In vivo synthesis of bacterial amyloid curli contributes to joint inflammation during S. Typhimurium infection

Miller, Amanda L.; Pasternak, J. Alex; Medeiros, Nicole J.; Nicastro, Lauren K.; Tursi, Sarah A.; Hansen, Elizabeth G.; Krochak, Ryan; Sokaribo, Akosiererem S.; MacKenzie, Keith D.; Palmer, Melissa B.; Herman, Dakoda J.; Watson, Nikole L.; Zhang, Yi; Wilson, Heather L.; Wilson, Ronald P.; White, Aaron P.; Tükel, Çaǧla

doi:10.1371/journal.ppat.1008591

Cited by 35 publications

(36 citation statements)

References 69 publications

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“…Although these conditions are somewhat artificial, the c-di-GMP regulatory principles could be an important observation. We recently discovered that curli can be synthesized by S. typhimurium during murine infections, with csgD transcription activated at 37 °C in vivo [ 91 ]. It is also of note that iron limitation [ 52 ] and exposure to bile [ 92 ] can alleviate temperature-based repression of csgD transcription.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Activation of CsgD in the Regulation of Salmonella Biofilms

et al. 2020

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Among human food-borne pathogens, gastroenteritis-causing Salmonella strains have the most real-world impact. Like all pathogens, their success relies on efficient transmission. Biofilm formation, a specialized physiology characterized by multicellular aggregation and persistence, is proposed to play an important role in the Salmonella transmission cycle. In this manuscript, we used luciferase reporters to examine the expression of csgD, which encodes the master biofilm regulator. We observed that the CsgD-regulated biofilm system responds differently to regulatory inputs once it is activated. Notably, the CsgD system became unresponsive to repression by Cpx and H-NS in high osmolarity conditions and less responsive to the addition of amino acids. Temperature-mediated regulation of csgD on agar was altered by intracellular levels of RpoS and cyclic-di-GMP. In contrast, the addition of glucose repressed CsgD biofilms seemingly independent of other signals. Understanding the fine-tuned regulation of csgD can help us to piece together how regulation occurs in natural environments, knowing that all Salmonella strains face strong selection pressures both within and outside their hosts. Ultimately, we can use this information to better control Salmonella and develop strategies to break the transmission cycle.

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Section: Discussionmentioning

confidence: 99%

Metabolic Activation of CsgD in the Regulation of Salmonella Biofilms

et al. 2020

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“…However, antibodies to curli have been detected in the serum of patients recovering from NTS infection and recent work in mice orally infected with S . Typhimurium demonstrated the production of curli amyloids in the gastrointestinal tract, suggesting that expression of biofilm genes does occur on some level during human infection ( Tursi and Tukel, 2018 ; Miller et al, 2020 ).…”

Section: Salmonella Biofilms Within the Infected Hostmentioning

confidence: 99%

“…While persistent and/or recurrent NTS infections of the human intestine have been documented, reports of cases are limited and do not provide any concrete evidence that would implicate the involvement of biofilms (Musher and Rubenstein, 1973;Kazemi et al, 1974;Buchwald and Blaser, 1984;Marzel et al, 2016;Gal-Mor, 2019). However, antibodies to curli have been detected in the serum of patients recovering from NTS infection and recent work in mice orally infected with S. Typhimurium demonstrated the production of curli amyloids in the gastrointestinal tract, suggesting that expression of biofilm genes does occur on some level during human infection (Tursi and Tukel, 2018;Miller et al, 2020).…”

Section: Salmonella Biofilms Within the Infected Hostmentioning

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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“…The infected mice generated increased levels of anti-dsDNA autoantibodies and joint inflammation. They hypothesized that the study provided the relation between bacterial amyloids like curli and human amyloids and their association with diseases such as Alzheimer's Disease (52).…”

Section: Salmonellamentioning

confidence: 99%

Bacterial molecular mimicry in autoimmune diseases

Palma

2021

Curr Biosci

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Bacterial molecular mimicry in autoimmune diseases is one of the leading mechanisms by which microorganisms may induce autoimmunity and survive in the host. The main purpose of the current study was to determine the main microbes that elicit autoimmune reactions through molecular mimicry and identify the most relevant approaches to investigate this mechanism. A classic example is the M protein of Streptococcus pyogenes, which induces antibody cross-reactivity with a cardiac protein and causes rheumatic fever. Another notable example is the protein from Porphyromonas gingivalis that closely resembles the human heat shock protein and accelerates atherosclerotic. There is evidence that antibodies against Helicobacter pylori CagA interact with different parts of smooth muscle and endothelial cells enhancing atherosclerotic vascular disease. Recently, one cause of infertility has been associated with Staphylococcus aureus molecular mimicry that triggers an antibody response that cross-reacts with human spermatozoa proteins. Further examples of bacterial molecular mimicry are associated with Chlamydia pneumoniae, Escherichia coli, Yersinia, and Salmonella. From the literature, the most widely used methods in this field are Basic Local Alignment Search Tool (BLAST), serological assays, and phage display. The subjects of particular concern are vaccine cross-reactivity and immunosuppressive drugs side-effects, therefore alternative approaches are needed. Such an approach is phage display where therapeutic antibody fragments obtained by this technique have been used in the treatment of autoimmune diseases by neutralizing the pathological effects of autoantibodies. Phage display libraries are constructed from the antibody repertoires of autoimmune disease patients. Antibody fragments without the Fc domain can not interact with Fc receptors and proteins of the complement system and trigger autoimmune diseases. Another approach is to block the Fc receptors. In conclusion, this review highlights key aspects of bacterial molecular mimicry to better understand the factors associated with autoimmune diseases and encourage further research in this field.

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In vivo synthesis of bacterial amyloid curli contributes to joint inflammation during S. Typhimurium infection

Cited by 35 publications

References 69 publications

Metabolic Activation of CsgD in the Regulation of Salmonella Biofilms

Metabolic Activation of CsgD in the Regulation of Salmonella Biofilms

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

Bacterial molecular mimicry in autoimmune diseases

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