Gastrointestinal nematode expulsion in IL-4 knockout mice is IL-13 dependent

Bancroft, Allison J.; Artis, David; Donaldson, Deborah D.; Sypek, Joseph P.; Grencis, Richard K.

doi:10.1002/1521-4141(200007)30:7<2083::aid-immu2083>3.0.co;2-3

Cited by 116 publications

(78 citation statements)

References 26 publications

(15 reference statements)

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“…It is widely accepted that the Th2-like response induced via the STAT6-mediated signaling pathway (through IL-4/IL-13 receptors) plays a critical role in mediating protective immunity against most helminths (17)(18)(19). For example, STAT6-mediated signaling promotes protective immunity against Trichinella spiralis (13) and N. brasiliensis (12).…”

Section: Resultsmentioning

confidence: 99%

Cutting Edge: Susceptibility to the Larval Stage of the Helminth ParasiteTaenia crassicepsIs Mediated by Th2 Response Induced Via STAT6 Signaling

Rodrı́guez-Sosa

David

Bojalil

et al. 2002

The Journal of Immunology

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Using STAT6−/− BALB/c mice, we analyzed the role of STAT6-induced Th2 response in determining the outcome of murine cysticercosis caused by the helminth parasite Taenia crassiceps. After T. crassiceps infection, wild-type BALB/c mice developed a strong Th2-like response; produced high levels of IgG1, IgE, IL-4, as well as IL-13; and remained susceptible to T. crassiceps. In contrast, similarly infected STAT6−/− mice mounted a strong Th1-like response; produced high levels of IgG2a, IL-12, IFN-γ, as well as nitric oxide; and efficiently controlled T. crassiceps infection. These findings demonstrate that Th2-like response induced via STAT6-mediated signaling pathway mediates susceptibility to T. crassiceps and, furthermore, that unlike the case in most helminths, immunity against T. crassiceps is mediated by a Th1-like rather than Th2-like response.

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Section: Resultsmentioning

confidence: 99%

Cutting Edge: Susceptibility to the Larval Stage of the Helminth ParasiteTaenia crassicepsIs Mediated by Th2 Response Induced Via STAT6 Signaling

Rodrı́guez-Sosa

David

Bojalil

et al. 2002

The Journal of Immunology

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“…Inhibition of IL-9 impaired Trichuris muris clearance (10), whereas IL-9 overexpression accelerated expulsion of T. muris or Trichinella spiralis (9,33). Similarly, mice treated with anti-IL-13 Abs or deficient in IL-13 fail to expel T. muris (8,34). However, the mechanism involved in worm clearance remains controversial, and might depend on the nematode species.…”

Section: Discussionmentioning

confidence: 99%

IL-9 Promotes IL-13-Dependent Paneth Cell Hyperplasia and Up-Regulation of Innate Immunity Mediators in Intestinal Mucosa

Steenwinckel

Louahed²,

Lemaire³

et al. 2009

The Journal of Immunology

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IL-9 contributes to lung inflammatory processes such as asthma, by promoting mast cell differentiation, B cell activation, eosinophilia, and mucus production by lung epithelial cells. The observation that IL-9 overexpressing mice show increased mast cell numbers in the intestinal mucosa suggests that this cytokine might also play a role in intestinal inflammation. In colons from IL-9 transgenic mice, the expression of Muc2, a major intestinal mucin gene, was up-regulated, together with that of CLCA3 chloride channel and resistin like α, which are goblet cell-associated genes. Additional IL-9 up-regulated genes were identified and included innate immunity genes such as angiogenin 4 and the PLA2g2a phospholipase A2, which are typical Paneth cell markers. Histochemical staining of Paneth cells by phloxine/tartrazine showed that IL-9 induces Paneth cell hyperplasia in Lieberkühn glands of the small intestine, and in the colonic mucosa, where this cell type is normally absent. Expression of Paneth cell markers, including angiogenin 4, PLA2g2a, and cryptdins, was induced in the colon of wild-type mice after two to four daily administrations of IL-9. By crossing IL-9 transgenic mice with IL-13−/− mice, or by injecting IL-9 into IL-4R−/− mice, we showed that IL-13 was required for the up-regulation of these Paneth cell-specific genes by IL-9. Taken together, our data indicate that Paneth cell hyperplasia and expression of their various antimicrobial products contribute to the immune response driven by TH2 cytokines, such as IL-9 and IL-13 in the intestinal mucosa.

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“…In vitro, clearance of apoptotic neutrophils is mediated through phagocytosis by macrophages 36 . Both lung and gut are frequently involved with allergic inflammation and, not surprisingly, their lumens are sites of inflammatory cell clearance 37,38 . In acute allergic airway inflammation, eosinophils and macrophages constitute >80% of total recovered leukocytes 3,5,14 .…”

Section: Discussionmentioning

confidence: 99%

Decreased allergic lung inflammatory cell egression and increased susceptibility to asphyxiation in MMP2-deficiency

et al. 2002

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Clearance of recruited immune cells is necessary to resolve inflammatory reactions. We show here that matrix metalloproteinase 2 (MMP2), as part of an interleukin 13 (IL-13)-dependent regulatory loop, dampens inflammation by promoting the egress of inflammatory cells into the airway lumen. MMP2 −/− mice showed a robust asthma phenotype and increased susceptibility to asphyxiation induced by allergens. However, whereas the lack of MMP2 reduced the influx of cells into bronchoalveolar lavage (BAL), numerous inflammatory cells accumulated in the lung parenchyma. BAL of MMP2 −/− mice lacked normal chemotactic activity, whereas lung inflammatory cells from the same mice showed appropriate chemotactic responses. Thus, MMP2 establishes the chemotactic gradient required for egression of lung inflammatory cells and prevention of lethal asphyxiation.

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Gastrointestinal nematode expulsion in IL-4 knockout mice is IL-13 dependent

Cited by 116 publications

References 26 publications

Cutting Edge: Susceptibility to the Larval Stage of the Helminth ParasiteTaenia crassicepsIs Mediated by Th2 Response Induced Via STAT6 Signaling

Cutting Edge: Susceptibility to the Larval Stage of the Helminth ParasiteTaenia crassicepsIs Mediated by Th2 Response Induced Via STAT6 Signaling

IL-9 Promotes IL-13-Dependent Paneth Cell Hyperplasia and Up-Regulation of Innate Immunity Mediators in Intestinal Mucosa

Decreased allergic lung inflammatory cell egression and increased susceptibility to asphyxiation in MMP2-deficiency

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