Malevolent Designer News - The Brilliance of Creationism's Divine Sadist

Scanning electron micrograph of Salmonella typhimurium invading a human epithelial cell.

New insights into what helps Salmonella cause infections | Carl R. Woese Institute for Genomic Biology

Salmonella

The brilliance of creationism's favourite sadist was on display again recently, when researchers from the Department of Microbiology, University of Illinois at Urbana Champaign, Urbana, Illinois, USA, showed how the pathogen, Salmonella, is designed to not only survive being engulfed by the macrophages in our blood that are supposedly designed to protect us, but positively thrives and multiplies inside them. Although rarely fatal, Salmonella infection can be distressing and unpleasant with vomiting and diarrhoea, as I can attest from my childhood in rural Oxfordshire at a time when food and water hygiene left much to be desired.

So, it looks like creationism’s intelligent [sic] designer won that particular arms race with itself, in favour of the nasty pathogen designed to increase the suffering in the world. At least, that's the sort of nonsense creationists needs to believe to retain the childish belief that living things are made by a magic man in the sky.

The fact that salmonella can live happily inside a macrophage supposedly designed to kill pathogens has been known for some time, but what the University of Illinois researchers have discovered is just how it manages the trick. It's all down to the structure and function of the bacterium's surface membrane which detects and adjusts to the conditions in which the organism finds itself.
First, a little AI background on the pathogen:

Tell me all about Salmonella, what it does and how it evolved, please. Salmonella is a genus of bacteria that includes a variety of species, some of which can cause illness in humans and animals. The most common types associated with human infections are Salmonella enterica and Salmonella bongori. Salmonella enterica is further divided into numerous serotypes, each with distinct characteristics.

Pathogenic Strains:

1. Salmonella typhi and Salmonella paratyphi:
   • These strains cause typhoid fever and paratyphoid fever, respectively.
   • Transmission is primarily through contaminated food and water.
2. Non-Typhoidal Salmonella (NTS):
   • Causes gastroenteritis.
   • Commonly transmitted through contaminated food, such as undercooked poultry, eggs, and unpasteurized dairy products.

Symptoms:

Symptoms of Salmonella infection include diarrhea, abdominal cramps, fever, nausea, and vomiting. In severe cases, the infection can lead to systemic illness and may require medical intervention.

Evolution:

Salmonella has evolved through various mechanisms, including genetic mutations, horizontal gene transfer, and adaptation to different environments. Evolutionary processes have led to the development of different serotypes with varying pathogenicity and host specificity.

Horizontal Gene Transfer:
Salmonella can exchange genetic material with other bacteria through horizontal gene transfer, allowing for the acquisition of virulence factors and antibiotic resistance genes.

Host Adaptation:
Different Salmonella serotypes have adapted to specific hosts. For instance, some strains are adapted to infect humans, while others primarily affect animals. This host adaptation is a result of the evolutionary pressure exerted by the host's immune system and environmental factors.

Transmission:

Salmonella is often transmitted through the consumption of contaminated food or water. Contaminated surfaces, inadequate food handling, and improper cooking practices can contribute to the spread of the bacteria. Additionally, contact with infected animals or their environments can lead to transmission.

Prevention and Control:

Preventing Salmonella infections involve practicing good hygiene, proper food handling, and thorough cooking of potentially contaminated foods. Public health measures, including surveillance and monitoring of food production and distribution, are essential to control outbreaks.

Treatment:

the In most cases, Salmonella infections resolve on their own, and supportive care is provided to manage symptoms. However, severe cases may require antibiotic treatment. It is crucial to use antibiotics judiciously to avoid the development of antibiotic-resistant strains.

In summary, Salmonella is a diverse group of bacteria that can cause gastroenteritis and more severe systemic infections in humans. The evolution of different serotypes, adaptation to hosts, and the ability to exchange genetic material contribute to the pathogenicity and persistence of Salmonella in various environments. Public health measures and proper food safety practices are crucial for preventing and controlling Salmonella infections.

