IL-17A And TNF-± Exert Synergistic Effects On Expression Of CXCL5 By Alveolar Type II Cells In Vivo And In Vitro

Liu, Yuhong; Mei, Junjie; Gonzales, Linda W.; Wang, Ping; Dai, Ning; Guang, Yang; Zhang, Peggy; Worthen, Scott

doi:10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6787

Cited by 26 publications

(41 citation statements)

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“…We previously showed that lung resident cells are the predominant source of Cxcl5 in the alveolar space during lung inflammation (21,27). To further determine whether lung epithelial cells express measurable Cxcl5 under basal conditions, we used a small-volume lavage procedure to minimize dilution, and we detected low-level Cxcl5 expression ( Figure 4B).…”

Section: Cxcr2mentioning

confidence: 89%

“…We previously demonstrated that under normal conditions, Cxcl5 in blood is derived from platelets (21), whereas in mouse models of lung inflammation, resident cells (which we have suggested are AE II cells; refs. 21,27) are the only source of Cxcl5 in the bronchoalveolar lavage fluid (BALF). To determine the origin of the Cxcl5 contributing to neutrophil homeostasis, we generated BM chimeric mice using WT and Cxcl5 -/-mice and found that only Cxcl5 -/-recipient mice displayed increased percentages of neutrophil in the BM ( Figure 4A), indicating that resident cell-derived Cxcl5 is responsible for regulating neutrophil homeostasis.…”

Section: Cxcr2mentioning

confidence: 99%

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Cxcr2 and Cxcl5 regulate the IL-17/G-CSF axis and neutrophil homeostasis in mice

Mei¹,

Liu²,

Dai³

et al. 2012

J. Clin. Invest.

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153

134

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Neutrophils are essential for maintaining innate immune surveillance under normal conditions, but also represent a major contributor to tissue damage during inflammation. Neutrophil homeostasis is therefore tightly regulated. Cxcr2 plays a critical role in neutrophil homeostasis, as Cxcr2 -/-mice demonstrate mild neutrophilia and severe neutrophil hyperplasia in the bone marrow. The mechanisms underlying these phenotypes, however, are unclear.

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Section: Cxcr2mentioning

confidence: 89%

Section: Cxcr2mentioning

confidence: 99%

Cxcr2 and Cxcl5 regulate the IL-17/G-CSF axis and neutrophil homeostasis in mice

Mei¹,

Liu²,

Dai³

et al. 2012

J. Clin. Invest.

Self Cite

153

134

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“…In contrast to in vitro cell culture consisting solely of AECII, other cell types likewise responding to M. tuberculosis challenge, e.g., by cytokine secretion, are present in the bronchoalveolar spaces in vivo. In fact, various inflammatory mediators secreted by cells other than pneumocytes are reportedly capable of inducing CXCL5 release by epithelia (49,59), among which at least IL-1β and TNF-α were detected at day 15 p.i. in WT and Tlr2 -/-mice, albeit at low concentrations (G. Nouailles, unpublished observations).…”

Section: Discussionmentioning

confidence: 99%

CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis

Nouailles¹,

Dorhoi²,

Koch³

et al. 2014

J. Clin. Invest.

187

185

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Successful host defense against numerous pulmonary infections depends on bacterial clearance by polymorphonuclear leukocytes (PMNs); however, excessive PMN accumulation can result in life-threatening lung injury. Local expression of CXC chemokines is critical for PMN recruitment. The impact of chemokinedependent PMN recruitment during pulmonary Mycobacterium tuberculosis infection is not fully understood. Here, we analyzed expression of genes encoding CXC chemokines in M. tuberculosis-infected murine lung tissue and found that M. tuberculosis infection promotes upregulation of Cxcr2 and its ligand Cxcl5. To determine the contribution of CXCL5 in pulmonary PMN recruitment, we generated Cxcl5 -/-mice and analyzed their immune response against M. tuberculosis. Both Cxcr2 -/-mice and Cxcl5 -/-mice, which are deficient for only one of numerous CXCR2 ligands, exhibited enhanced survival compared with that of WT mice following high-dose M. tuberculosis infection. The resistance of Cxcl5 -/-mice to M. tuberculosis infection was not due to heightened M. tuberculosis clearance but was the result of impaired PMN recruitment, which reduced pulmonary inflammation. Lung epithelial cells were the main source of CXCL5 upon M. tuberculosis infection, and secretion of CXCL5 was reduced by blocking TLR2 signaling. Together, our data indicate that TLR2-induced epithelial-derived CXCL5 is critical for PMN-driven destructive inflammation in pulmonary tuberculosis.

