Yersinia‐triggered arthritis in IL‐12p40‐deficient mice: relevant antigens and local expression of Toll‐like receptor mRNA

Genaro, María Silvia Di; Cargnelutti, Diego Esteban; Castro, D. O.; Eliçabe, Ricardo Javier; Gutierrez, Johana; Correa, Silvia G.; Guzmán, A.M.

doi:10.1080/03009740600906651

Cited by 9 publications

(4 citation statements)

References 39 publications

(59 reference statements)

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“…These findings are consistent with recent studies implying a functional cross-talk between TNF and IL-12p40 in in vitro studies (54), collagen-induced arthritis (42), experimental autoimmune encephalomyelitis (55), and streptococcal cell wall-induced arthritis (32). In this regard, we observed a self-limiting Yersinia-induced ReA in p40 2/2 mice (14). Taken together, these data and the severe and progressive arthritis that developed in TNFRp55 2/2 mice indicate a critical role for this common cytokine subunit in modulating Th1 and Th17 responses during the development of ReA.…”

Section: Discussionsupporting

confidence: 82%

Lack of TNFR p55 Results in Heightened Expression of IFN-γ and IL-17 during the Development of Reactive Arthritis

Eliçabe¹,

Cargnelutti²,

Serer³

et al. 2010

The Journal of Immunology

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Reactive arthritis (ReA) is a type of arthritis originating from certain gastrointestinal or genitourinary infections. In previous studies, we reported the development of progressive Yersinia enterocolitica-induced ReA in mice lacking TNFR p55; however, the mechanisms underlying this effect are still uncertain. In this study, we investigated the impact of TNFR p55 deficiency in modulating Ag-specific Th1 and Th17 responses during this arthritogenic process. We found more severe ReA in TNFRp55−/− mice compared with their wild-type (WT) counterparts. This effect was accompanied by increased levels of Yersinia LPS in the joints of knockout mice. Analysis of the local cytokine profile revealed greater amounts of IFN-γ and IL-17 in arthritic joints of TNFRp55−/− mice compared with WT mice at day 21 postinfection. Moreover, altered IL-17 and IFN-γ production was observed in mesenteric and inguinal lymph nodes of Yersinia-infected TNFRp55−/− mice, as well as in spleen cells obtained from infected mice and restimulated ex vivo with bacterial Ags. Increased levels of cytokine secretion were associated with a greater frequency of CD4+IL-17+, CD4+IFN-γ+, and IL-17+IFN-γ+ cells in TNFRp55−/− mice compared with WT mice. Remarkably, Ab-mediated blockade of IL-17 and/or IFN-γ resulted in reduced joint histological scores in TNFRp55−/− mice. A mechanistic analysis revealed the involvement of p40, a common subunit of heterodimeric IL-12 and IL-23, in the generation of augmented IFN-γ and IL-17 production under TNFR p55 deficiency. Taken together, these data indicate that, in the absence of TNFR p55 signaling, Th1 and Th17 effector cells may act in concert to sustain the inflammatory response in bacterial-induced arthritogenic processes.

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Section: Discussionsupporting

confidence: 82%

Lack of TNFR p55 Results in Heightened Expression of IFN-γ and IL-17 during the Development of Reactive Arthritis

Eliçabe¹,

Cargnelutti²,

Serer³

et al. 2010

The Journal of Immunology

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“…At this time, we detected different bacterial load in PP, MLN and spleen between WT and KO mice. These data confirm our previous results [31] and suggest again that IL-12p40 plays a central role in early protection against Yersinia infection [31,32]. Late after the infection (day 21), the bacterial load in PP, MLN, spleen and joints decreased in both groups of mice.…”

Section: Discussionsupporting

confidence: 81%

“…To determine whether IL-12 deficiency affected systemic and mucosal Yersinia clarification, we assessed the bacteria number in PP, MLN, spleen, and lung at day 3 and 21 after infection. Moreover, since Y. enterocolitica O:3 causes reactive arthritis as sequelae of infection, we assessment the bacterial load in joints during early (day 3) and late (day 21) time after infection [31]. Since the initial immune response to bacteria or their antigenic components at mucosal surface level could influence the extent of their dissemination to the lung, we studied the bacterial load early after infection (day 3).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-12p40 contributes to protection against lung injury after oral Yersinia enterocolitica infection

Gutiérrez

Valdéz²,

Genaro

et al. 2008

Inflamm. res.

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“…On gestational day 18 at CT7 (middle of rest period), ankle joints were excised as previously described in Di Genaro et al [33]. The frozen tissue was placed in 1 mL of TRIzol reagent (Invitrogen, San Diego, CA, USA) and RNA extraction was performed as described by the manufacturer.…”

Section: Methodsmentioning

confidence: 99%

Peripheral Neuroimmunoendocrine Interactions: Contribution of TNFRp55 to the Circadian Synchronization of Progesterone and Cytokine Production in Joints of Mice in Late Pregnancy

Arias

Mayordomo

Silva

et al. 2018

Neuroimmunomodulation

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Objective: Circadian rhythms are generated by the suprachiasmatic nucleus of the hypothalamus and involve rhythmic expression of clock genes and proteins. This rhythmicity is transferred to peripheral tissues by neural and hormonal signals. Late pregnancy is considered a state of inflammation which impacts on peripheral tissues such as joints. Tumor necrosis factor (TNF) mediates inflammatory and circadian responses through its p55 receptor (TNFRp55). Neuroimmunoendocrine interactions in joints have not been studied completely. The purpose of this study was to analyze these interactions, investigating the circadian rhythms of progesterone (Pg) and pro- and anti-inflammatory cytokines in the joints at the end of pregnancy (gestational day 18). Moreover, the impact of TNFRp55 deficiency on these temporal oscillations was explored. Methods: Wild-type and TNFRp55-deficient (KO) C57BL/6 mice were kept under constant darkness in order to study their endogenous circadian rhythms. The expression of the clock genes Bmal1 and Per1 at circadian time 7 was studied by reverse transcription polymerase chain reaction in the ankle joints of nonpregnant and pregnant (gestational day 18) mice. In late pregnancy, Pg and the cytokines interleukin 17 (IL-17), IL-6, and IL-10 were measured in the joints throughout a 24-h period by radioimmunoassay and enzyme-linked immunosorbent assay, respectively. Results: A significant increase in Bmal1 and Per1 mRNA expression was detected in the joints of pregnant KO mice. Furthermore, KO mice displayed a desynchronization of articular Pg and cytokine production. Conclusions: Our results show that TNF, via TNFRp55 signaling, modulates articular Pg and cytokine circadian rhythms in late pregnancy. These findings suggest a temporal neuroimmunoendocrine association in peripheral tissues in late pregnancy.

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Yersinia‐triggered arthritis in IL‐12p40‐deficient mice: relevant antigens and local expression of Toll‐like receptor mRNA

Abstract: Yersinia-triggered arthritis in IL-12p40 deficient mice: relevant antigens and local expression of Toll-like receptor mRNA.

Cited by 9 publications

References 39 publications

Lack of TNFR p55 Results in Heightened Expression of IFN-γ and IL-17 during the Development of Reactive Arthritis

Lack of TNFR p55 Results in Heightened Expression of IFN-γ and IL-17 during the Development of Reactive Arthritis

Interleukin-12p40 contributes to protection against lung injury after oral Yersinia enterocolitica infection

Peripheral Neuroimmunoendocrine Interactions: Contribution of TNFRp55 to the Circadian Synchronization of Progesterone and Cytokine Production in Joints of Mice in Late Pregnancy

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