And some explanation of the technical terms used:

What is PhoPQ and what function does it have? PhoPQ is a two-component regulatory system found in bacteria, and it plays a crucial role in the response to environmental stress, particularly in the context of virulence and survival within host organisms. This system is commonly associated with Gram-negative bacteria, including Salmonella enterica, which we mentioned in the previous response. Here's a breakdown of the PhoPQ system and its function:

1. Two-Component Regulatory System:
   • PhoP: This is a transcriptional regulator protein.
   • PhoQ: This is a sensor kinase protein.
2. Activation Mechanism:
   • PhoPQ operates as a classic two-component signal transduction system. PhoQ, the sensor kinase, is activated by external signals, such as changes in the environment, including low magnesium or low pH. When these signals are detected, PhoQ undergoes autophosphorylation.
   • Phosphorylated PhoQ then transfers the phosphate group to PhoP, activating it. Activated PhoP acts as a transcription factor, regulating the expression of specific genes.
3. Function:
   • Virulence and Survival:
     • In the context of bacteria like Salmonella enterica, the PhoPQ system is often associated with virulence and survival within host organisms.
     • Activation of PhoP induces the expression of various genes that contribute to the bacteria's ability to survive in the host environment, including within macrophages.
   • Adaptation to Stress Conditions:
     • PhoPQ helps bacteria adapt to environmental stress conditions. For example, during infection, the host environment presents challenges such as low magnesium and acidic conditions. PhoPQ-regulated genes help the bacteria overcome these challenges.
   • Lipopolysaccharide Modification:
     • PhoPQ can regulate the modification of lipopolysaccharides (LPS) in the bacterial outer membrane. This modification is important for evading the host immune response.
   • Resistance to Antimicrobial Peptides:
     • The PhoPQ system also contributes to resistance against antimicrobial peptides produced by the host as part of the immune response.

Understanding the role of the PhoPQ system provides insights into the strategies bacteria employ to survive and establish infections in their hosts. It also presents potential targets for the development of antimicrobial therapies aimed at disrupting bacterial virulence and survival mechanisms.

The researcher’s work is described in the University of Illinois news release and in their published paper in the Journal of Bacteriology:

Salmonella is a foodborne pathogen that causes more than a million infections each year in the U.S. Concerningly, it can kill young, old, and immunocompromised individuals. What makes these bacteria especially dangerous is their ability to evade our immune responses.

Macrophages are designed to kill bacteria by spraying them with antibacterial products, exposing them to acidic environments, and withholding magnesium, all of which target the outer layers of the bacteria. Salmonella, however, has evolved mechanisms to survive and grow in this environment.

Under normal conditions, Salmonella uses a complex called Bam to assemble certain proteins that are transported to its outer membrane layer. In previous studies, the group have shown that inside macrophages, the complex is compromised and, as a result, Salmonella depends on the PhoPQ system to sense the environment and orchestrate necessary changes in the outer membrane.

Studies in other bacteria have shown that the TamAB complex performs similar functions to Bam, which led the researchers of the present study to ask whether it might be important in Salmonella. They found that the genes that were responsible for producing TamAB were being controlled by PhoPQ.

“We knew from other studies that TamA was similar to BamA in its structure. When we realized that PhoPQ was controlling this TamAB complex, we hypothesized that the Bam complex struggles in the macrophage and TamA is induced by PhoPQ to help,” said James Slauch (IGOH), a professor of microbiology.

To test their hypothesis, the researchers first removed TamAB from Salmonella. To their surprise, these mutants were still able to cause an infection in mice. However, when they also crippled the Bam complex, the mutants that lacked TamAB struggled.

The researchers also saw similar results when they recreated the macrophage-like conditions in test tubes and tested the different Salmonella mutants. They observed that mutants that lacked both the Bam and TamAB complexes were sensitive to vancomycin. This result is particularly intriguing because vancomycin is not used to treat Salmonella since it can't cross the outer membrane. This sensitivity suggests that the two complexes have a function in creating or maintaining the outer membrane, although the mechanism is not clear.

