Elevation of macrophage-derived chemokine in eosinophilic pneumonia: a role of alveolar macrophages

Manabe, Kenji; Nishioka, Yasuhiko; Kishi, Jun; Inayama, Mami; Aono, Yoshinori; Nakamura, Yoichi; Ogushi, Fumitaka; Bando, Hiroyasu; Tani, Kenji; Sone, Saburo

doi:10.2152/jmi.52.85

Cited by 12 publications

(22 citation statements)

References 29 publications

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“…We have also observed increased expression of CCL11 and CCL26 in alve- The CCR4 ligands, CCL17 and CCL22, were upregulated in the liver by LD ATRA in A suum-infected pigs at 7 DAI. CCL17 and CCL22 are induced by IL4 and IL13 in various cell types and are associated with Th2 cells and eosinophilic infiltration into the human lung (30,38). We observed that IL4 and IL13 induced the expression of CCL17 and CCL22 in porcine alveolar macrophages.…”

Section: Vol 77 2009mentioning

confidence: 64%

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Localized Th1-, Th2-, T Regulatory Cell-, and Inflammation-Associated Hepatic and Pulmonary Immune Responses inAscaris suum-Infected Swine Are Increased by Retinoic Acid

et al. 2009

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Pigs infected with Ascaris suum or controls were given 100 g (low-dose) or 1,000 g (high-dose) all-trans retinoic acid (ATRA)/kg body weight in corn oil or corn oil alone per os on days after inoculation (DAI) ؊1, ؉1, and ؉3 with infective eggs. Treatment with ATRA increased interleukin 4 (IL4) and IL12p70 in plasma of infected pigs at 7 DAI and augmented bronchoalveolar lavage (BAL) eosinophilia observed at 7 and 14 DAI. To explore potential molecular mechanisms underlying these observations, a quantitative real-time reverse transcription (RT)-PCR array was used to examine mRNA expression in tissue. Ascaris-infected pigs had increased levels of liver mRNA for T-helper-2 (Th2)-associated cytokines, mast cell markers, and T regulatory (Treg) cells, while infected pigs given ATRA had higher IL4, IL13, CCL11, CCL26, CCL17, CCL22, and TPSB1 expression. Gene expression for Th1-associated markers (IFNG, IL12B, and TBX21), the CXCR3 ligand (CXCL9), IL1B, and the putative Treg marker TNFRSF18 was also increased. Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. To determine a putative cellular source of eosinophil chemoattractants, alveolar macrophages were treated with IL4 and/or ATRA in vitro. IL4 induced CCL11, CCL17, CCL22, and CCL26 mRNA, and ATRA increased the basal and IL4-stimulated expression of CCL17 and CCL22. Thus, ATRA augments a diverse Th1-, Th2-, Treg-, and inflammation-associated response in swine infected with A. suum, and the increased BAL eosinophilia may be related to enhanced induction of eosinophil chemokine activity by alveolar macrophages.

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Section: Vol 77 2009mentioning

confidence: 64%

“…The role of retinoids or VA in the functional development and recruitment of eosinophils is confounded by data from a variety of both in vitro (30,34,39) and in vivo (8,17,53) studies. Our studies demonstrated that oral ATRA supple- FIG.…”

Section: Discussionmentioning

confidence: 99%

Localized Th1-, Th2-, T Regulatory Cell-, and Inflammation-Associated Hepatic and Pulmonary Immune Responses inAscaris suum-Infected Swine Are Increased by Retinoic Acid

et al. 2009

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“…BAL was performed as described previously [14,15]. Briefly, a flexible fibreoptic bronchoscope (Model 1T20; Olympus Co., Tokyo, Japan) was wedged into a segmental or subsegmental bronchus of the middle lobe or lingula, and lavage was performed with a total volume of 150 ml of sterile 0·9% saline warmed at 37°C in three 50-ml aliquots.…”

Section: Bronchoalveolar Lavagementioning

confidence: 99%

“…The total number of cells was counted using the trypan-blue dye exclusion test. Differential counts on 400 cells were carried out on smears of sedimented cells stained with Diff-Quik stain (Baxter Dade AG, Duedingen, Switzerland) [14,15]. Blood samples were collected at the time of diagnosis.…”

Section: Bronchoalveolar Lavagementioning

confidence: 99%

CXCL9 and 11 in patients with pulmonary sarcoidosis: a role of alveolar macrophages

