Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner

Rice, Teresa C.; Armocida, Stephanie M.; Kuethe, Joshua W.; Jain, Ayushi; Hildeman, David; Healy, Daniel P.; Gulbins, Erich; Caldwell, Charles C.

doi:10.1016/j.cellimm.2016.12.004

Cited by 12 publications

(12 citation statements)

References 58 publications

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“…Butyrate is well known for regulating T-cell function and the systemic immune response [ 31 ]. We have previously shown that colonic butyrate levels decrease following burn injury [ 26 ] and that butyrate reduces T cell death in an acid sphingomyelinase-dependent manner [ 32 ]. T cell depletion is a key component in burn-induced immunosuppression and enhanced susceptibility to opportunistic infections.…”

Section: Discussionmentioning

confidence: 99%

Burn injury alters the intestinal microbiome’s taxonomic composition and functional gene expression

2018

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Burn patients have a high risk of sepsis-related mortality even after surviving the initial injury. Immunosuppression increases the risk of sepsis after burn injury, as does the disruption of the intestinal epithelial barrier, which allows the translocation of bacteria and bacterial products into the circulation. The integrity of the intestinal epithelial barrier is largely maintained by the intestinal microbiota. Burn injury has been reported to result in significant changes in the intestinal microbiome composition. In this mouse study, we confirm these taxonomic differences in a full-thickness scald injury model using CF-1 mice. For the first time, we also address alterations in functional gene expression of the intestinal microbiota after burn injury to assess the microbiome’s physiological capabilities for overgrowth and pathogenic invasion: 38 pathways were differentially abundant between the sham and burn injury mice, including bacterial invasion of epithelial cells and gap- and adherens junction pathways.

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Section: Discussionmentioning

confidence: 99%

Burn injury alters the intestinal microbiome’s taxonomic composition and functional gene expression

2018

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“…The following cell types were identified using the following antibody combinations: Neutrophils: Ly-6G and CD11b; Resident macrophages: F4/80 and CD11b; Total CD4 T cells: CD4 and TCRβ (naïve: CD62L high ); Total CD8 T cells: CD8 and TCRβ (naïve: CD62L high ); and immature macrophages: Ly-6G − , Ly-6C + , and CD31 low . Cells were analyzed using an Attune Acoustic Focusing Cytometer and accompanying software (Life Technologies, Carlsbad, CA, USA), as previously described [ 38 ]. The BAL IL-6 and G-CSF levels were determined by a cytometric bead array per the manufacturer’s instructions (BD Biosciences) and as previously described [ 39 ].…”

Section: Methodsmentioning

confidence: 99%

A Murine Model of Persistent Inflammation, Immune Suppression, and Catabolism Syndrome

Pugh

Auteri

Goetzman

et al. 2017

IJMS

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Critically ill patients that survive sepsis can develop a Persistent Inflammation, Immunosuppression, and Catabolism Syndrome (PICS), which often leads to extended recovery periods and multiple complications. Here, we utilized a cecal ligation and puncture (CLP) method in mice with the goal of creating a model that concurrently displays all the characteristics of PICS. We observed that, after eight days, mice that survive the CLP develop persistent inflammation with significant myelopoiesis in the bone marrow and spleen. These mice also demonstrate ongoing immune suppression, as evidenced by the decreased total and naïve splenic CD4 and CD8 T cells with a concomitant increase in immature myeloid cells. The mice further display significant weight loss and decreased muscle mass, indicating a state of ongoing catabolism. When PICS mice are challenged with intranasal Pseudomonas aeruginosa, mortality is significantly elevated compared to sham mice. This mortality difference is associated with increased bacterial loads in the lung, as well as impaired neutrophil migration and neutrophil dysfunction in the PICS mice. Altogether, we have created a sepsis model that concurrently exhibits PICS characteristics. We postulate that this will help determine the mechanisms underlying PICS and identify potential therapeutic targets to improve outcomes for this patient population.

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“…Patients with extensive burns have burn-related immunosuppression [7, 8]. However, reports on the reactivation of latent VZV manifesting as either shingles or disseminated zoster in burn patients are rare.…”

Section: Discussionmentioning

confidence: 99%

Disseminated zoster in an adult patient with extensive burns: a case report

Kubota

Kosaka

Hokazono

et al. 2019

Virol J

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Background: Shingles (localized zoster) and disseminated zoster are caused by the reactivation of latent varicella zoster virus (VZV). Reactivation of VZV is related to impaired cell-mediated immunity. Extensive burns affecting a patient result in burn-related immunosuppression and cytokine storm. Despite immunosuppression in burn patients, the reactivation of VZV is extremely rare, whereas eczema herpeticum, caused by reactivation of latent herpes simplex virus (HSV), is common. We have found only 1 published case of VZV reactivation during burn treatment in the literature. Case presentation: A 51-year-old man was burned in a fire, which affected 60% of his total body surface area (TBSA), and also received inhalation injury (day 0). Despite fluid resuscitation, he showed persistent renal failure. Continuous hemodialysis and filtration (CHDF) combined with polymyxin B-immobilized fiber column direct hemoperfusion (PMX-DHP) therapy was used for cytokine modulation. Autologous and allogeneic skin grafting was performed. On day 15, multiple-drug-resistant Pseudomonas aeruginosa (MDRP) was detected from a blood specimen, and the patient developed multiple organ failure (MOF). On day 31, compact aggregations of small vesicles appeared on the intact skin of his left knee and left buttock. The vesicles were located within the 4th lumbar (L4) spinal dermatome. From day 32 to day 34, similar new vesicles arose on his intact skin and epithelializing skin-graft donor sites. We diagnosed disseminated zoster, based on the patient's age, the characteristic occurrence of the initial vesicles within a limited area of intact skin in the left L4 dermatome, and a positive Tzank smear. Serologic testing on day 36 showed a high level of anti-VZV immunoglobulin (Ig)G with low levels of anti-VZV IgM, anti-HSV IgG, and anti-HSV IgM. The patient was isolated in a negative-pressure room to avoid airborne spread of VZV. On day 52, the patient died. Conclusions: To the best of our knowledge, our patient is the second case of reactivation of VZV during burn treatment. It is unclear why reactivation of VZV is rare in patients with burn-related immunosuppression, whereas HSV reactivation is common. Cytokine modulation throughout the treatment period using CHDF combined with PMX-DHP might have been related to the rare reactivation of VZV in our patient. Our case provides an additional information on the relationship between the immune status of a patient with extensive burns and reactivation of latent VZV or HSV.

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Burn injury influences the T cell homeostasis in a butyrate-acid sphingomyelinase dependent manner

Cited by 12 publications

References 58 publications

Burn injury alters the intestinal microbiome’s taxonomic composition and functional gene expression

Burn injury alters the intestinal microbiome’s taxonomic composition and functional gene expression

A Murine Model of Persistent Inflammation, Immune Suppression, and Catabolism Syndrome

Disseminated zoster in an adult patient with extensive burns: a case report

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