ESCHERICHIA COLI RECEPTORS AND PATHOGENETIC MECHANISMS

Caraffa Al, Pellegrino R.  Escherichia coli receptors and pathogenetic mechanisms. International Journal of Infection. 2022;6(2):56-60

Al. Caraffa¹ and R. Pellegrino^2*

¹ School of Pharmacy, University of Camerino, Camerino, Italy;
² Physiatrist and Pain Therapist, Lecce, Italy.

*Correspondence to:
Dr. Raffaello Pellegrino,
Physiatrist and Pain Therapist,
Lecce-Castromediano/Cavallino,
Via S. Pelico 34,
73100 Lecce, Italy.
e-mail: drpellegrino@yahoo.it

Received: 02 May, 2022 Accepted: 12 August, 2022

ISSN 1972-6945 [online] Copyright 2022 © by Biolife-publisher This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: all authors report no conflicts of interest relevant to this article.

ABSTRACT

Escherichia coli (E. coli) is a group of bacteria found in humans and animals. Some strains can be highly pathogenic and cause severe immune and inflammatory reactions. E. coli is a member of the Enterobacteriaceae family and is a Gram-negative rod-shaped bacteria that has peritrichous flagella, which allow the bacteria to move. Pathogenic E. coli produces various toxins such as Shiga toxin (Stx) that disrupt normal cellular functions, inhibit protein synthesis, and cause cellular. Heat-labile (LT) and heat-stable (ST) enterotoxins are produced by enterotoxigenic E. coli (ETEC), and can cause intestinal ion alteration and diarrhea. Pathogenic E. coli is capable of injecting virulence factors directly into host cells and uses some antigens to carry out its pathogenic action. E. coli also uses immune mechanisms, such as alteration of surface antigens, to escape the immune response. Inhibition of E. coli and prevention with the use of vaccines or specific antibodies improves the infectious state and human health.

KEYWORDS: Escherichia coli, Gram-negative bacterium, pathogenetic mechanism, E. Coli receptor, virulence

INTRODUCTION

Escherichia coli (E. coli) is a diverse group of bacteria commonly found in the intestines of humans and animals. While most strains are harmless, some can cause serious food poisoning, infections, and diseases. E. coli is a Gram-negative bacterium that frequently exists in the lower intestine of warm-blooded organisms. This rod-shaped bacterium is a member of the Enterobacteriaceae family and is one of the most extensively studied prokaryotic model organisms in microbiology.

E. coli has specific morphological characteristics. It is a rod-shaped cylindrical bacillus and typically appears as short rods. It has a dimension of about 2 to 4 micrometers (µm) in length and 0.4 to 0.7 µm in diameter (1,2). In the laboratory, this Gram-negative bacillus does not retain the crystal violet stain used in the Gram stain procedure and appears red or pink under the microscope due to counterstaining, usually with safranin or fuchsin.

E. coli is usually found as single bacterium or in pairs. E. coli bacteria do not form clusters or chains, which distinguishes them from other types of bacteria. Many strains of E. coli possess peritrichous flagella, which are flagella distributed over the entire surface of the cell that allow the bacteria to move. Some strains of E. coli have a polysaccharide capsule surrounding the cell, which can help evade the host immune system and increase virulence (3). As a Gram-negative bacterium, E. coli has a characteristic cell wall structure consisting of a thin layer of peptidoglycan surrounded by an outer membrane containing lipopolysaccharides (LPS) (4). The outer membrane also contains proteins, lipoproteins, and porins (5). E. coli does not form endospores, which are a type of dormant, hardy, non-reproductive structure that some bacteria produce to withstand unfavorable conditions (6). These morphological traits aid in the identification and study of E. coli in various microbiological and medical research contexts.

DISCUSSION

E. coli presents various molecular mechanisms and biochemical processes essential for its survival, growth, and pathogenicity. Of the molecular mechanisms of E. coli, DNA replication is important, which originates from the replication of the circular chromosome, a single origin of replication called oriC (7). E. coli primarily uses DNA polymerase III for chromosome replication, with DNA polymerase I involved in the removal of RNA primers and DNA repair (8). Transcription occurs through RNA polymerase which transcribes DNA into mRNA. Sigma factors are proteins that bind to RNA polymerase and direct it to specific promoters.

Translation occurs through ribosomes which translate mRNA into proteins. E. coli has 70S ribosomes, composed of 50S and 30S subunits (9). Gene regulation in E. coli occurs through the lac Operon which controls lactose metabolism and includes the lacZ, lacY, and lacA genes, regulated by the lac repressor and catabolite activator protein (CAP) (10).

