Salmonella infections in immunocompromised adults

Gordon, Michael A.

doi:10.1016/j.jinf.2008.03.012

Cited by 394 publications

(345 citation statements)

References 88 publications

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“…S. enterica Typhimurium is a Gram-negative facultative intracellular pathogen that resides within membrane-bound vacuoles [17,18]. Infections with non-typhoidal strains of S. enterica, primarily the serovars Typhimurium and Enteritidis, cause a variety of clinical syndromes ranging from self-limiting gastroenteritis to life-threatening systemic disease seen in infants and HIV-infected adults, particularly in Africa [19,20]. Systemic infection is established after ingestion of contaminated food/ water and dissemination of bacteria from the intestine or mesenteric lymph nodes to other tissues including the spleen and liver [18].…”

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confidence: 99%

Death receptor 3 is essential for generating optimal protective CD4¹ T‐cell immunity against Salmonella

et al. 2012

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The TNF receptor superfamily member death receptor 3 (DR3) exacerbates Th2-and Th17-cell-mediated inflammatory and autoimmune conditions, yet no role in host defence has been reported. Here, we examined the role of DR3 during infection with Salmonella enterica serovar Typhimurium. Infection resulted in protracted expression of the DR3 ligand TL1A but not the related TNF superfamily proteins OX40L or CD30L. TL1A expression was localized to splenic F4/80 1 macrophages where S. enterica Typhimurium replicates, and temporally coincided with the onset of CD4 1 -cell expansion. To address the relevance of the TL1A-DR3 interaction, we examined immune responses to S. enterica Typhimurium in mice lacking DR3. Infected DR3 À/À mice harboured reduced numbers of antigen-experienced and proliferating CD4 1 T cells compared with WT mice. Furthermore, the frequency of IFN-c 1 CD4 1 T cells in DR3 À/À mice was lower throughout the time of bacterial clearance. Importantly, bacterial clearance, which is dependent on Th1 cells, was also impaired in DR3 À/À mice. This defect was intrinsic to CD4 1 T cells as evidenced by an increase in bacterial burden in RAG2-deficient mice receiving DR3 À/À CD4 1 T cells compared with WT CD4 1 -cell recipients. These data establish for the first time a role for DR3 in a host defence response.Key words: Costimulation . DR3 . Th1 cells . TNF receptor superfamily . TNFRSF25 Supporting Information available online IntroductionMembers of the tumour necrosis factor receptor superfamily (TNFRSF), such as CD27, CD30, OX40 and 4-1BB, are key players in the regulation of T-cell-mediated immune responses [1,2]. Collectively, these receptors provide costimulatory signals to antigen-stimulated T cells that enhance their expansion and survival. Thus, costimulation by various members of the TNFRSF augments the magnitude of the primary and/or secondary T-cell response and contributes to host protection against infection [3,4]. The involvement of different TNFRSF members in regulating T-cell responses varies however, with some TNFRSF members contributing preferentially towards enhanced memory generation [3] or local responses within the inflamed tissue [5]. The requirement for multiple TNFRSF members probably arises due to distinct temporal patterns of costimulatory receptor and ligand expression, which are likely to be controlled by factors such as pathogen type and virulence [4,6].Death receptor 3 (DR3, TNFRSF25) is a member of the TNFRSF that is most similar in sequence to TNFR1 [7]. DR3 Eur. J. Immunol. 2012. 42: 580-588 580 contains a death domain that binds to TRADD (TNFR1-associated death domain protein), a component of the TNFR1 signalosome that is capable of recruiting pro-caspase 8 as well as activating NF-kB [7]. Unlike TNFR1 however, which is widely expressed, expression of DR3 is limited primarily to T cells, cells of the monocyte/macrophage lineage and lymphoid tissue inducer (LTi) cells [8][9][10]. DR3 interacts with TL1A (TNFSF15), a TNF-like protein that is expressed on activated macrophages,...

