Evasion of MAIT cell recognition by the African<i>Salmonella</i>Typhimurium ST313 pathovar that causes invasive disease

Preciado-Llanes, Lorena; Aulicino, Anna; Canals, Rocı́o; Moynihan, Patrick J.; Zhu, Xiaojun; Jambo, Ndaru; Nyirenda, Tonney S.; Kadwala, Innocent; Gerós, Ana Sousa; Owen, Siân V.; Jambo, Kondwani; Kumwenda, Benjamin; Veerapen, Natacha; Besra, Gurdyal S.; Gordon, Melita A.; Hinton, Jay C. D.; Napolitani, Giorgio; Salio, Mariolina; Simmons, Alison

doi:10.1073/pnas.2007472117

Cited by 24 publications

(15 citation statements)

References 75 publications

(123 reference statements)

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“…Further, a recent study showed that Lineage 2 isolates of S . Typhimurium ST313 escape early immune recognition by MAIT cells (mucosal immune cells), via overexpression of the bacterial enzyme RibB 53 . Similar to ST313, our initial observations suggest that Salmonella 4,[5],12:i:- Lineages 2 and 3 may have also evolved specific immune evasion mechanisms to maintain the viability of host cells and confer a competitive advantage over Lineage 1 isolates and possibly other biphasic NTS.…”

Section: Discussionmentioning

confidence: 99%

Evolutionary dynamics of multidrug resistant Salmonella enterica serovar 4,[5],12:i:- in Australia

et al. 2021

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Salmonella enterica serovar 4,[5],12:i:- (Salmonella 4,[5],12:i:-) is a monophasic variant of Salmonella Typhimurium that has emerged as a global cause of multidrug resistant salmonellosis. We used Bayesian phylodynamics, genomic epidemiology, and phenotypic characterization to describe the emergence and evolution of Salmonella 4,[5],12:i:- in Australia. We show that the interruption of the genetic region surrounding the phase II flagellin, FljB, causing a monophasic phenotype, represents a stepwise evolutionary event through the accumulation of mobile resistance elements with minimal impairment to bacterial fitness. We identify three lineages with different population dynamics and discrete antimicrobial resistance profiles emerged, likely reflecting differential antimicrobial selection pressures. Two lineages are associated with travel to South-East Asia and the third lineage is endemic to Australia. Moreover antimicrobial-resistant Salmonella 4,[5],12:i- lineages efficiently infected and survived in host phagocytes and epithelial cells without eliciting significant cellular cytotoxicity, suggesting a suppression of host immune response that may facilitate the persistence of Salmonella 4,[5],12:i:-.

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Section: Discussionmentioning

confidence: 99%

Evolutionary dynamics of multidrug resistant Salmonella enterica serovar 4,[5],12:i:- in Australia

et al. 2021

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“…Furthermore, antigen availability may differ across different isolates of the same pathogen, as shown for Steptococcus pneumoniae, resulting in differential MAIT cell activation (Hartmann et al, 2018;Kurioka et al, 2017). A novel mechanism of evasion from MAIT cell recognition has been reported for the African Salmonella typhimurium ST313 isolate that causes invasive disease (Preciado-Llanes et al, 2020). In this isolate, overexpression of ribB, encoding for a key enzyme in the riboflavin biosynthetic pathway, increases the overall amount of non-agonist metabolites such as riboflavin, flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), so that infected cells fail to effectively activate MAIT cells (Preciado-Llanes et al, 2020).…”

Section: Evasion Of Mr1-dependent Antigen Presentationmentioning

confidence: 99%

“…A novel mechanism of evasion from MAIT cell recognition has been reported for the African Salmonella typhimurium ST313 isolate that causes invasive disease (Preciado-Llanes et al, 2020). In this isolate, overexpression of ribB, encoding for a key enzyme in the riboflavin biosynthetic pathway, increases the overall amount of non-agonist metabolites such as riboflavin, flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), so that infected cells fail to effectively activate MAIT cells (Preciado-Llanes et al, 2020). Importantly, these results also suggest that weak MAIT cell agonists of the lumazine family (Corbett et al, 2014) do not accumulate at concentrations sufficient to elicit MAIT cell activation and are rapidly converted into non antigenic riboflavin, FMN, and FAD (Preciado-Llanes et al, 2020).…”

Section: Evasion Of Mr1-dependent Antigen Presentationmentioning

confidence: 99%

Understanding and modulating the MR1 metabolite antigen presentation pathway

McWilliam

Salio

2021

Molecular Immunology

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“…This adaptation results in hyper-dissemination of Salmonella via CD11b + CCR7 + migratory DCs (migDCs) through the lymphatics ( Carden et al, 2017 ). ST313 has evolved other mechanisms to promote invasive disease such as overexpression of ribB to avoid detection by Mucosal-associated Invariant T cells by reducing their activation ( Preciado-Llanes et al, 2020 ). SseI, a known immunogen that induces a potent and sustained CD4 + T cell response, inhibits the migration of infected DCs ( Kurtz et al, 2014 ; Carden et al, 2017 ).…”

Section: Adaptive Immune Responses To Intestinal Salmonellamentioning

confidence: 99%

Salmonella Biofilm Formation, Chronic Infection, and Immunity Within the Intestine and Hepatobiliary Tract

Harrell

Hahn

D’Souza

et al. 2021

Front. Cell. Infect. Microbiol.

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Within the species of Salmonella enterica, there is significant diversity represented among the numerous subspecies and serovars. Collectively, these account for microbes with variable host ranges, from common plant and animal colonizers to extremely pathogenic and human-specific serovars. Despite these differences, many Salmonella species find commonality in the ability to form biofilms and the ability to cause acute, latent, or chronic disease. The exact outcome of infection depends on many factors such as the growth state of Salmonella, the environmental conditions encountered at the time of infection, as well as the infected host and immune response elicited. Here, we review the numerous biofilm lifestyles of Salmonella (on biotic and abiotic surfaces) and how the production of extracellular polymeric substances not only enhances long-term persistence outside the host but also is an essential function in chronic human infections. Furthermore, careful consideration is made for the events during initial infection that allow for gut transcytosis which, in conjunction with host immune functions, often determine the progression of disease. Both typhoidal and non-typhoidal salmonellae can cause chronic and/or secondary infections, thus the adaptive immune responses to both types of bacteria are discussed with particular attention to the differences between Salmonella Typhi, Salmonella Typhimurium, and invasive non-typhoidal Salmonella that can result in differential immune responses. Finally, while strides have been made in our understanding of immunity to Salmonella in the lymphoid organs, fewer definitive studies exist for intestinal and hepatobiliary immunity. By examining our current knowledge and what remains to be determined, we provide insight into new directions in the field of Salmonella immunity, particularly as it relates to chronic infection.

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Evasion of MAIT cell recognition by the AfricanSalmonellaTyphimurium ST313 pathovar that causes invasive disease

Cited by 24 publications

References 75 publications

Evolutionary dynamics of multidrug resistant Salmonella enterica serovar 4,[5],12:i:- in Australia

Evolutionary dynamics of multidrug resistant Salmonella enterica serovar 4,[5],12:i:- in Australia

Understanding and modulating the MR1 metabolite antigen presentation pathway

Salmonella Biofilm Formation, Chronic Infection, and Immunity Within the Intestine and Hepatobiliary Tract

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