Critical role of CCL4 in eosinophil recruitment into the airway

Kobayashi, Yoshiki; Konno, Yasunori; Kanda, Akira; Yamada, Yoshiyuki; Yasuba, Hirotaka; Sakata, Yoshiko; Fukuchi, Mineyo; Tomoda, Koichi; Iwai, Hiroshi; Ueki, Shigeharu

doi:10.1111/cea.13382

Cited by 26 publications

(33 citation statements)

References 38 publications

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“…Several studies have confirmed that CCR3 ligands are upregulated in the airways of bronchial asthma or EP patients [34][35][36][37]. Furthermore, the role of CCR5 and its ligands in the development of eosinophilic inflammation has been reported [38]. The concentration of macrophage inflammatory protein (MIP) 1β (CCL4), a CCR5 ligand, is increased in the BALF of EP patients [38].…”

Section: Mechanisms For the Development Of Eosinophilic Airway Inflammentioning

confidence: 95%

“…Furthermore, the role of CCR5 and its ligands in the development of eosinophilic inflammation has been reported [38]. The concentration of macrophage inflammatory protein (MIP) 1β (CCL4), a CCR5 ligand, is increased in the BALF of EP patients [38].…”

Section: Mechanisms For the Development Of Eosinophilic Airway Inflammentioning

confidence: 99%

“…The constitutive and/or inducible expression of CCR1, CCR3, CCR5, CXC chemokine receptor (CXCR) 1, CXCR2, CXCR3, and CXCR4 in human peripheral blood eosinophils has been reported [38,[43][44][45]. However, proteomic studies of eosinophils found or described only CCR1, CCR3, and CXCR4 as being present on human blood eosinophils [46,47].…”

Section: Role Of Ccr3 Ligands or Ccr5 Ligands In The Eosinophil Accummentioning

confidence: 99%

“…MIP-1β differs from the other chemokines in that it is a specific CCR5 ligand [52]. Kobayashi et al reported that the concentration of the CCR5 ligand MIP-1β is elevated in the BALF of EP patients [38]. Eosinophils constitutively secrete MIP-1β, which induces eosinophil migration, and MIP-1β secretion is enhanced by IL-5 [38].…”

Section: Role Of Ccr3 Ligands or Ccr5 Ligands In The Eosinophil Accummentioning

confidence: 99%

“…Kobayashi et al reported that the concentration of the CCR5 ligand MIP-1β is elevated in the BALF of EP patients [38]. Eosinophils constitutively secrete MIP-1β, which induces eosinophil migration, and MIP-1β secretion is enhanced by IL-5 [38]. CCR5-deficient mice show decreased airway eosinophilic inflammation and hyperresponsiveness [53].…”

Section: Role Of Ccr3 Ligands or Ccr5 Ligands In The Eosinophil Accummentioning

confidence: 99%

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Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia

Nakagome

Nagata

2020

Biomolecules

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Eosinophilic pneumonia (EP), including acute EP and chronic EP, is characterized by the massive pulmonary infiltration of eosinophils into the lung. However, the mechanisms underlying the selective accumulation of eosinophils in EP have not yet been fully elucidated. We reported that bronchoalveolar lavage fluid (BALF) from EP patients induced the transmigration of eosinophils across endothelial cells in vitro. The concentrations of eotaxin-2 (CCL24) and monocyte chemotactic protein (MCP)-4 (CCL13), which are CC chemokine receptor (CCR) 3 ligands, were elevated in the BALF of EP patients, and anti-CCR3 monoclonal antibody inhibited the eosinophil transmigration induced by the BALF of EP patients. The concentration of macrophage inflammatory protein 1β (CCL4), a CCR5 ligand that induces eosinophil migration, was increased in the BALF of EP patients. Furthermore, the concentration of interleukin (IL) 5 was increased in the BALF of EP patients, and it has been reported that anti-IL-5 antibody treatment resulted in remission and the reduction of glucocorticoid use in some cases of chronic EP. The concentrations of lipid mediators, such as leukotriene (LT) B 4 , damage-associated molecular pattern molecules (DAMPs), such as uric acid, or extracellular matrix proteins, such as periostin, were also increased in the BALF of EP patients. These findings suggest that chemokines, such as CCR3/CCR5 ligands, cytokines, such as IL-5, lipid mediators, such as LTB 4 , DAMPs, and extracellular matrix proteins may play roles in the accumulation or activation of eosinophils in EP.Biomolecules 2020, 10, 638 2 of 12 mechanisms of eosinophil accumulation in the airway of EP patients are discussed. The aim of this review is to better understand the mechanisms of eosinophil accumulation and activation in EP. AEP and CEPAEP is characterized by acute febrile illness with diffuse pulmonary infiltrates, severe hypoxemia, and increased eosinophils in bronchoalveolar lavage fluid (BALF) [3]. AEP is diagnosed based on the following: acute onset of respiratory failure, diffuse pulmonary infiltrates on chest roentgenogram, and increased numbers of eosinophils in BALF (more than 25% of total cells) [3]. Although the mechanisms of AEP have not yet been fully established, inhaled agents, such as cigarette smoke or chemical agents, are known causes of AEP [1,2,[5][6][7][8][9]. For example, a relationship was observed between the recent onset of cigarette smoking and the development of AEP [5][6][7]. Even short-term passive smoking can induce AEP [7]. The collapse of the World Trade Center towers [8] and the desert of the Middle East [9] have also been reported to induce AEP.

