IL-9 expression by human eosinophils: Regulation by IL-1β and TNF-α

Gounni, Abdelilah Soussi; Nutku, Esra; Koussih, Latifa; Aris, Fadi; Louahed, Jamila; Levitt, Roy C.; Nicolaides, Nicholas C.; Hamid, Qutayba

doi:10.1067/mai.2000.109172

Cited by 82 publications

(51 citation statements)

References 26 publications

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“…IL-1b is known to activate eosinophils directly to stimulate cytokine release (23). IL-1 may also affect eosinophil reactivity, since IL-1 receptor antagonists decrease hypodense eosinophils in bronchoalveolar lavage of antigen-challenged animals (22), suggesting that IL-1 contributes to eosinophil activation.…”

Section: Discussionmentioning

confidence: 99%

“…Interleukin 1b (IL-1b) is a central mediator of inflammation that increases granulocyte hematopoiesis (18), induces chemokines and adhesion molecules (19)(20)(21), and activates eosinophils (22,23). Inhibiting IL-1b or blocking IL-1 receptors prevents virus-induced, toluene diisocyanate-induced, and antigen challenge-induced hyperreactivity in animals (24)(25)(26)(27).…”

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confidence: 99%

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IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Verhein¹,

Jacoby

Fryer

2008

Am J Respir Cell Mol Biol

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Ozone exposure in the lab and environment causes airway hyperreactivity lasting at least 3 days in humans and animals. In guinea pigs 1 day after ozone exposure, airway hyperreactivity is mediated by eosinophils that block neuronal M 2 muscarinic receptor function, thus increasing acetylcholine release from airway parasympathetic nerves. However, mechanisms of ozone-induced airway hyperreactivity change over time, so that depleting eosinophils 3 days after ozone makes airway hyperreactivity worse rather than better. Ozone exposure increases IL-1b in bone marrow, which may contribute to acute and chronic airway hyperreactivity. To test whether IL-1b mediates ozone-induced airway hyperreactivity 1 and 3 days after ozone exposure, guinea pigs were pretreated with an IL-1 receptor antagonist (anakinra, 30 mg/kg, intraperitoneally) 30 minutes before exposure to filtered air or to ozone (2 ppm, 4 h). One or three days after exposure, airway reactivity was measured in anesthetized guinea pigs. The IL-1 receptor antagonist prevented ozoneinduced airway hyperreactivity 3 days, but not 1 day, after ozone exposure. Ozone-induced airway hyperreactivity was vagally mediated, since bronchoconstriction induced by intravenous acetylcholine was not changed by ozone. The IL-1 receptor antagonist selectively prevented ozone-induced reduction of eosinophils around nerves and prevented ozone-induced deposition of extracellular eosinophil major basic protein in airways. These data demonstrate that IL-1 mediates ozone-induced airway hyperreactivity at 3 days, but not 1 day, after ozone exposure. Furthermore, preventing hyperreactivity was accompanied by decreased eosinophil major basic protein deposition within the lung, suggesting that IL-1 affects eosinophil activation 3 days after ozone exposure.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Verhein¹,

Jacoby

Fryer

2008

Am J Respir Cell Mol Biol

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“…Similarly, TNF-␣ plays a central role in the activation of macrophages, granulocytes, and cytotoxic T cells in an acute immune response (15,39). Using epithelial cells from the gastrointestinal tract and cervical epithelial cells, Kagnoff and colleagues demonstrated the secretion of interleukin-8, GRO alpha, granulocyte-macrophage colony-stimulating factor, and interleukin-6 in response to Chlamydia infection (40).…”

Section: Discussionmentioning

confidence: 99%

Effect ofEscherichia coliandLactobacillus rhamnosuson Macrophage Inflammatory Protein 3α, Tumor Necrosis Factor Alpha, and Transforming Growth Factor β Release by Polarized Rat Uterine Epithelial Cells in Culture

