Sepsis-Surviving Mice Are More Susceptible to a Secondary Kidney Insult*

Portella, Viviane Gomes; Silva-Filho, João Luiz; Landgraf, Sharon Schilling; Rico, Thais Baldez de; Vieira, Maria Aparecida Ribeiro; Takiya, Christina Maeda; Souza, Mariana C.; Henriques, Maria das Graças; Canetti, Cláudio; Pinheiro, Ana Acácia S.; Benjamim, Cláudia F.; Caruso-Neves, Celso

doi:10.1097/ccm.0b013e3182746696

Cited by 24 publications

(59 citation statements)

References 32 publications

(52 reference statements)

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“…Severe sepsis was performed in mice using a clinically relevant model of polymicrobial peritonitis induced by caecal ligation and puncture (CLP), which has been used extensively to investigate sepsis12132324252627. BALB/c mice undergoing lethal CLP were treated with antibiotics (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population

et al. 2017

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Patients who survive sepsis can develop long-term immune dysfunction, with expansion of the regulatory T (Treg) cell population. However, how Treg cells proliferate in these patients is not clear. Here we show that IL-33 has a major function in the induction of this immunosuppression. Mice deficient in ST2 (IL-33R) develop attenuated immunosuppression in cases that survive sepsis, whereas treatment of naive wild-type mice with IL-33 induces immunosuppression. IL-33, released during tissue injury in sepsis, activates type 2 innate lymphoid cells, which promote polarization of M2 macrophages, thereby enhancing expansion of the Treg cell population via IL-10. Moreover, sepsis-surviving patients have more Treg cells, IL-33 and IL-10 in their peripheral blood. Our study suggests that targeting IL-33 may be an effective treatment for sepsis-induced immunosuppression.

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Section: Resultsmentioning

confidence: 99%

IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population

et al. 2017

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“…Many authors agree that the renal effects of sepsis per se should not be underestimated. Recently, Portella et al found that sepsis-surviving mice were more susceptible to a secondary kidney insult [26], indicating that modifications induced by sepsis could aggravate a second kidney insult. Therefore, use of CMS may play a role as a secondary insult in patients with septic shock.…”

Section: Discussionmentioning

confidence: 99%

Colistin treatment in carbapenem-resistant Acinetobacter baumannii pneumonia patients: Incidence of nephrotoxicity and outcomes

Kwon

Yoon

et al. 2015

International Journal of Antimicrobial Agents

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“…Moreover, complement activation by albumin is a powerful underlying mechanism of tubular and interstitial injury via cytotoxic, proinflammatory, and fibrogenic effects, which often occur in renal diseases where proteinuria is present (Portella et al , 2013). In an experiment conducted in proximal tubular cells incubated with serum proteins, in vitro complement activation was observed, which could be associated with changes in the cytoskeleton, production of superoxide anion, hydrogen peroxide, and proinflammatory cytokines, such as IL-6 and TNF-α (Abbate et al , 2006).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of acute kidney injury induced by experimental Lonomia obliqua envenomation

et al. 2014

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Background Lonomia obliqua caterpillar envenomation causes acute kidney injury (AKI), which can be responsible for its deadly actions. This study evaluates the possible mechanisms involved in the pathogenesis of renal dysfunction. Methods To characterize L. obliqua venom effects we subcutaneously injected rats and examined renal functional, morphological and biochemical parameters at several time points. We also performed discovery based proteomic analysis to measure protein expression to identify molecular pathways of renal disease. Results L. obliqua envenomation causes acute tubular necrosis, which is associated with renal inflammation; formation of hematic casts, resulting from intravascular hemolysis; increase in vascular permeability and fibrosis. The dilation of Bowman’s space and glomerular tuft is related to fluid leakage and intra-glomerular fibrin deposition, respectively, since tissue factor procoagulant activity increases in the kidney. Systemic hypotension also contributes to these alterations and to the sudden loss of basic renal functions, including filtration and excretion capacities, urinary concentration and maintenance of fluid homeostasis. In addition, envenomed kidneys increases expression of proteins involved in cell stress, inflammation, tissue injury, heme-induced oxidative stress, coagulation and complement system activation. Finally, the localization of the venom in renal tissue agrees with morphological and functional alterations, suggesting also a direct nephrotoxic activity. Conclusions Mechanisms of L. obliqua-induced AKI are complex involving mainly glomerular and tubular functional impairment and vascular alterations. These results are important to understand the mechanisms of renal injury and may suggest more efficient ways to prevent or attenuate the pathology of Lonomia’s envenomation.

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Sepsis-Surviving Mice Are More Susceptible to a Secondary Kidney Insult*

Abstract: These results suggest that sepsis induces long-term effects in kidney structure aggravating tubule damage in a second kidney insult.

Cited by 24 publications

References 32 publications

IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population

IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population

Colistin treatment in carbapenem-resistant Acinetobacter baumannii pneumonia patients: Incidence of nephrotoxicity and outcomes

Mechanisms of acute kidney injury induced by experimental Lonomia obliqua envenomation

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