Nishioka

Manabe

Kishi

et al. 2007

Clinical and Experimental Immunology

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SummaryInterferon-inducible protein-10 (IP-10)/CXCL10, which is a ligand for CXC chemokine receptor 3 (CXCR3), is known to be involved in the pathogenesis of pulmonary sarcoidosis. However, the roles of monokine induced by interferon g (Mig)/CXCL9 and interferon-inducible T cell a chemoattractant (I-TAC)/CXCL11, which are also CXCR3 ligands, remain unclear. Mig/ CXCL9, IP-10/CXCL10 and I-TAC/CXCL11 in both bronchoalveolar lavage fluid (BALF) and serum in patients with pulmonary sarcoidosis were measured by enzyme-linked immunosorbent assay (ELISA). The expression of these chemokines in alveolar macrophages was examined using ELISA, quantitative real-time polymerase chain reaction and immunostaining. In BALF, Mig/CXCL9 and IP-10/CXCL10 were significantly elevated in stage II sarcoidosis as compared with the levels in healthy volunteers. In serum, Mig/CXCL9 and I-TAC/CXCL11 were increased in stage II of the disease. The levels of all CXCR3 ligands in BALF were correlated with the numbers of both total and CD4 + lymphocytes. Alveolar macrophages were stained positive for all CXCR3 ligands and produced increased amounts of these chemokines. Positive staining of the three chemokines was also observed in the epithelioid and giant cells in the sarcoid lungs. These findings suggest that Mig/CXCL9 and I-TAC/ CXCL11 as well as IP-10/CXCL10 play important roles in the accumulation of Th1 lymphocytes in sarcoid lungs.

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“…In addition, the T-cell chemotactic factor TARC has been found to be elevated both in humans (Manabe et al, 2005) and models of lung inflammation (Ritter et al, 2005). The induction of nitric oxide (NO) through inducible NO synthase (iNOS) also plays a significant role in the inflammatory response, and its inhibition attenuates endotoxin-induced lung injury in rats (Su et al, 2007;Xia et al, 2007).…”

mentioning

confidence: 99%

Treatment of Sepsis-Induced Acquired Protein C Deficiency Reverses Angiotensin-Converting Enzyme-2 Inhibition and Decreases Pulmonary Inflammatory Response

Richardson

Gupta²,

O’Brien³

et al. 2008

J Pharmacol Exp Ther

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The protein C (PC) pathway plays an important role in vascular and immune function, and acquired deficiency during sepsis is associated with increased mortality in both animal models and in clinical studies. However, the association of acquired PC deficiency with the pathophysiology of lung injury is unclear. We hypothesized that low PC induced by sepsis would associate with increased pulmonary injury and that replacement with activated protein C (APC) would reverse the activation of pathways associated with injury. Using a cecal ligation and puncture (CLP) model of polymicrobial sepsis, we examined the role of acquired PC deficiency on acute lung injury assessed by analyzing changes in pulmonary pathology, chemokine response, inducible nitric-oxide synthase (iNOS), and the angiotensin pathway. Acquired PC deficiency was strongly associated with an increase in lung inflammation and drivers of pulmonary injury, including angiotensin (Ang) II, thymus and activation-regulated chemokine, plasminogen activator inhibitor (PAI)-1, and iNOS. In contrast, the protective factor angiotensin-converting enzyme (ACE)-2 was significantly suppressed in animals with acquired PC deficiency. The endothelial protein C receptor, required for the cytoprotective signaling of APC, was significantly increased post-CLP, suggesting a compensatory up-regulation of the signaling receptor. Treatment of septic animals with APC reduced pulmonary pathology, suppressed the macrophage inflammatory protein family chemokine response, iNOS expression, and PAI-1 activity and up-regulated ACE-2 expression with concomitant reduction in AngII peptide. These data demonstrate a clear link between acquired PC deficiency and pulmonary inflammatory response in the rat sepsis model and provide support for the concept of APC as a replacement therapy in acute lung injury associated with acquired PC deficiency.Acute lung injury (ALI) leading to acute respiratory distress syndrome (ARDS) is a significant issue in the intensive care unit, with an incidence of 10 to 15% (Vincent and Zambon, 2006). Despite advances in the understanding of the pathophysiology of ALI/ARDS and improved supportive care with optimal ventilation and fluid balance, mortality rates range from 30 to 50% (Bastarache et al., 2006). ARDS is a systemic disease with the majority of patients dying from multiorgan dysfunction (Vincent and Zambon, 2006), and there remains a significant need for new therapeutic interventions.Infection is a common cause of pulmonary injury, and in sepsis, the lung is the most often affected organ (Vincent et al., 2003;Bastarache et al., 2006). The lung is a major source of various inflammatory mediators that affect both local and systemic immune response (Ritter et al., 2005), and recent studies have identified specific markers associated with pulmonary dysfunction. For example, chemokines associated with leukocyte migration and activation such as MIP-1␣ and MIP-2 have been found in close association in pulmonary lesions (Sun et al., 2006) and associated with ...

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Elevation of macrophage-derived chemokine in eosinophilic pneumonia: a role of alveolar macrophages

Cited by 12 publications

References 29 publications

Localized Th1-, Th2-, T Regulatory Cell-, and Inflammation-Associated Hepatic and Pulmonary Immune Responses inAscaris suum-Infected Swine Are Increased by Retinoic Acid

Localized Th1-, Th2-, T Regulatory Cell-, and Inflammation-Associated Hepatic and Pulmonary Immune Responses inAscaris suum-Infected Swine Are Increased by Retinoic Acid

CXCL9 and 11 in patients with pulmonary sarcoidosis: a role of alveolar macrophages

Treatment of Sepsis-Induced Acquired Protein C Deficiency Reverses Angiotensin-Converting Enzyme-2 Inhibition and Decreases Pulmonary Inflammatory Response

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