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Death receptor 3 is essential for generating optimal protective CD4¹ T‐cell immunity against Salmonella

et al. 2012

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“…Bunlar; malignansiler, romatolojik hastalıklar, tümör nekroz faktörü blokajı (örn. etanersept veya infliksimab), transplantasyon, insan immünyetmezlik virüsü (HIV) infeksiyonu ve konjenital immündefektlerdir [5][6][7][8] . Diğer predispozan faktörler ise hemoglobinopatiler (özellikle orak hücreli anemi), karaciğer hastalıkları, şistozomiyaz ve kronik granülomatöz hastalıklardır.…”

Section: Discussionunclassified

Bacteremia Due to Quinolone Resistant Salmonella enteritidis: A Case Report

Mert¹,

Yilmaz²,

Kılıçaslan³

et al. 2017

FLORA

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“…Sin embargo, en pacientes con compromiso inmunológico como diabéticos 1 , cirróticos 2 , personas con infección por VIH 3 y ancianos 4 puede causar cuadros graves y de presentación atípica como abscesos cerebrales, suprarrenales, hepáticos, esplénicos, ováricos, musculares y cervicales, entre otras localizaciones. Dentro de las infecciones por Salmonella no Typhi, las infecciones focales se estiman entre 7-12% 5 .…”

Section: Introductionunclassified

Tumor cervical por Salmonella Typhimurium como forma de presentación clínica de SIDA en un paciente con infección por VIH

Echavarri

et al. 2011

Rev. chil. infectol.

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Caso Clínicowww.sochinf.cl 363Tumor cervical por Salmonella Typhimurium como forma de presentación clínica de SIDA en un paciente con infección por VIHSebastián Paredes E., Constanza Norambuena N., Sylvia Echavarri V. y Martín Lasso B.Cervical mass caused by Salmonella Typhimurium as a clinical presentation of AIDS in a HIV-positive patientInfections due to non-typhi salmonellae (NTS) generally cause a mild and self-limited gastrointestinal disease. However, there have been reports of atypical and severe presentations in immunocompromised patients. We report the case of a male patient who consulted with a cervical mass. He was found to be HIV-positive and Salmonella Typhimurium was isolated in one blood culture and cervical mass tissue culture. We discuss the relevance of infections by NTS in immunodefi cient patients because they present with more severe illness than normal population. We emphasize the importance of NTS bacteremia as a marker of underlying immunodefi ciency. We present some localized infection sites reported in the literature and their relation with particular diseases. We discuss the future relevance that an early start of antiretroviral therapy (ART) may have in HIV patients with NTS acute bacteremia or focal infections. Because infections by NTS can be severe and highly lethal they must be considered in the differential diagnosis of causative organisms of localized infections and bacteremia in HIV patients.

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Salmonella infections in immunocompromised adults

Cited by 394 publications

References 88 publications

Death receptor 3 is essential for generating optimal protective CD4¹ T‐cell immunity against Salmonella

Death receptor 3 is essential for generating optimal protective CD4¹ T‐cell immunity against Salmonella

Bacteremia Due to Quinolone Resistant Salmonella enteritidis: A Case Report

Tumor cervical por Salmonella Typhimurium como forma de presentación clínica de SIDA en un paciente con infección por VIH

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Salmonella infections in immunocompromised adults

Cited by 394 publications

References 88 publications

Death receptor 3 is essential for generating optimal protective CD41 T‐cell immunity against Salmonella

Death receptor 3 is essential for generating optimal protective CD41 T‐cell immunity against Salmonella

Bacteremia Due to Quinolone Resistant Salmonella enteritidis: A Case Report

Tumor cervical por Salmonella Typhimurium como forma de presentación clínica de SIDA en un paciente con infección por VIH

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Death receptor 3 is essential for generating optimal protective CD4¹ T‐cell immunity against Salmonella

Death receptor 3 is essential for generating optimal protective CD4¹ T‐cell immunity against Salmonella