In metabolic processes, E. coli breaks down glucose through glycolysis to produce pyruvate, ATP, and NADH (11). The TCA cycle (Krebs Cycle) processes acetyl-CoA to produce ATP, NADH, and FADH2. Furthermore, E. coli can perform oxidative phosphorylation under aerobic conditions, using the electron transport chain to generate ATP (12). Under anaerobic conditions, E. coli can perform oxidative phosphorylation using the electron transport chain to generate ATP (13). Again, in anaerobic conditions, E. coli can ferment sugars, producing organic acids, alcohol, and gases as end products (14). E. coli synthesizes all 20 standard amino acids and nucleotides de novo (15). Furthermore, in cell wall synthesis, E. coli synthesizes peptidoglycan, an important component of its cell wall, which involves the assembly of N-acetylglucosamine and N-acetylmuramic acid (16).

E. coli acts through Tar and Tsr receptors, which sense chemical gradients in the environment and mediate chemotaxis, allowing bacteria to move toward attractants or away from repellents (17). The outer membrane receptors are porins such as OmpF and OmpC that form channels through which small molecules can diffuse (18). TonB-dependent receptors are FepA and FhuA receptors which are involved in the uptake of scarce resources such as iron by use of energy derived from the TonB complex (19). Regarding fimbrial adhesions, type 1 pili mediate adhesion to tissue and are important in the early stages of infection (20). The P Pili are involved in the attachment to the urinary tract epithelium, which is crucial for uropathogenic E. coli (UPEC) (21). Understanding these molecular mechanisms, biochemical processes, and receptor functions provides insights into how E. coli survives, adapts, and sometimes causes disease in host organisms.

E. Coli is broadly classified into six groups of pathogenic strains (Table I). Each pathogenic group has specific virulence factors that enable it to cause disease. These include adhesins, toxins, invasins, and secretion systems.

Table I. The broadly classified pathogenic strains of Escherichia coli.

Pathogenic E. coli produces various toxins, such as Shiga toxins (Stx), that disrupt normal cellular functions (22). These toxins produced by enterohemorrhagic E. coli (EHEC) inhibit protein synthesis, leading to cell death (23). Heat-labile (LT) and Heat-stable (ST) enterotoxins are produced by enterotoxigenic E. coli (ETEC), causing diarrhea by altering ion transport in the intestines (24).

Invasins are proteins that facilitate bacterial invasion of host cells. Invasion plasmid antigens (Ipa) are used by enteroinvasive E. coli (EIEC) to invade and multiply within intestinal cells (25). Pathogenic E. coli employs sophisticated secretion systems to inject virulence factors directly into host cells. The type III secretion system (T3SS) is used by enteropathogenic E. coli (EPEC) and EHEC to inject effector proteins into host cells, disrupting cellular processes and facilitating colonization (26).

ETEC adheres to the small intestine using colonization factor antigens (CFA) and produces enterotoxins (LT and ST) that stimulate fluid secretion, leading to diarrhea (27). The virulence factors are CFAs, LT, and ST. EPEC attaches to intestinal epithelial cells using bundle-forming pili (BFP) and forms characteristic attaching and effacing (A/E) lesions through the T3SS (28). Virulence factors are BFP, T3SS, Esp proteins. EHEC, in particular O157, adheres to the colon using intiman and T3SS, producing Stx that cause severe damage to intestinal and renal cells (29). UPEC colonizes the urinary tract using P type 1 pili and fimbriae, producing hemolysin and cytotoxic necrotizing factor 1 (CNF1) to damage host cells (30). The genes encoding these virulence factors are often located on plasmids, which are extrachromosomal DNA elements that can be transferred between bacteria and contribute to the spread of virulence traits.

The E. coli pathogen interacts with host cells in several ways such as adhesion, invasion, toxin production, and immune evasion. In adhesion, initial attachment to the host cell surface is achieved by adhesins. Invasion intends the entry into host cells (e.g. EIEC). Toxin production refers to the disruption of host cellular functions. And immune evasion refers to the mechanisms used by the microorganism to avoid host immune responses, such as alteration of surface antigens (31).

CONCLUSIONS

The molecular aspects of E. coli pathogenesis have crucial clinical implications. Diagnosis occurs through molecular techniques, such as PCR and sequencing, that can identify specific virulence genes. Targeting specific virulence factors (e.g., anti-adhesive therapies, neutralizing toxins) can improve treatment outcomes, while prevention is achieved through the use of vaccines targeting the main virulence factors for some E. coli pathotypes.

Conflict of interest

The authors declare that they have no conflict of interest.

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