Anti-inflammatory action of type I interferons deduced from mice expressing interferon β

Bodelón, Oscar G.; Hortelano, Sonsoles; Casellas, Alba; Bosch, F. Xavier

doi:10.1038/sj.gt.3301179

Cited by 22 publications

(16 citation statements)

References 59 publications

(70 reference statements)

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“…Similarly, it has been shown to inhibit monocyte migration across human brain-derived endothelial cells (Seguin et al, 2003) and reduce cellular infiltration into damaged brain regions (Veldhuis et al, 2003b). On a cellular level, IFNβ has been shown to reduce reactive oxygen species (Lopez-Collazo et al, 1998, Stewart et al, 1998, Hua et al, 2002), suppress inflammatory cytokine production and induce IL-1Ra (Bosca et al, 2000, Palmer et al, 2004), promote nerve growth factor production by astrocytes (Boutros et al, 1997) and protect neurons from toxicity induced by activated microglia (Jin et al, 2007). In addition, systemic administration of IFNβ has been shown to reduce infarct damage in rat and rabbit models of ischemic stroke (Liu et al, 2002, Veldhuis et al, 2003a).…”

Section: Mechanisms Of Neuroprotection—reprogramming Tlr Signalingmentioning

confidence: 99%

Toll-like receptor signaling in endogenous neuroprotection and stroke

2009

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Stroke and other cerebral vascular diseases are a leading cause of morbidity and mortality in the United States. Despite intensive research to identify interventions that lessen cerebrovascular injury, no major therapies exist. Development of stroke prophylaxis involves an understanding of the mechanisms of damage following cerebral ischemia, and elucidation of the endogenous mechanisms that combat further brain injury. Toll-like receptors (TLRs) are critical components of the innate immune system that have been shown recently to mediate ischemic injury. Paradoxically, TLR ligands administered systemically induce a state of tolerance to subsequent ischemic injury. Herein we suggest that stimulation of TLRs prior to ischemia reprograms TLR signaling that occurs following ischemic injury. Such reprogramming leads to suppressed expression of pro-inflammatory molecules and enhanced expression of numerous anti-inflammatory mediators that collectively confer robust neuroprotection. Our findings indicate that numerous preconditioning stimuli lead to TLR activation, an event that occurs prior to ischemia and ultimately leads to TLR reprogramming. Thus genomic reprogramming of TLR signaling may be a unifying principle of tolerance to cerebral ischemia.

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Section: Mechanisms Of Neuroprotection—reprogramming Tlr Signalingmentioning

confidence: 99%

Toll-like receptor signaling in endogenous neuroprotection and stroke

2009

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“…It is a type I interferon (IFN), which includes IFN alpha (IFNA), IFN beta (IFNB), IFN delta (IFND), and IFN omega (IFNW). After binding to a common receptor, IFNA receptor 1 (IFNAR1), and IFNAR2, type I IFNs affect the production of inflammatory cytokines such as interleukin- (IL-) 1 β and tumor necrosis factor α (TNF- α ) [6, 7]. Thus, type I IFNs have widely recognized roles in inflammatory diseases, such as experimental allergic encephalomyelitis, multiple sclerosis, and spontaneous autoimmune diabetes [5, 8–10].…”

Section: Introductionmentioning

confidence: 99%

Interferon Tau Affects Mouse Intestinal Microbiota and Expression of IL-17

Ren¹,

Chen²,

Zhang

et al. 2016

Mediators of Inflammation

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This study was conducted to explore the effects of interferon tau (IFNT) on the intestinal microbiota and expression of interleukin 17 (IL-17) in the intestine of mice. IFNT supplementation increased microbial diversity in the jejunum and ileum but decreased microbial diversity in the feces. IFNT supplementation influenced the composition of the intestinal microbiota as follows: (1) decreasing the percentage of Firmicutes and increasing Bacteroidetes in the jejunum and ileum; (2) enhancing the percentage of Firmicutes but decreasing Bacteroidetes in the colon and feces; (3) decreasing Lactobacillus in the jejunum and ileum; (4) increasing the percentage of Blautia, Bacteroides, Alloprevotella, and Lactobacillus in the colon; and (5) increasing the percentage of Lactobacillus, Bacteroides, and Allobaculum, while decreasing Blautia in the feces. Also, IFNT supplementation decreased the expression of IL-17 in the intestines of normal mice and of an intestinal pathogen infected mice. In conclusion, IFNT supplementation modulates the intestinal microbiota and intestinal IL-17 expression, indicating the applicability of IFNT to treat the intestinal diseases involving IL-17 expression and microbiota.

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“…8 The mechanism by which IFN-␤ mediates these contrasting effects on Th1 cell generation operates, at least in part, by regulating DC expression of interleukin-12 (IL-12) family cytokines. Bosca et al 9 showed in mice that systemic administration of IFN-␤ might influence the response to proinflammatory stimuli, in particular Th1 cell-derived cytokines, through antagonism of IFN-␥ signaling.…”

Section: Introductionmentioning

confidence: 98%

Diverse Production of Interferonsα,β, andγby Airway Leukocytes of Asthmatics with Regard to Cigarette Smoking and Corticosteroid Treatment

Liebhart

Cembrzyńska-Nowak²,

Kulczak

et al. 2007

Journal of Interferon & Cytokine Research

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The production of interferon-alpha(IFN-alpha), IFN-beta, and IFN-gamma by airway leukocytes from induced sputa (IS) of asthmatics was investigated. The groups consisted of 32 corticosteroid-free asthmatics (A), with 13 nonsmokers (nS) and 19 smokers (S), and 30 inhaled corticosteroid-treated asthmatics (cA) with 14 nS and 16 S. The control healthy group (H) comprised 11 nS and 15 S. The levels of IFNs in media from cultures of IS leukocytes were assessed by ELISA. The cells of the smokers produced lower amounts of IFN-alpha than those of nonsmokers in groups H, A, and cA (p = 0.0417, 0.0002, 0.0495, respectively) and significantly higher amounts of IFNbeta than nonsmokers in groups H (p = 0.0044) and cA (p = 0.0007). No differences in the levels of IFN-gamma were observed between S and nS in groups H (p = 0.8148), A (p = 0.8339), and cA (p = 0.0722). In the entire group of smokers, smoking indices correlated negatively with IFN-alpha (R(S) = -0.4374, p = 0.0006), and positively with IFN-beta (R(S) = 0.4239, p = 0.0009). There was no correlation with IFN-gamma (R(S) = 0.0471, p = 0.7004). The results suggest that production of IFNs by the airway leukocytes of cA may be modified by cigarette smoking toward deficient production of IFN-alpha and excess production of IFN-beta, which may have implications in the pathophysiology of asthma.

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Anti-inflammatory action of type I interferons deduced from mice expressing interferon β

Cited by 22 publications

References 59 publications

Toll-like receptor signaling in endogenous neuroprotection and stroke

Toll-like receptor signaling in endogenous neuroprotection and stroke

Interferon Tau Affects Mouse Intestinal Microbiota and Expression of IL-17

Diverse Production of Interferonsα,β, andγby Airway Leukocytes of Asthmatics with Regard to Cigarette Smoking and Corticosteroid Treatment

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