“Basically, TamAB helps create favorable conditions for the Bam complex to work but it's indirect,” said Yekaterina Golubeva, a research scientist in the Slauch lab.

It is still unclear what the indirect effect might be. “The problem is that studying the outer membrane is complicated because everything is interconnected. If you mess up the Bam complex, it disrupts additional machineries required for synthesis of the outer membrane. As a result, understanding the contributions of these proteins is difficult,” Slauch said.

Nonetheless, the researchers are now interested in figuring out how TamAB helps. To do so, they will be using suppressor mutants that have accumulated different types of mutations that can help them grow even if their Bam and Tam complexes are defective, providing insights into Salmonella’s outer membrane structure and function.

“There are efforts underway in biotechnology companies that are targeting the Bam complex as a way to treat Salmonella infections,” Slauch said. “Understanding the structure of the outer membrane when Salmonella is in a macrophage can help us understand what will affect its sensitivity to drugs and our results with vancomycin is consistent with that.”

ABSTRACT

Salmonella survive and replicate in macrophages, which normally kill bacteria by exposing them to a variety of harsh conditions and antimicrobial effectors, many of which target the bacterial cell envelope. The PhoPQ two-component system responds to the phagosome environment and induces factors that protect the outer membrane, allowing adaptation and growth in the macrophage. We show that PhoPQ induces the transcription of the tamAB operon both in vitro and in macrophages. The TamA protein is structurally similar to BamA, an essential protein in the Bam complex that assembles β-barrel proteins in the outer membrane, while TamB is an AsmA-family protein implicated in lipid transport between the inner and outer membranes. We show that the Bam machinery is stressed in vitro under low Mg²⁺, low pH conditions that mimic the phagosome. Not surprisingly, mutations affecting Bam function confer significant virulence defects. Although loss of TamAB alone confers no virulence defect, a tamAB deletion confers a synthetic phenotype in bam mutant backgrounds in animals and macrophages, and in vitro upon treatment with vancomycin or sodium dodecyl sulfate. Mutations affecting YhdP, which functions in partial redundancy with TamB, also confer synthetic phenotypes with bam mutations in the animal, but this interaction is not evident in vitro. Thus, in the harsh phagocytic environment of the macrophage, the outer membrane Bam machinery is compromised, and the TamAB system, and perhaps other PhoPQ-regulated factors, is induced to compensate. It is most likely that TamAB and other systems assist the Bam complex indirectly by affecting outer membrane properties.

IMPORTANCE

The TamAB system has been implicated in both outer membrane protein localization and phospholipid transport between the inner and outer membranes. We show that the β-barrel protein assembly complex, Bam, is stressed under conditions thought to mimic the macrophage phagosome. TamAB expression is controlled by the PhoPQ two-component system and induced in macrophages. This system somehow compensates for the Bam complex as evidenced by the fact that mutations affecting the two systems confer synthetic phenotypes in animals, macrophages, and in vitro in the presence of vancomycin or SDS. This study has implications concerning the role of TamAB in outer membrane homeostasis. It also contributes to our understanding of the systems necessary for Salmonella to adapt and reproduce within the macrophage phagosome.

Ramezanifard Rouhallah; Golubeva Yekaterina A.; Palmer Alexander D.; Slauch James M.
TamAB is regulated by PhoPQ and functions in outer membrane homeostasis during Salmonella pathogenesis
Journal of Bacteriology 205(10) e00183-23. DOI: 10.1128/jb.00183-23

© 2023 American Society for Microbiology.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

So, creationism's intelligent [sic] designer has designed an ingenious way to help Salmonella survive the mechanism it intelligently [sic] designed to protect us from pathogens like Salmonella. And creationist frauds make a fortune out of selling the notion of intelligent design to scientifically illiterate fools who have not the slightest understanding of the detail beneath the superficial appearance of design, and no intention of learning about it.

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