<p>Molecular Mechanisms of <em>Salmonella</em> Effector Proteins: A Comprehensive Review</p>

Abstract

Salmonella can be categorized into many serotypes, which are specific to known hosts or broadhosts. It makes no difference which one of the serotypes would penetrate the gastrointestinal tract because they all face similar obstacles such as mucus and microbiome. However, following their penetration, some species remain in the gastrointestinal tract; yet, others spread to another organ like gallbladder. Salmonella is required to alter the immune response to sustain its intracellular life. Changing the host response requires particular effector proteins and vehicles to translocate them. To this end, a categorized gene called Salmonella pathogenicity island (SPI) was developed; genes like Salmonella pathogenicity island encode aggressive or modulating proteins. Initially, Salmonella needs to be attached and stabilized via adhesin factor, without which no further steps can be taken. In this review, an attempt has been made to elaborate on each factor attached to the host cell or to modulating and aggressive proteins that evade immune systems. This review includes four sections: (A) attachment factors or T3SS-independent entrance, (B) effector proteins or T3SS-dependent entrance, (c) regulation of invasive genes, and (D) regulation of immune responses.

Involvement of the Heat Shock Protein HtpG of Salmonella Typhimurium in Infection and Proliferation in Hosts

“…In severe cases, it can cause sepsis and systemic infections ( Desin et al., 2013 ). At present, the role of various effect factors of S. Typhimurium in the infected host has been fully explained ( LaRock et al., 2015 ; Azimi et al., 2020 ; dos Santos et al., 2020 ); however, the role of chaperone proteins is frequently ignored. Heat shock protein 90 (HSP90/HtpG) belongs to the family of heat shock proteins, which is highly conserved genetically and widely found in eukaryotes and prokaryotes ( Picard, 2002 ).…”

SAC1 regulates autophagosomal phosphatidylinositol-4-phosphate for xenophagy-directed bacterial clearance

“…Intracellular bacteria are known to manipulate host cell processes to develop replication-competent niches or avoid defense mechanisms ( Asrat et al, 2014 ; Case and Samuel, 2016 ; Kimmey and Stallings, 2016 ; Pao and Rape, 2019 ). Salmonella , as well as other pathogens, produces an array of effector proteins—with functions ranging from inducing uptake to developing a replication-competent vacuole ( Cardenal-Muñoz and Ramos-Morales, 2011 )—that act both redundantly and cooperatively to ensure survival ( Azimi et al, 2020 ; Ghosh and O’Connor, 2017 ). Our results highlight the importance of innate host defense to restrict bacterial replication and the role of bacterial factors in intracellular survival.…”

Detection of antimicrobial resistance, pathogenicity, and virulence potentials of non-typhoidal Salmonella isolates at the Yaounde abattoir using whole genome sequencing technique

“…About 82% of Salmonella isolates in the present study were endowed with not all but the necessary virulence factors (SipA, SipC, SopB, SopD, SopE, SopE2, SipB, EnvE, EnvF, InvA, InvE, SipD, Sii E, IagB, SptP, OrgB, PhoP, MisL, ShdA, rtn) to gain access into the host cells in order to esblish infection. Interestingly, all the effectors described in this phase of the infection are all SPI-1 encoded, indicating its active role in the Salmonella entry process [28–29]. Putative fimbriae usher (FimA, FimC, FimZ, HilD), pilin chaperon (ecpD1, CsgD) and flagellin (proteins FliZ, FliT) collectively called adhesion factors are additional virulence determinants to ensure successful colonization and persistence of Salmonella in the hosts [23].…”

“…Putative fimbriae usher (FimA, FimC, FimZ, HilD), pilin chaperon (ecpD1, CsgD) and flagellin (proteins FliZ, FliT) collectively called adhesion factors are additional virulence determinants to ensure successful colonization and persistence of Salmonella in the hosts [23]. Moreover, the expression of SipA and SipC required for invasion efficiency and of SopE and SopE2 for internalization efficiency [28–29] reinforced the pathogenicity potentials of our isolates. Despite the absence of SseI, SseJ, SspH and SifA, the expression of other effectors including SopB, SopE, SopA, SopD, SpiC, SpvB, SseB, SseC, and SseD, PipB2, SptP, SopE2 and antigen presentation proteins SpaK, SpaN, SpaS, and SpaR could still enable Salmonella isolates to achieve the maturation and tracfficking process of the Salmonella-containing vacuole, to replicate within the SCV and to control the host immune responses.…”