koga¹,

Migita

Sato

et al. 2016

Medicine

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The precise cytokine networks in the serum of individuals with familial Mediterranean fever (FMF) that are associated with its pathogenesis have been unknown. Here, we attempted to identify specific biomarkers to diagnose or assess disease activity in FMF patients.We measured serum levels of 45 cytokines in 75 FMF patients and 40 age-matched controls by multisuspension cytokine array. FMF in “attack” or “remission” was classified by Japan College of Rheumatology-certified rheumatologists according to the Tel Hashomer criteria. Cytokines were ranked by their importance by a multivariate classification algorithm. We performed a logistic regression analysis to determine specific biomarkers for discriminating FMF patients in attack. To identify specific molecular networks, we performed a cluster analysis of each cytokine.Twenty-nine of the 45 cytokines were available for further analyses. Eight cytokines’ serum levels were significantly elevated in the FMF attack versus healthy control group. Nine cytokines were increased in FMF attack compared to FMF remission. Multivariate classification algorithms followed by a logistic regression analysis revealed that the combined measurement of IL-6, IL-18, and IL-17 distinguished FMF patients in attack from the controls with the highest accuracy (sensitivity 89.2%, specificity 100%, and accuracy 95.5%). Among the FMF patients, the combined measurement of IL-6, G-CSF, IL-10, and IL-12p40 discriminated febrile attack periods from remission periods with the highest accuracy (sensitivity 75.0%, specificity 87.9%, and accuracy 84.0%).Our data identified combinational diagnostic biomarkers in FMF patients based on the measurement of multiple cytokines. These findings help to improve the diagnostic performance of FMF in daily practice and extend our understanding of the activation of the inflammasome leading to enhanced cytokine networks.

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Section: Discussionmentioning

confidence: 99%

Multiple Serum Cytokine Profiling to Identify Combinational Diagnostic Biomarkers in Attacks of Familial Mediterranean Fever

Koga¹,

Migita

Sato

et al. 2016

Medicine

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“…In sarcoidosis, TNF-α induced the expression of intracellular adhesion molecule-1 (ICAM-1) on AMs, leading to cellular aggregation (66). Additionally, leukocyte adhesion molecule (LeuCAM) expression, such as CD11a/b/c and CD18 (67), is increased in sarcoid AMs compared with controls.…”

Section: Granuloma Formationmentioning

confidence: 99%

Granuloma Formation in Pulmonary Sarcoidosis

et al. 2013

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Sarcoidosis is a granulomatous disorder of unknown cause, affecting multiple organs, but mainly the lungs. The exact order of immunological events remains obscure. Reviewing current literature, combined with careful clinical observations, we propose a model for granuloma formation in pulmonary sarcoidosis. A tight collaboration between macrophages, dendritic cells, and lymphocyte subsets, initiates the first steps toward granuloma formation, orchestrated by cytokines and chemokines. In a substantial part of pulmonary sarcoidosis patients, granuloma formation becomes an on-going process, leading to debilitating disease, and sometimes death. The immunological response, determining granuloma sustainment is not well understood. An impaired immunosuppressive function of regulatory T cells has been suggested to contribute to the exaggerated response. Interestingly, therapeutical agents commonly used in sarcoidosis, such as glucocorticosteroids and anti-TNF agents, interfere with granuloma integrity and restore the immune homeostasis in autoimmune disorders. Increasing insight into their mechanisms of action may contribute to the search for new therapeutical targets in pulmonary sarcoidosis.

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“…Activated macrophages obtain increased cytokine production and enhanced tumoricidal and microbicidal function (6,7). In various inflammatory and granulomatous conditions, IFN-γ is critical in enhancing and sustaining macrophage activation (8,9). However, its precise mechanism remains largely unknown and elucidating its role is essential in order to gain further understanding of the pathogenesis of inflammation.…”

Section: Introductionmentioning

confidence: 99%

Interferon-γ enhances phorbol myristate acetate-induced cell attachment and tumor necrosis factor production via the NF-κB pathway in THP-1 human monocytic cells

Kurihara

Furue

2013

Molecular Medicine Reports

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During inflammation, activated macrophages express adhesion molecules and produce cytokines that interact with other hematopoietic and stromal cells. THP-1 non-adherent human monocytic cells differentiate into plastic-adherent macrophages via αVβ3 integrin, by ERK activation in the presence of phorbol myristate acetate (PMA). This has proven to be a valuable model for investigating functional monocyte/macrophage diversity. Interferon-γ (IFN-γ) is a Th1-cytokine that is crucial in macrophage activation. In this study, we investigated the effects of IFN-γ on adhesion and the secretion of tumor necrosis factor (TNF) by PMA-stimulated THP-1 cells. IFN-γ is incapable of inducing cell attachment and TNF production; however, it cumulatively upregulated PMA-induced basal adhesion and TNF production. IFN-γ increased αV integrin, ICAM-1 and VCAM-1 expression and among these PMA-induced cell surface adhesion molecules, the blocking antibody for αV integrin suppressed adhesion and TNF production. Furthermore, IFN-γ enhanced PMA-induced NF-κB phosphorylation and not ERK phosphorylation. Accordingly, the NF-κB pathway inhibitor (BAY 11-7082) inhibited the enhancing effect of IFN-γ on adhesion and TNF production. By contrast, the MEK inhibitor (U0126) almost completely eliminated PMA-induced basal adhesion and TNF production. In conclusion, IFN-γ regulates macrophage activation by mediating the NF-κB signaling pathway.

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Role of ICAM‐1 in the aggregation and adhesion of human alveolar macrophages in response to TNF‐α and INF‐γ

Cited by 17 publications

References 25 publications

Multiple Serum Cytokine Profiling to Identify Combinational Diagnostic Biomarkers in Attacks of Familial Mediterranean Fever

Multiple Serum Cytokine Profiling to Identify Combinational Diagnostic Biomarkers in Attacks of Familial Mediterranean Fever

Granuloma Formation in Pulmonary Sarcoidosis

Interferon-γ enhances phorbol myristate acetate-induced cell attachment and tumor necrosis factor production via the NF-κB pathway in THP-1 human monocytic cells

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