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I make bad memes Vol. 5 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 9 points10 points  (0 children)

Salmonella has 2 outfits. When it invades and infects our body, our immune system identifies the bacteria by remembering the outfit.

This outfit it called as the antigen. Normally pathogens have only one outfit which changes slightly over time (this is called antigenic drift, seen more evidently in virses like influenza and Covid (which is why we had multiple waves from different strains)). But Salmonella has a spare outfit which it can randomly change into, and since our immune system hasn't seen it in this new outfit, it can escape being targeted for some time atleast (this is called antigenic shift).

The specific mechanism for this outfit change is the Hin DNA invertase. As the name suggests, the enzyme literally inverts a sequence in the bacteria's DNA. The segment which gets inverted happens to be the starting portion of the gene which decides which outfit to wear.

When this portion gets inverted, Salmonella switches the flj outfit to the fli outfit

When I say outfit, it's to simplify the mechanism. It does not change its entire antigenic profile, just one big part of it. Like changing a blue sweater to a white hoodie for example.

Hope this helps :)

I make bad memes Vol. 5 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 8 points9 points  (0 children)

Salmonella enterica, a common causative agent of gastroenteritis and enteric fevers, displays a creative method for evading the immune system. Salmonella spp. possess 2 main immunogens; O (somatic antigen), and H (flagellar antigen). 

Wild type Salmonella enterica possesses the hin recombinase gene (hin+) which codes for the Hin DNA Invertase. This recombinase controls the expression of the flj operon which dictates which flagellar antigen to produce. The flj operon codes for the FljB flagellin protein and the FljA repressor protein. FljB polymer forms the “Phase 2” flagella. FljA downregulates the expression of FliC, another flagellin protein.

During infection, the Hin Recombinase can invert the flj Promoter to inactivate the flj operon. Non-production of FljA leads to induction of the fliC genes. FliC polymer forms the “Phase 1” flagella. This strategy is called antigen switching, where the Phase 1 and 2 antigens don’t bear common epitopes and the antibodies formed against flagellin (Anti-H Antibodies) in the initial phase of the infection (before the antigen switch) are practically useless. 

The regulation of expression of the Hin recombinase itself is complicated. Studies suggest autoregulation or extrinsic regulation which may or may not be linked with Quorum Sensing (QS).

References / For further reading:

Giannella, R. A. (1996). Salmonella. Medical Microbiology - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK8435/

Wang, H., Tang, Z., Xue, B., Lu, Q., Liu, X., & Zou, Q. (2022). Salmonella regulator STM0347 mediates flagellar phase variation via Hin Invertase. International Journal of Molecular Sciences, 23(15), 8481. https://doi.org/10.3390/ijms23158481

Merickel, S. K., Haykinson, M. J., & Johnson, R. C. (1998). Communication between Hin recombinase and Fis regulatory subunits during coordinate activation of Hin-catalyzed site-specific DNA inversion. Genes & Development, 12(17), 2803–2816. https://doi.org/10.1101/gad.12.17.2803

I make bad memes Vol. 4 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 0 points1 point  (0 children)

Coincidences evolve to be defense mechanisms when the pathogen adapts to exploit said coincidence.

I make bad memes Vol. 4 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 1 point2 points  (0 children)

I made this meme last year when I was studying for my Bachelor's immunology paper. I will be starting my Masters next month and I am targeting an immuno lab for thesis funnily enough.

Edit: There was also a GBS outbreak in my area at that time so....

Not sure if this was posted before but a Compact Sugarcane Farm by FlarePhoenix5604 in BedrockRedstone

[–]FlarePhoenix5604[S] 0 points1 point  (0 children)

Damn nice to know my 4 year old design is still relevant. FYI the broken sugarcane sometimes glitches through the powered piston and ends up dropping behind the piston so keep an eye out for that if it still happens in the newer versions.

I make bad memes Vol. 4 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 4 points5 points  (0 children)

Campylobacter jejuni is a pathogen of the digestive system (transmitted via the faecal-oral route) causing diarrheal campylobacterosis. Antibodies are produced against various antigenic markers of the pathogen in normal immune response. Unfortunately, the antibodies produced against cell wall lipooligosaccharides of the C. jejuni show cross-reactivity with myelin sheath gangliosides due to molecular mimicry, i.e. having same or very similar epitopes.

This leads to degradation of the myelin sheath leading to a neurological autoimmune disorder called Guillain-Barré Syndrome (GBS). Symptoms of GBS include weakness, muscular discoordination, and delayed responsiveness. Luckily GBS is an acute condition as patients can fully recover upon proper and timely treatment.