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“…2A, 2B). One potential mechanism by which neutrophils are recruited into the airways is via IL-17-induced production of two CXC chemokines (CXCL1 and CXCL5) (19,20,41). Interestingly, mRNA levels of each of these chemokines (Fig.…”

Section: Intranasal Delivery Of Ril-13 Induces Ahr Airway Inflammatimentioning

confidence: 99%

“…More recently, IL-17 has also been implicated specifically in severe asthma (12)(13)(14)(15). Elevated levels of IL-17 are thought to participate in increased airway neutrophilia in this group of asthmatics (13,16,17) owing to IL-17-mediated production of chemokines that promote neutrophil recruitment (18)(19)(20)(21). The role of IL-17 in murine models of allergic airways disease is unclear.…”

mentioning

confidence: 99%

Dose-Dependent Effects of IL-17 on IL-13–Induced Airway Inflammatory Responses and Airway Hyperresponsiveness

Kinyanjui

Shan

Nakada

et al. 2013

The Journal of Immunology

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The Th2 cytokine IL-13 regulates several aspects of the asthmatic phenotype, including airway inflammation, airway hyperresponsiveness, and mucus production. The Th17 cytokine IL-17A is also implicated in asthma and has been shown to both positively and negatively regulate Th2-dependent responses in murine models of allergic airways disease. Our objective in this study was to better understand the role of IL-17 in airway inflammation by examining how IL-17 modifies IL-13–induced airway inflammatory responses. We treated BALB/c mice intranasally with IL-13 or IL-17 alone or in combination for 8 consecutive days, after which airway hyperresponsiveness, inflammatory cell influx into the lung, and lung chemokine/cytokine expression were assessed. As expected, IL-13 increased airway inflammation and airway hyperresponsiveness. IL-13 also increased numbers of IL-17–producing CD4+ and γδ T cells. Treating mice with a combination of IL-13 and IL-17 reduced infiltration of IL-17+ γδ T cells, but increased the number of infiltrating eosinophils. In contrast, coadministration of IL-13 with a higher dose of IL-17 decreased all IL-13–induced inflammatory responses, including infiltration of both IL-17+CD4+ and γδ T cells. To examine the inhibitory activity of IL-17–expressing γδ T cells in this model, these cells were adoptively transferred into naive recipients. Consistent with an inhibitory role for γδ T cells, IL-13–induced infiltration of eosinophils, lymphocytes, and IL-17+CD4+ T cells was diminished in recipients of the γδ T cells. Collectively, our data indicate that allergic airway inflammatory responses induced by IL-13 are modulated by both the quantity and the cellular source of IL-17.

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IL-17A And TNF-± Exert Synergistic Effects On Expression Of CXCL5 By Alveolar Type II Cells In Vivo And In Vitro

Cited by 26 publications

References 0 publications

Cxcr2 and Cxcl5 regulate the IL-17/G-CSF axis and neutrophil homeostasis in mice

Cxcr2 and Cxcl5 regulate the IL-17/G-CSF axis and neutrophil homeostasis in mice

CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis

Dose-Dependent Effects of IL-17 on IL-13–Induced Airway Inflammatory Responses and Airway Hyperresponsiveness

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