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Section: Mechanisms For the Development Of Eosinophilic Airway Inflammentioning

confidence: 95%

Section: Mechanisms For the Development Of Eosinophilic Airway Inflammentioning

confidence: 99%

Section: Role Of Ccr3 Ligands or Ccr5 Ligands In The Eosinophil Accummentioning

confidence: 99%

Section: Role Of Ccr3 Ligands or Ccr5 Ligands In The Eosinophil Accummentioning

confidence: 99%

Section: Role Of Ccr3 Ligands or Ccr5 Ligands In The Eosinophil Accummentioning

confidence: 99%

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Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia

Nakagome

Nagata

2020

Biomolecules

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Gram‐negative microbiota is related to acute exacerbation in children with asthma

Kim

Jang

Kim

et al. 2021

Clinical & Translational All

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Background The upper‐airway microbiota may be associated with the pathogenesis of asthma and useful for predicting acute exacerbation. However, the relationship between the lower‐airway microbiota and acute exacerbation in children with asthma is not well understood. We evaluated the characteristics of the airway microbiome using induced sputum from children with asthma exacerbation and compared the microbiota‐related differences of inflammatory cytokines with those in children with asthma. Methods We analysed the microbiome using induced sputum during acute exacerbation of asthma in children. We identified microbial candidates that were prominent in children with asthma exacerbation and compared them with those in children with stable asthma using various analytical methods. The microbial candidates were analysed to determine their association with inflammatory cytokines. We also developed a predictive functional profile using PICRUSt. Results A total of 95 children with allergic sensitisation including 22 with asthma exacerbation, 67 with stable asthma, and 6 controls were evaluated. We selected 26 microbial candidates whose abundances were significantly increased, decreased, or correlated during acute exacerbation in children with asthma. Among the microbial candidates, Campylobacter , Capnocytophaga , Haemophilus , and Porphyromonas were associated with inflammatory cytokines including macrophage inflammatory protein (MIP)‐1β, programmed death‐ligand 1, and granzyme B. Both Campylobacter and MIP‐1β levels were correlated with sputum eosinophils. Increased lipopolysaccharide biosynthesis and decreased glycan degradation were observed in children with asthma exacerbation. Conclusion Gram‐negative microbes in the lower airway were related to acute exacerbation in children with asthma. These microbes and associated cytokines may play a role in exacerbating asthma in children.

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Human bocavirus 1 coinfection is associated with decreased cytokine expression in the rhinovirus‐induced first wheezing episode in children

Hurme,

Sahla,

Rückert

et al. 2023

Clinical & Translational All

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BackgroundRhinovirus (RV)‐induced first wheezing episodes in children are associated with a markedly increased risk of asthma. Previous studies have suggested that human bocavirus 1 (HBoV1) may modify RV‐induced immune responses in young children. We investigated cytokine profiles of sole RV‐ and dual RV‐HBoV1‐induced first wheezing episodes, and their association with severity and prognosis.MethodsFifty‐two children infected with only RV and nine children infected with dual RV‐HBoV1, aged 3–23 months, with severe first wheezing episodes were recruited. At acute illness and 2 weeks later, peripheral blood mononuclear cells were isolated, and stimulated with anti‐CD3/anti‐CD28 in vitro. Multiplex ELISA was used to quantitatively identify 56 different cytokines at both study points. Patients were prospectively followed for 4 years.ResultsThe mean age of the children was 14.3 months, and 30% were sensitized. During the acute illness, the adjusted analyses revealed a decrease in the expression of IL‐1b, MIP‐1b, Regulated upon activation, normal T cell expressed and presumably secreted (CCL5), TNF‐a, TARC, and ENA‐78 in the RV‐HBoV1 group compared with the RV group. In the convalescence phase, the RV‐HBoV1 group was characterized by decreased expression of Fractalkine, MCP‐3, and IL‐8 compared to the RV group. Furthermore, the hospitalization time was associated with the virus group and cytokine response (interaction p < 0.05), signifying that increased levels of epidermal growth factor and MIP‐1b were related with a shorter duration of hospitalization in the RV‐HBoV1 coinfection group but not in the RV group.ConclusionsDifferent cytokine response profiles were detected between the RV and the RV‐HBoV1 groups. Our results show the idea that RV‐induced immune responses may be suppressed by HBoV1.

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Critical role of CCL4 in eosinophil recruitment into the airway

Cited by 26 publications

References 38 publications

Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia

Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia

Gram‐negative microbiota is related to acute exacerbation in children with asthma

Human bocavirus 1 coinfection is associated with decreased cytokine expression in the rhinovirus‐induced first wheezing episode in children

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