Severe gram positive bacterial infection in an ulcerative colitis patient treated with Infliximab

Marques, Margarida; Rodrigues, Susana; Mariz, Eva; Pinto, José; Videira, Taciana; Brito, Juan P.; Reis, Carina; Simões-Ventura, F.; Magro, Fernando

doi:10.1016/j.crohns.2009.08.005

Cited by 8 publications

(4 citation statements)

References 6 publications

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“…141 , 142 When the colonic epithelial barrier is disrupted, a negative immune response is triggered after exposure to Lachnospiraceae . 143 Our study shows a significantly decrease in the OTU of bacteria from Lachnospiraceae , but other gram-positive bacteria such as Peptococcaceae, Eubacteriaceae, Tissierellaceae, Streptococcaceae, Veillonellaceae, Coprobacillus , and Leuconostocaceae were all significantly increased in abundance within the gut microbiota of PNA animals.…”

Section: Discussionmentioning

confidence: 99%

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

et al. 2018

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Background: Conditions of excess androgen in women, such as polycystic ovary syndrome (PCOS), often exhibit intergenerational transmission. One way in which the risk for PCOS may be increased in daughters of affected women is through exposure to elevated androgens in utero. Hyperandrogenemic conditions have serious health consequences, including increased risk for hypertension and cardiovascular disease. Recently, gut dysbiosis has been found to induce hypertension in rats, such that blood pressure can be normalized through fecal microbial transplant. Therefore, we hypothesized that the hypertension seen in PCOS has early origins in gut dysbiosis caused by in utero exposure to excess androgen. We investigated this hypothesis with a model of prenatal androgen (PNA) exposure and maternal hyperandrogenemia by single-injection of testosterone cypionate or sesame oil vehicle (VEH) to pregnant dams in late gestation. We then completed a gut microbiota and cardiometabolic profile of the adult female offspring. Results: The metabolic assessment revealed that adult PNA rats had increased body weight and increased mRNA expression of adipokines: adipocyte binding protein 2, adiponectin, and leptin in inguinal white adipose tissue. Radiotelemetry analysis revealed hypertension with decreased heart rate in PNA animals. The fecal microbiota profile of PNA animals contained higher relative abundance of bacteria associated with steroid hormone synthesis, Nocardiaceae and Clostridiaceae, and lower abundance of Akkermansia, Bacteroides, Lactobacillus, Clostridium. The PNA animals also had an increased relative abundance of bacteria associated with biosynthesis and elongation of unsaturated short chain fatty acids (SCFAs). Conclusions: We found that prenatal exposure to excess androgen negatively impacted cardiovascular function by increasing systolic and diastolic blood pressure and decreasing heart rate. Prenatal androgen was also associated with gut microbial dysbiosis and altered abundance of bacteria involved in metabolite production of short chain fatty acids. These results suggest that early-life exposure to hyperandrogenemia in daughters of women with PCOS may lead to long-term alterations in gut microbiota and cardiometabolic function.

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Section: Discussionmentioning

confidence: 99%

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

et al. 2018

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“…TNF-␣ supports host antibacterial defenses through several mechanisms, including potentiation of the killing of bacteria by neutrophils and upregulation of vascular and adhesion molecules, which are necessary for neutrophil recruitment (40). In this regard, treatment of inflammatory diseases, such as lupus or rheumatoid arthritis, with neutralizing antibodies to TNF-␣ has led to increased risks of infectious diseases (41,42), including infections caused by S. aureus (43).…”

Section: Discussionmentioning

confidence: 99%

Shedding of Tumor Necrosis Factor Receptor 1 Induced by Protein A Decreases Tumor Necrosis Factor Alpha Availability and Inflammation during Systemic Staphylococcus aureus Infection

et al. 2013

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Staphylococcus aureus infections are an important public health concern due to their increasing incidence and high rates of mortality. The success of S. aureus as a pathogen is highly related to its enormous capacity to evade the host immune response. The critical role of tumor necrosis factor alpha (TNF-␣) in the initial host defense against systemic staphylococcal infection has been demonstrated in experimental models and may partially explain the lack of significant benefits observed in clinical trials attempting to neutralize this cytokine in septic patients. S. aureus protein A plays a key role in regulating inflammation through its ability to bind and signal through the TNF-␣ receptor 1 (TNFR1). In this study, we demonstrate that S. aureus, via protein A-mediated signaling, induces early shedding of TNFR1, which precedes the secretion of TNF-␣ in vitro and in vivo. The results obtained using a protein A-deficient mutant and tnfr1 ؊/؊ mice strongly suggest that the increased levels of soluble TNFR1 present during experimental S. aureus infection may neutralize circulating TNF-␣ and impair the host inflammatory response. Early shedding of TNFR1 induced by protein A may constitute a novel mechanism by which S. aureus subverts the host immune response.

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“…This finding was in stark contrast with bacterial sepsis in adults, for which beneficial effects from systemic TNF-a inhibition have repeatedly been reported (52,(55)(56)(57)(58). Serious infections of adults after treatment with etanercept have only occasionally been observed (59)(60)(61). Recently, the importance of TNF-a for the leukocyte recruitment in cytomegalovirus-infected newborn mice (62) has been reported.…”

Section: Discussionmentioning

confidence: 94%

Constitutive TNF‐α signaling in neonates is essential for the development of tissue‐resident leukocyte profiles at barrier sites

et al. 2019

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Newborn infants have a high disposition to develop systemic inflammatory response syndromes (SIRSs) upon inflammatory or infectious challenges. Moreover, there is a considerable trafficking of hematopoietic cells to tissues already under noninflammatory conditions. These age‐specific characteristics suggest a hitherto unappreciated crucial role of the vascular endothelium during the neonatal period. Here, we demonstrate that healthy neonates showed already strong endothelial baseline activation, which was mediated by a constitutively increased production of TNF‐α. In mice, pharmacological inhibition of TNF‐α directly after birth prevented subsequent fatal SIRS but completely abrogated the recruitment of leukocytes to sites of infection. Importantly, in healthy neonates, blocking TNF‐α at birth disrupted the physiologic leukocyte trafficking, which resulted in persistently altered leukocyte profiles at barrier sites. Collectively, these data suggest that constitutive TNF‐α—mediated sterile endothelial activation in newborn infants contributes to the increased risk of developing SIRS but is needed to ensure the postnatal recruitment of leukocytes to organs and interfaces.—Bickes, M. S., Pirr, S., Heinemann, A. S., Fehlhaber, B., Halle, S., Völlger, L., Willers, M., Richter, M., Böhne, C., Albrecht, M., Langer, M., Pfeifer, S., Jonigk, D., Vieten, G., Ure, B., von Kaisenberg, C., Förster, R., von Köckritz‐Blickwede, M., Hansen, G., Viemann, D. Constitutive TNF‐α signaling in neonates is essential for the development of tissue‐resident leukocyte profiles at barrier sites. FASEB J. 33, 10633–10647 (2019). http://www.fasebj.org

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Severe gram positive bacterial infection in an ulcerative colitis patient treated with Infliximab

Cited by 8 publications

References 6 publications

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

Shedding of Tumor Necrosis Factor Receptor 1 Induced by Protein A Decreases Tumor Necrosis Factor Alpha Availability and Inflammation during Systemic Staphylococcus aureus Infection

Constitutive TNF‐α signaling in neonates is essential for the development of tissue‐resident leukocyte profiles at barrier sites

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