Crane-Godreau¹,

Wira²

2004

Infect Immun

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Entry of bacteria from the vagina into the uterus raises the question of uterine epithelial cell (UEC) signaling in response to the presence of bacteria. Our model system helps to define microbially elicited UEC basolateral cytokine release, important in regulating underlying stromal immune cell protection. UECs from adult rats were grown in cell culture inserts to establish a confluent polarized monolayer as was determined by transepithelial resistance (TER). Polarized epithelial cell cultures were treated apically with live or heat-killed Escherichia coli or Lactobacillus rhamnosus prior to collection of basolateral media after 24 h of incubation. Coculture of polarized UECs with live E. coli had no effect on epithelial cell TER. In response to exposure to live E. coli, epithelial cell basolateral release of macrophage inflammatory protein 3␣ (MIP3␣) and tumor necrosis factor alpha (TNF-␣) increased at a time when basolateral release of biologically active transforming growth factor ␤ (TGF-␤) decreased. Incubation of UECs with heat-killed E. coli resulted in an increased basolateral release of MIP3␣ and TNF-␣, without affecting TER or TGF-␤. In contrast to E. coli, live or heat-killed L. rhamnosus had no effect on TER or cytokine release. These studies indicate that polarized rat UECs respond to gram-negative E. coli by releasing the cytokines MIP3␣ and TNF-␣, signals important to both the innate and adaptive immune systems. These findings suggest that UEC responses to bacteria are selective and important in initiating and regulating immune protection in the female reproductive tract.

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“…Since its discovery as a T-cell [1,2] and mast-cell [3] growth factor that plays an essential role in helminth elimination [4] and in pulmonary mast cell and goblet cell accumulation [5], IL-9 has been considered a Th2 cytokine [6,7], although, in asthmatic humans, eosinophils have also been identified as an IL-9 source [8]. A recent publication, however, showed that, in the presence of IL-4 and TGF-b, naïve T cells could be programmed to selective IL-9 production [9] and failed to express T-bet, GATA3, Foxp3, or RORgt, suggesting that these cells could represent a novel Th subset, an idea confirmed in another report [10].…”

Section: Introductionmentioning

confidence: 99%

TGF‐β interactions with IL‐1 family members trigger IL‐4‐independent IL‐9 production by mouse CD4⁺ T cells

2010

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TGF-b and IL-4 were recently shown to selectively upregulate IL-9 production by naïve CD4 1 T cells. We report here that TGF-b interactions with IL-1a, IL-1b, IL-18, and IL-33 have equivalent IL-9-stimulating activities that function even in IL-4-deficient animals. This was observed after in vitro antigenic stimulation of immunized or unprimed mice and after polyclonal T-cell activation. Based on intracellular IL-9 staining, all IL-9-producing cells were CD4 1 and 80-90% had proliferated, as indicated by reduced CFSE staining. In contrast to IL-9, IL-13 and IL-17 were strongly stimulated by IL-1 and either inhibited (IL-13) or were unaffected (IL-17) by addition of TGF-b. IL-9 and IL-17 production also differed in their dependence on IL-2 and regulation by IL-1/IL-23. As IL-9 levels were much lower in Th2 and Th17 cultures, our results identify TGF-b/IL-1 and TGF-b/IL-4 as the main control points of IL-9 synthesis.

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IL-9 expression by human eosinophils: Regulation by IL-1β and TNF-α

Cited by 82 publications

References 26 publications

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Effect ofEscherichia coliandLactobacillus rhamnosuson Macrophage Inflammatory Protein 3α, Tumor Necrosis Factor Alpha, and Transforming Growth Factor β Release by Polarized Rat Uterine Epithelial Cells in Culture

TGF‐β interactions with IL‐1 family members trigger IL‐4‐independent IL‐9 production by mouse CD4⁺ T cells

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IL-9 expression by human eosinophils: Regulation by IL-1β and TNF-α

Cited by 82 publications

References 26 publications

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Effect ofEscherichia coliandLactobacillus rhamnosuson Macrophage Inflammatory Protein 3α, Tumor Necrosis Factor Alpha, and Transforming Growth Factor β Release by Polarized Rat Uterine Epithelial Cells in Culture

TGF‐β interactions with IL‐1 family members trigger IL‐4‐independent IL‐9 production by mouse CD4+ T cells

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TGF‐β interactions with IL‐1 family members trigger IL‐4‐independent IL‐9 production by mouse CD4⁺ T cells