Novel Effector Molecules in Type 2 Inflammation: Lessons Drawn from Helminth Infection and Allergy

Nair, Meera G.; Guild, Katherine J.; Artis, David

doi:10.4049/jimmunol.177.3.1393

Cited by 120 publications

(118 citation statements)

References 74 publications

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“…Soluble lectins like collectins and ficolins can opsonize bacteria and induce the lectin-dependent pathway of complement activation (Fujita, 2004;Lu, 2002). The identification of mouse intelectin expression in intestinal Paneth cells and the binding of recombinant human intelectin-1 to galactofuranose in vitro suggested that intelectins might play a role in immune defense (Nair, 2006;Tsuji, 2001). Using the helminth parasite N. brasiliensis, we confirmed previous reports using Trichinella spiralis or Trichiuris muris infection in mice to show strong induction of intelectin expression in secretory Paneth cells and goblet cells of the intestine (Datta, 2005;Pemberton, 2004a).…”

Section: Discussionmentioning

confidence: 99%

Nippostrongylus brasiliensis: Identification of intelectin-1 and -2 as Stat6-dependent genes expressed in lung and intestine during infection

Voehringer

Stanley

Cox

et al. 2007

Experimental Parasitology

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Elimination of the helminth parasite Nippostrongylus brasiliensis from infected mice is mediated by IL-4 or IL-13 and dependent on the IL-4Rα chain and the transcription factor Stat6 in nonhematopoietic cells. However, it is not clear which Stat6-dependent effector molecules mediate worm expulsion. We identified intelectin-1 and -2 as Stat6-dependent genes that are induced during infection. Intelectins can bind galactofuranose, a sugar present only in microorganisms and might therefore serve as microbial pattern element. To analyze whether constitutive expression of intelectin-1 or -2 leads to accelerated pathogen clearance, transgenic mice were generated which express high levels of these genes selectively in the lung. Infection with N. brasiliensis or Mycobacterium tuberculosis did not result in accelerated pathogen clearance in transgenic as compared to wild-type mice. Further, no significant modulation of the immune response in lung or lymph nodes was observed. Thus, under these conditions, intelectins did not enhance pathogen clearance.

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Section: Discussionmentioning

confidence: 99%

Nippostrongylus brasiliensis: Identification of intelectin-1 and -2 as Stat6-dependent genes expressed in lung and intestine during infection

Voehringer

Stanley

Cox

et al. 2007

Experimental Parasitology

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“…Species such as Trichinella spiralis generate an intestinal immune response during which gut function is severely affected and, as the immune response intensifies, so worm numbers decline. Concurrently marked changes in a range of cellular and soluble mediators can be detected, reflected for example in mastocytosis on the one hand (mast cell numbers increase and degranulate, releasing their highly toxic compounds) and in changes in the expression of receptors of signals from cytokines, including adhesion molecules, on the other hand (Else and Finkelman, 1999 ;Gause, Urban and Stadecker, 2003 ;Nair, Guild and Artis, 2006).…”

Section: The Immune Response As An E N V I R O N M E N T a L S T R E mentioning

confidence: 99%

Structure in parasite component communities in wild rodents: predictability, stability, associations and interactions .... or pure randomness?

Behnke

2008

Parasitology

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SUMMARYExperimental data establish that interactions exist between species of intestinal helminths during concurrent infections in rodents, the strongest effects being mediated through the host's immune responses. Detecting immune-mediated relationships in wild rodent populations has been fraught with problems and published data do not support a major role for interactions in structuring helminth communities. Helminths in wild rodents show predictable patterns of seasonal, host age-dependent and spatial variation in species richness and in abundance of core species. When these are controlled for, patterns of co-infection compatible with synergistic interactions can be demonstrated. At least one of these, the positive relationship betweenHeligmosomoides polygyrusand species richness of other helminths has been demonstrated in three totally independent data-sets. Collectively, they explain only a small percentage of the variance/deviance in abundance data and at this level are unlikely to play a major role in structuring helminth communities, although they may be important in the more heavily infected wood mice. Current worm burdens underestimate the possibility that earlier interactions through the immune system have taken place, and therefore interactions may have a greater role to play than is immediately evident from current worm burdens. Longitudinal studies are proposed to resolve this issue.

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“…Interestingly, these family members each show unique tissue distribution, raising the possibility of their differential roles in the pathogenesis of diseases. Retnla is expressed mainly by hematopoietic cells and stromal vascular cells but not by adipocytes in WAT 12,37,43,44 . Retnlb is expressed abundantly in the colon in both mouse and human, and expression can also be induced in macrophages under the proper inflammatory conditions 12,44,45 .…”

Section: Discussionmentioning

confidence: 99%

“…Retnla is expressed mainly by hematopoietic cells and stromal vascular cells but not by adipocytes in WAT 12,37,43,44 . Retnlb is expressed abundantly in the colon in both mouse and human, and expression can also be induced in macrophages under the proper inflammatory conditions 12,44,45 . In mice, resistin is primarily produced in adipocytes, whereas in humans, resistin is mainly derived from monocytes and macrophages 19,46 .…”

Section: Discussionmentioning

confidence: 99%

The adipokine Retnla modulates cholesterol homeostasis in hyperlipidemic mice

et al. 2014

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Hyperlipidemia is a well-recognized risk factor for atherosclerosis and can be regulated by adipokines. Expression of the adipokine resistin-like molecule alpha (Retnla) is regulated by food intake; whether Retnla has a role in the pathogenesis of hyperlipidemia and atherosclerosis is unknown. Here we report that Retnla has a cholesterol-lowering effect and protects against atherosclerosis in low-density lipoprotein receptor-deficient mice. On a high-fat diet, Retnla deficiency promotes hypercholesterolaemia and atherosclerosis, whereas Retnla overexpression reverses these effects and improves the serum lipoprotein profile, with decreased cholesterol in the very low-density lipoprotein fraction concomitant with reduced serum apolipoprotein B levels. We show that Retnla upregulates cholesterol-7-a-hydroxylase, a key hepatic enzyme in the cholesterol catabolic pathway, through induction of its transcriptional activator liver receptor homologue-1, leading to increased excretion of cholesterol in the form of bile acids. These findings define Retnla as a novel therapeutic target for treating hypercholesterolaemia and atherosclerosis.

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Novel Effector Molecules in Type 2 Inflammation: Lessons Drawn from Helminth Infection and Allergy

Cited by 120 publications

References 74 publications

Nippostrongylus brasiliensis: Identification of intelectin-1 and -2 as Stat6-dependent genes expressed in lung and intestine during infection

Nippostrongylus brasiliensis: Identification of intelectin-1 and -2 as Stat6-dependent genes expressed in lung and intestine during infection

Structure in parasite component communities in wild rodents: predictability, stability, associations and interactions .... or pure randomness?

The adipokine Retnla modulates cholesterol homeostasis in hyperlipidemic mice

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