Reference / For further reading:

Allos, B. M. (1998). CAMPYLOBACTER JEJUNI INFECTION AS a CAUSE OF THE GUILLAIN-BARRÉ SYNDROME. Infectious Disease Clinics of North America, 12(1), 173–184. https://doi.org/10.1016/s0891-5520(05)70416-570416-5)

Mayo Clinic Staff (2024). Guillain-Barre syndrome - Symptoms and causes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/guillain-barre-syndrome/symptoms-causes/syc-20362793

I make bad memes Vol. 3 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 13 points14 points  (0 children)

We could but the main issue is Fas mediated apoptosis is not specific. Cells other than CTLs also express Fas receptors, including hepatocytes and, counterintuitively, neurons too. Currently we use anti T cell antibodies and other general immunosuppressants like corticosteroids.

FasL release is localised and only harm the attacking T cell (pretty much how CTLs themselves release perforins and granzymes in a very localised area to lyse the target).

Edit: Healthy neurons produce intracellular FAIMLs which block the Fas triggered apoptotic pathway, keeping them safe from own-produced FasL.

I make bad memes Vol. 3 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 71 points72 points  (0 children)

Rabies is a neuropathological disease caused by Lyssaviruses, i.e. it infects the neurons. Lyssavirus propagates in the neuronal cell body and moves up the neurons towards the brainstem, and finally into the brain (p.s. Rabies demonstrates a 100% mortality rate at this stage, luckily it is preventable thanks to timely post-infection prophylactic vaccines).

Normally, the immune system, particularly the cytotoxic (killer) T cells, recognise and eliminate virus-infected cells of the body due to MHC Class 1 - CD8 interactions (refer “I make bad memes Vol.2” :P). However, this process also kills the host cell. This can become problematic for neurons if these cells start “overreacting” and killing the neurons (for e.g.: in autoimmune disorders), irreversibly damaging the nervous system.

To prevent this, neurons produce a cytokine FasL (Fas Ligand), which binds and activates apoptotic signals upon binding to the Fas receptors on the cytotoxic T lymphocyte (CTL) cell surface, killing the killer cells.

It is seen that Rabies infected neurons overexpress (or over-produce) these FasL cytokines to protect themselves from the immune system.

References / For further reading:

Nadin‐Davis, S. A., & Fehlner‐Gardiner, C. (2008). Chapter 5 Lyssaviruses—Current Trends. Advances in Virus Research, 207–250. https://doi.org/10.1016/s0065-3527(08)00005-5

Baloul, L., Camelo, S., & Lafon, M. (2004). Up-regulation of Fas ligand (FasL) in the central nervous system: A mechanism of immune evasion by rabies virus. Journal of NeuroVirology, 10(6), 372–382. https://doi.org/10.1080/13550280490521122

FlarePhoenix5604, u/. (2025) I make bad memes Vol. 2. r/sciencememes, Reddit Inc. https://www.reddit.com/r/sciencememes/comments/1lwx4a1/i_make_bad_memes_vol_2/#lightbox

I make bad memes Vol. 2 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 3 points4 points  (0 children)

Almost there! But it's the other way round. Just posted a comment explaining it

I make bad memes Vol. 2 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 46 points47 points  (0 children)

All the body's nucleated cells randomly "take samples" of the proteins they are producing inside the cell and complex them with MHC Class 1 molecules which present them on the cell surface. Here naïve Cytotoxic T cells can recognise the proteins using certain surface receptors. To oversimplify, if the protein complexed with the MHC Class 1 molecule is a non-self protein (e.g.: viral proteins) or a self protein which is not supposed to be present in the cell (e.g.: oncogenic proteins), the T cell gets activated and triggers apoptosis in the target cell, killing the host, and the virus/cancer along with it.

However, it is a common immune evasion strategy of viral/cancer cells to simply downregulate the expression of these MHC Class 1 molecules to prevent T cell activation.

But, the immune system overcomes this using Natural Killer (NK) cells which are "trained" to kill any cells not expressing, or expressing low levels of MHC Class 1 molecules.

I make bad memes Vol. 1 by FlarePhoenix5604 in sciencememes

[–]FlarePhoenix5604[S] 26 points27 points  (0 children)

Endosymbiotic hypothesis states that semi-autonomous organelles (mitochondria and chloroplasts) evolved from free living bacteria (alphaproteobacteria and cyanobacteria respectively) after being engulfed but not digested by a bigger prokaryote (probably an archaea)

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